Toxemias of pregnancy

TOXEMIAS OF PREGNANCY * FOSTER Associate

in Obstetrics,

Harvard

MedicaI

S.

SchooI;

KELLOGG, Assistant

BOSTON,

A

CLASSIFICATION

The necessity for a universaIIy accepted cIassification is evident. Without this we have the present tower of Babe1 state of the whole affair. Only by using a universal cIassification can we within a reasonabIe time accumuIate sufficient group data to raise treatment from the IeveI of individual opinion to that of a reasoned rationaIe. So essentia1 is the immediate need to estabIish and use such a cIass&ation that those to whom this phase of the subject has been of particuIar interest can. afford to make concessions to one another’s views. The more so in that any such classification must be tentative and that its perfection depends entireIy on how it works out in practice in many cIinics. This statement was proved Harvard

Medical

Obstetrician,

Boston

Lying-In

Hospital

to us when in the course of a few months experience with a “ paper predesigned index,” it became absoIuteIy necessary to aIter it to fit the cases as they appeared, I shaI1 Iimit my discussion to two cIassifications and try to show that except for terminoIogy and the incIusion or excIusion of certain debatabIe entities they are much alike and far from irreconciIabIe. Within the confines of these two cIassifications this ground may be covered compIeteIy. The best and most recent presentation and exposition of the WiIIiams-Stander cIassification is to be found in Williams Text Book,l 7th Edition, Edited by Stander, Chapter XXIX entitIed “The Toxemias of Pregnancy.” The headings in the order in which they appear are: (I) Vomiting of Pregnancy; (2) Acute YeIIow Atropy of the Liver; (3) Low Reserve Kidney; (4) Chronic Nephritis CompIicating Pregnancy; (3) PreecIampsia; (6) EcIampsia; and (7) UncIassified Toxemias. The previous chapter of this book is devoted to pyelitis and pyeIonephritis and is not Iinked in any way to this cIassification. Diagram I presents the most recent deveIopment of the Boston Lying-In Hospital Classification2 with figures resuIting from the first eighteen months study. The origina scheme from which this deveIoped is to be found in Irving’s “A Text Book of This cIassification has for its Obstetrics.“3 primary concept the division of a11 cases into two great groups; (A), those presenting certain or presumptive evidence of disease independent of pregnancy and (B), those presenting no such evidence. Group A is cIassified on the basis of the VoIhard and Fahr cIassification of the nephropathies modified to suit our idea of the needs in

of facts and theories concerning the conditions at times grouped under this title, particuIarIy considered from a cIinica1 and practica1 viewpoint, is here designed. The term “Toxemia of Pregnancy ” and its various derivatives-for example “Nephritic Toxemia”-shouId be abandoned. In its place should be used, on the one hand, “ PreecIampsia ” and “ EcIampsia,” suffIcientIy discreet entities when seen in pure form; and on the other hand, such individua1 conditions as in the Iight of existing knowIedge or opinion at any given moment it seems reasonabIe to consider in reIationship to preecIampsia and to ecIampsia, as for example “Essential Hypertension.” Th e compIete omission from consideration of certain aiIments of pregnancy often ascribed to “toxemia of unknown origin” may serve to emphasize my beIief that the term “toxemia” obscures and does not iIIuminate.

of Obstetrics,

Visiting

MASS.

SUMMARY

* From the Department

M.D.

