William J. Dieckmann

Important procedures in the conservative treatment of eclampsia

Abstract Eclampsia is best treated by certain definite procedures which by their success or failure permit one to note the progress of the case. After delivery or death of the fetus a marked blood dilution takes place, during which period a diuresis occurs. Clinical improvement is closely associated with these phenomena. The eclamptic patient has an increased tolerance for glucose, probably due to the retention of chlorides found in pregnancy. The injection of large amounts of intravenous glucose solution will simulate temporarily at least the effect produced by delivery. The prognosis for the patient with a severe type of eclampsia is chiefly favored by delivery or early fetal death.

The hepatic lesion in eclampsia

I N DISCUSSING the etiology of eolampsia, a tliscxa,se which is charscterized by so n1an.y pathologic changes in various organs and in the blood and in which a large ov pressure. Also in Hinselmann’s monograph various aut,hors review important, facts regarding eclampsia. Bergell, who discusses the subject. from a chemical st,andpoint, reviews various existing theories and is forced to conclude that these views can only be definitely established as facts by much additional experimental work and further clinical observation. Recently Hofbauer, Louros, and Schmechel have given their attention to bhe production of pathologic lesions in the liver simulating the lesion of eclampsia. Lonros and Schmechel in reviewing the literature

American Gynecological Society Transactions of the Eightieth Annual MeetingTotal exchangeable sodium and space in normal and pre-eclamptic patients determined with sodium: Preliminary report☆☆☆

Abstract Radiosodium 22 with a half-life of 3 years is the ideal substance for determining the amount of sodium in the body and its elimination. The equilibration for sodium 22 as determined by the serum concentration and the total amount remaining in the body depends upon the sodium intake for the preceding period and days following the injection. The sodium space in patients who are ingesting 4 or more Gm. of sodium salts per day probably never reaches equilibrium. In the patient on a sodium intake of 4 or more Gm. per 24 hours, the radioactive sodium is no longer detectable by 14 weeks but in the patient on a sodium intake of less than 2 grams per 24 hours, the sodium was still determinable at the end of 18 weeks, and with a still smaller intake of sodium the turnover was still slower, reaching approximately 22 weeks. In the normal subject on an average or high intake of sodium chloride, although the turnover is more rapid, approximately 13 per cent of the injected sodium 22 at the end of 14 weeks is still unaccounted for and is probably stored in bone. A basis for comparing values between pregnant patients is extremely difficult, and will probably have to be based upon the total body water in the lean body mass. The sodium space is increased in normal pregnancy and markedly increased in pre-eclamptic patients and to a lesser degree in the hypertensive disease group. This is true whether one calculates it as the total sodium space, as the milliliters per kilogram, per centimeter of height, or per square meter of body surface. The total exchangeable sodium is increased approximately 10 per cent in the normal pregnant patient and is markedly increased in the pre-eclamptic patient as evidenced by a 32 per cent drop by the eighth postpartum day. The hypertensive disease group is characterized by a larger amount of total exchangeable sodium but if calculated on a per kilogram basis then the values are less than normal, indicating that fat does not contain as much water and electrolyte as does the lean body tissue.

Eclampsia without convulsions or coma

Abstract 1. 1. An unusual case of eclampsia without convuisions or coma is reviewed with special reference to some of its most outstanding clinical, laboratory, and postmortem features. 2. 2. Attention is again called to the prime importance of establishing and maintaining blood dilution in eclampsia. 3. 3. A possibly much more adequate therapeutic agent (acacia) for producing a more lasting hydration of the blood is suggested.

Further observations on the hepatic lesion in eclampsia

Abstract Although the lesion which has been produced in this series is not typically that of eclampsia, we feel that it is due to the coagulation of red blood cells in the portal vessels of the midzonal area with hemorrhage beginning at this point and a necrosis resulting in the involved tissue. In other words, the same mechanism produces this lesion which is apparently at work in the production of the lesion of eclampsia in the human. As a result of marked hemorrhage and necrosis as well as portal thrombosis produced in some of these cases, we think that substances which were absorbed from the intestinal tract and concentrated in the portal system overloaded this system under the conditions of the general circulatory injection of tissue fibrinogen and was an added factor in bringing about coagulation in the portal system within the liver. We feel that the idea of Mills that a marked shortening of coagulation time after the ingestion of a meal rich in meat protein is substantiated by these experiments. One of the striking features of lesions in this series was the rapidity with which extensive damage occurred in some of the cases. This is particularly well shown in Case 67, which is illustrated (Figs. 1, 2 and 3). This dog received 1 c.c. of lung extract one hour after a full meal and died three hours later and was autopsied at once. We feel that this might be evidence of the fact that when an extensive lesion occurs in human eclampsia it may occur rather abruptly and not over a period of a long time such as is characteristic of socalled preeclampsia. The period of so-called preeclampsia may be regarded as a precursor in most cases and a sudden production of a marked liver lesion might precipitate the attack of eclampsia. In concluding, although the lesions produced in this series are not entirely typical of hepatic lesions in eclampsia, we feel the mechanism of their production is similar to the lesion which occurs in the liver in human eclampsia and, therefore, we feel as we have stated in our first papers that we have further evidence that a hepatic lesion in eclampsia may result from a greater concentration of substances in the portal vein which can bring about thrombosis and which obviously must have their origin in great part from the intestinal tract. We also think this work further emphasizes the value of limiting the meat protein intake and the insistence on good intestinal hygiene in the patients in the last months of pregnancy, thereby averting at least the fulminating types of eclampsia.