SchooI and the CIinic of the Boston Lying-In

300

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No. 2

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of Pregnancy

pregnancy. Group B consists of the cornmonly accepted ones of preecIampsia and “ EcIamptic eclampsia (well called the CLINIC,

BOSTON

LYING-IN

HOSPITAL,

Hypertension

Group A-Evidence

of Disease

Independent

30 I

I

JANUARY

and/or Albuminuria

I,

1935-JULY

61 Cases

of Pregnancy

1936, 552

I,

CGES

of Pregnancy koup B-No Evidence of Disease Independentofpregnancy 491 Cases

I

PreecIampsia grade 414 cases

1 Nephropathies associated with arteria1 vascuJar -- disease Essential

Jor~rnnl of Su I~CI,L

them under separate headings, is unimportant. Whether one wishes to term the pigeon hole into which we f3e for future

DIAGRAM TOXEMIA

Amcricnn

1

i

hypertension

I

.I

hlalignant form form 7 cases 45 cases A. Cerebral change A. Endarteritis B. Cardiac failure Necrosis Uremia C. RfnaI faiIure ArterioscIerotic Kidney with uremia Benign

II Infiammatory I.E. nephritis Q , GIomeruIonephritis

I

Diffuse II Acute

nephropathies

II Preeclampsia 6j

grade II

cases

I

Pyelonephritis

I

Focal

I

I

Acute Chronic 5 cases

Chronic 4 cases III Degenerative nephropathies I.E. Nephroses 0 cases

I

I

A. ChemicaI poisoning B. Bacterial toxins

SpeciaI types A. Amyloid B. Lipoid

State” to emphasize identity) with a debatabIe group caIIed preecIampsia grade I. In the paper in which we first presented this cIassification we have discussed the Iimitations of this group.2 The discrepancies in these two cIassifications, if one reads carefuIIy the text which accompanies them, may be divided into those that are unimportant and those that are possibIy somewhat more important. Whether one prefers to incIude certain debatabIe entities, as for exampIe “Vomiting of Pregnancy,” or to regard

reference miId cases not yet studied far enough to identify “Low Reserve Kidney” or “Preeclampsia Grade L” is unimportant. The term “Low Reserve Kidney” is an academic one, and patients can only be so diagnosed sureIy months after deIivery. The term “PreecIampsia Grade I ” is a refusa1 to admit, particularly for teaching purposes, that any pregnant woman with hypertension and/or aIbuminuria can be trusted not to go on to ecIampsia. In practice each schooI is equaIIy vigilant of such a patient. “ EssentiaI Hypertension”

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and “The Arteriosclerotic Type of Chronic Nephritis ” mean the same thing. The difference is one of terminology. We prefer the former because the condition is presented to us so frequently first in pregnancy solely as a hypertension and because the term points to the diffuseness of the condition and away from kidney Iocahzation. PossibIy this may be considered as one of the more important differences. So we may concIude they are not basicahy so very different and that from them a generaIIy acceptabIe tentative classification might be fashioned. The Nephropathies (Group A). For a discussion of diagnostic criteria and difficuIties in this group (Diagram I) the reader is referred to our paper on cIassification.2 In summary to iIIustrate what we need to know I may make the foIlowing statements: (I) That in essentia1 hypertension with low hyperpiesis earIy in pregnancy, as for exampIe r~o/go at the third month, we have as yet no criteria on which to base a sufhcientIy sound prognosis to decide whether or not we shouId attempt to take the patient through pregnancy. If we try one of three things may happen: she may succeed-we do not know in advance at what cost; or she may fair, when in the effort to obtain a Iive baby we may find that we have done irreparabIe damage; or she may fai1 or succeed with no apparent change to her own heaIth. It is desirabIe that we shouId be abIe to predict each outcome in advance. (2) That acute gIomeruIonephritis as a compIication of pregnancy is extraordinariIy rare in our experience but that more careful study along the lines suggested by Dieckmann” may show it to be less rare than we think. (3) WhiIe we have the impression that mild cases of chronic gIomeruIar nephritis may pass successfuIIy through pregnancy we have as yet IittIe evidence to back up this statement. (4) That certain chronic glomerular nephritis is far less common with pregnancy than some other writers beIieve. (5) That pyeIonephritis in pregnancy in relation to the ecIamptic state is more

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FEBRUAHY, ,937

important than is currentIy beIieved. (6) That nephrosis is a hazardous diagnosis to make in pregnancy4 if we define this term as in our classification paper.2 It is apparent that the “nephropathies” (Group A) must be considered as compIications of pregnancy to be treated in present knowIedge according to the behavior of each individua1 case as it is observedthe uterus to be emptied by the best means depending on the obvious conditions in the patient and baby-in the event that she becomes worse in spite of medical treatment. It is I think, equaIIy true that some of these conditions must be viewed as we11 as etioIogica1 factors of the ecIamptic state. Etiolog~y oJ the Eclamptic State. It is impossible and undesirable here to attempt to cover a11theories concerning the etioIogy of the eclamptic state. An examination of recent contributions to this question shows the net resuIt to be an accumulation of a vast amount of interesting and suggestive data, with weak Iinks in every chain. It cannot be said that Hofbauer’s” deveIopment of the posterior pituitary theory of the cause of ecIampsia is not correct, but it can be said that it is not yet proved. FaiIure to find pressor and antidiuretic substances in the bIood of patients cIassed as “toxemic” by Hurwitz and BuIIock6 and Byron and WiIson7 show the weakest point in this thesis. Further work may prove that this faiIure is due to technical fault. Even so the identity of the two substances, i.e. postpituitary and the x of the ecIamptic bIood, remains to be shown. Various descriptions of pIacenta1 pathoIogy are advanced by different students in an effort to Iink these with the etioIogy of eclampsia. I compare, again for example and not to cover this heId, two recent sets of observation in the years 1932 to 1936. Tenny” observed a thickening of the basement membranes of the viIIi in ecIampsia and preecIampsia and Iaterg an increase over the norma amount and severity of syncytia1 degeneration in the toxemias sufhcientIy marked to be of diagnostic vaIue. BarthoIomew and Krackel”sl’

find changes in similar pIacentas in the form of infarcts akin to the choIestero1 induced changes in the coronary arteries of rabbits, (as shown by Leary) and on this basis have buiIt a compIete hyperchoIesteroI explanation of the ecIamptic state. Since these observations are things that can be seen under the microscope with the trained pathoIogica1 eye they have the merit--not universa1 in the reaIm of etioIogy of ecIampsia-of being soon proved or disproved. BarthoIomew and Kracke” furthermore state that “ hyperchoIesteremia is probabIy responsibIe for nausea and vomiting of pregnancy through an increased secretion into the biIe unti1 storage of this material can take pIace in the reticuIo-endotheIia1 system.” Whereas HayesI’ says, “I have treated” (by relief of back pressure by kidney peIvis drainage) “prior to deIivery 39 cases of pernicious vomiting, preecIamptic toxemia or ecIampsia. AI1 the mothers showed an immediate improvement after the kidneys were drained, and a11 uItimateIy recovered.” Nineteen of the 39 cases were pernicious vomiting. There is a marked discrepancy between the ideas here expressed, for if the former are right the Iatter shouId perhaps have drained the gaI1 bladder and not the kidney peIvis. Yet, Peters13t1” and others have stressed the reIationship of pyeIonephritis to preeclampsia, and remarkabIe as the cIaims of Hayes appear, it must be admitted that in our hands at Ieast the genitourinary aspect has been negIected. So has the matter of irridation of the pituitary and adrenaIs which is thought by some to offer possibiIities in view of reported good resuIts in essentia1 hypertension. l5 The primary etioIogy must be Ieft, by one who has no notion as to the cause of ecIampsia, in a quite confused state; the endocrines and the pIacenta having first caI1 at present, Ieading to “a disease vascuIar in nature best expIained on the basis of arterioIar spasm.“16 Certain factors acting as secondary or contributing causes must be considered. I

have referred to two aspects in which it seems wise to view the nephropathies, one as direct complications of pregnancy to be treated as each case behaves, the other as contributing causes of the eclamptic state. EssentiaI hypertension and suspected chronic gIomeruIar nephritis have been shown by Corwin and Herrick17 and Herrick and TiIIman’* to beIong in the Iatter category. Peters1”,14 especiaIIv has emphasized the causal reIationsh:p of pyelonephritis and the ecIamptic state. The exact and percentage reIationship between these conditions and the eclamptic state has yet to be worked out in a great group of ca,ses folIowed to autopsy; but a more or Iess genera1 acceptance of this point of view is aIready apparent, and hence, patients showing these conditions require the most constant observation possible if the existing state of the disease warrants continuation of pregnancy. Around focal infection has grown a voluminous Iiterature in this reIationship---both of itseIf directIy, and indirectIy, in reIation to pIacenta1 infarction and far fetched conclusions have been drawn from observations concerning this. For example, that, reIeased by foca1 infection, tyramine is responsible. “If we are able to produce convuIsive seizures in a dog by the use of tyramine, then we fee1 that the poisonous amines are responsibIe for the toxemias of pregnancy.“lg It may be said that each propounder of a compIete soIution of ecIampsia reasons somewhat in this fashion. The’ acceptance of one individuaI’s theory by the creator of a different one wouId be impressive but so far as I know this phenomenon is not yet recorded. However, the eIimination of obvious foca1 infection is heId by most obstetricians to be a wise prophyIaxis against the eclamptic state, aIthough PaImerzO has pointed out that foci of infection are somewhat more common in patients (non-pregnant) without hypertension than in those with hypertension. He further concIudes that the two chief etioIogica1 factors in hypertension are inherited predisposition and obesity. From

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a practica1 point of view it is my opinion based on experience that obesity is the most important secondary etioIogica1 factor in the production of ecIampsia. FortunateIy, obesity and fauIty eIimination, another important factor, can be readiIy prevented. Exposure to coId and wet, infections, worry, Ioss of sIeep and overwork and tiredness have repeatedIy been the immediate precursors of “toxemia.” The Diferential Diagnosis between the “ Nephropathies” and Preeclampsia as an Immediate Clinical Problem. It is apparentIy beIieved by some that the differentia1 diagnosis between the nephropathies and preecIampsia in pure form or mixed is aIways possibIe within the narrow time Iimit of one pregnancy. In our experience we have not found this to be true. The cIinica1 importance of so distinguishing it is sometimes not of great account at any given moment, opportunity for more proIonged observation without detriment to the patient often answers the question. Sometimes again an immediate differentia1 diagnosis is of great cIinica1 importance. For exampIe, a primipara with essentia1 hypertension of 14a/go at the beginning of pregnancy, at the thirtieth week has deveIoped headache, aIbumin, edema, subjective and objective eye symptoms, irritabiIity and a bIood pressure of 250/ 150. How much is essentia1 hypertension, how much is preecIampsia? What may we expect her to do? ShouId we try to carry the patient for another week or ten days in an effort to get a better baby that wiI1 probabIy be her Iast? WiII the baby die in utero if we do? WiII she have convuIsions; wiII she separate the pIacenta or have a “cerebra1 accident”; wiI1 she get cardiac decompensation? I do not know the answer to any of these questions. In this particuIar patient and with the advice of a pediatrician who said the baby was better off out of than in this woman, I did a hysterotomy, got a good Iooking and active baby weighing three pounds, five ounces. The pediatrician assured me the baby wouId do weI1, and it died; within twenty-four hours of massive

of Pregnancy

FEBRUARY. 193,

ateIectasis. Six months Iater the patient’s bIood pressure was 180/120. Was my judgment good or bad? In any event, a quick test to prove the presence or absence of a preecIamptic eIement wouId have pIaced me in a stronger position to decide the moment for interference. Another exampIe; Mrs. C., a para IV, thirty-nine years oId, entered the hospita1 JuIy 8, 1935, because of marked edema, dyspnea and orthopnea. She had three other Iiving chiIdren, a11 dehvered at home; the second one was induced for “edema.” She gave a history of hypertension and aIbuminuria before the fifth month in this pregnancy. Her IocaI doctor said she had no hypertension or albumin or cardiac symptoms before she became pregnant this time. On entrance, she weighed 301 pounds; she was thirty-two weeks pregnant; her bIood pressure was 200/120. The urine boiIed solid; and the specific gravity was I .037; urea cIearance was 45 per cent once and 144per cent a few days Iater. She remained in the hospita1 tweIve days under observation. During this time, everybody on reguIar and specia1 service saw her, and the diagnosis vaciIIated between primary hypertension with cardiac asthma, and myocardiaI insuffIciency (in an oIder day “cardiorenaI” disease) on the one hand, and preecIampsia, grade II on the other, or a mixture of both. FinaIIy because she seemed to be getting worse, irrespective of the diagnosis, I emptied her uterus with a bougie and pack. Four months Iater from another hospita1 came the diagnosis “subsiding gIomeruIar nephritis.” Her bIood pressure was then 100/80. She had no cardiac enIargement. Thirteen months after deIivery we observed her bIood pressure at 122/82; the urine showed norma urea cIearance and no aIbumin. PathoIogicaI examination of the pIacenta had shown “MuItipIe areas of infarction and necrosis. OId and recent hemorrhage, necrosis and atheromatous degeneration of arteria1 sinusoids.” So far as studied one year this patient had preecIampsia

after deIivery, grade II and

not the other suspected condition at the time of her deIivery. Had we had a sure method of diagnosing this patient, we wouId not have carried her so Iong as tweIve days

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while the preecIampsia got worse, to a point where her recovery seemed doubtfu1. ExampIes of the desirabihty of knowing

of Pregnancy

chart of Smith and Smith, original Charts 5 and 6.

sureIy and at once the presence of a preecIamptic eIement might be muItipIied. AI1 Iiver function tests are of no heIp. BIood vesse1 changes in the eye grounds except in the pronounced cases, give contradictory and not concIusive evidence in different observers’ experience. Rena1 function tests are not dependabIe. Urea cIearance is indeed of vaIue in foIIowing patients over a Iong period of time, but not in the Iast months of pregnancy. The diIution concentration tests give abnorma1 vaIues in norma pregnancy thus at present vitiating resuhs in this connection.21,22 The “coId test “23 gives different resuIts in different observers’ experience and does not disprove superimproved preecIampsia on hypertension any way. The posterior pituitary test

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of Dieckmann and MicheIz4 is likeiy enough a rea1 differentiation test, and is aIso interesting in the Iight of the posterior pituitary Chad 5 %rumOeildruwimz~ I FJ =Dmbel
CHART I. ProIan and estrin composite

A merican

,,__Lp-

Late

,T e n-uc + ( +$y,

I and 2 and dotted line, Charts

theory of etioIogy. However, the production of added oIiguria and added hypertension to the preecIamptic state seems too risky to make it appIicabIe. The possible production of acute puImonary edema or separation of the pIacenta as reported by them is too hazardous. BIood chemistry, specificaIIy increased uric acid in the bIood and diminished CO2 combining power fai1 frequentIy to identify the presence of preecIampsia. Recent work of Smith and Smith2” is interesting from the point of view of differential diagnosis. These workers regard their observations aIso from etioIogicaI and therapeutic standpoints. EtioIogicaIIy, it seems to me in their own words “a matter of conjecture,” and therapeuticaIIy viewed, it seems worthy of a

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triaI. As a test of the presence or absence of preecIampsia or (occasionaIIy in the differentia1 diagnosis of ecIampsia from other types of convuIsions associated with pregnancy) it seems immediately of great vaIue. Chart I, kindIy suppIied by the authors, shows their findings in essence. The eclamptic state aIone gives abnormaIIy high proIan and abnormaIIy Iow estrin curves as compared with those in the norma1 pregnant woman, the pregnant hypertensive and patients with chronic nephritis, and the pregnant diabetic. The high proIan has been observed to occur in at Ieast 6 cases six weeks before a cIinica1 diagnosis of preecIampsia couId be made. This would seem to show the test to be one of great deIicacy. A reasonabIe degree of accuracy in the test can be obtained in five days. From the point of view of etioIogy and therapeutics, they maintain that if the high proIan which is pIacenta1 proIan, together with Iow estrin, is responsibIe for the ecIamptic state, (the pathoIogica1 process invoIved being to their minds akin to menstruation), then the raising of the estrin IeveI by injections, may with its antagonistic action to the proIan Iower it and correct the imbaIance. Here again are a series of observations capabIe of check. PATHOLOGY

This section covers certain aspects of the pathoIogy which Hertig has presented to the staff of the Boston Lying-In HospitaI during his term of offIce in the pathoIogica1 department of that hospita1. ExampIes of fata cases of preeclampsia are rare in the Iiterature and are aImost whoIIy confined to those cases of so-caIIed “ecIampsia without convuIsions.” The onIy fatal case of acute preecIamptic toxemia studied at postmortem in this clinic was that of a patient who died suddenIy during an attack of cardiac asthma. WhiIe many of the pathoIogica1 fmdings, such as edema of myocardial stroma, marked puImonary congestion and edema, hydropericardium and biIatera1 hydrothorax, were Iinked with the sudden cardiac death, there were

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definite Iesions in the liver, kidneys and brain which differed in no way except in degree from those of fata ecIampsia. The aImost invariabIe subcapsuIar and periportal or porta petechial hemorrhages found in ecIampsia were present in the Iiver of this patient. EarIy degenerative Iesions, in much earIier state of deveIopment than those found in true ecIampsia, were also present in the Iiver (Fig. I). They consisted of fragmented Iiver coIumns, periportaIIy arranged, the ceIIs of which contained “ bird’s_eye bodies,” Iesions pathognomonic of ceI1 damage, aIthough the ceIIs had not yet reached the stage of necrosis. The renal gIomeruIar epitheIium and endotheIium were the seat of necrosis and fatty degeneration, whiIe the capiIIary tufts occasionaIIy contained fibrin thrombi. The basement membrane, however, had not yet reached the stage of irreguIar thickening shown by Be11 to be characteristic of ecIamptic kidneys. This suggests that the thickening is a secondary or at Ieast a later appearing phenomenon. PoIymorphonucIear Ieucocytes were present in moderate numbers within capiIIary Ioops of the gIomeruIi. The convoIuted tubuIes showed evidence of fatty and hyaIine degeneration whiIe their Iumina contained granular precipitate and damaged desquamated epitheIia1 ceIIs but no hemorrhage or hemogIobin casts. RecentIy we have had the opportunity to study a fata case of puImonary emboIism who had suffered from severe preecIamptic toxemia ten days prior to her death. The Iiver showed no Lesion other than a prefatty infiItration, and the kidneys showed no Iesion other than a pre-existing subacute pyeIonephritis. AI1 of the Iesions described in the preceding fata case of preeclampsia, compIicated by cardiac asthma, with the exception of the gIomeruIar fibrin thrombi, could have existed in the Iast mentioned case and yet have been repaired by the time the patient died ten days after deIivery of a disease unassociated with her toxemia. The absence of gIomeruIar fibrin thrombi in the Iast mentioned case is of no

h’,iw

,F,H,FS

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significance since these Iesions are by no means universal even in the kidneys of full blown ecIampsia. The following summary of the pathoIogical anatomy of ecIampsia was gained from experience with I I fatal cases, 9 of true ecIampsia and 2 cases of ecIampsia without convulsions. No significant difference was noted in the pathoIogy of the two cIinica1 types of toxemia. The hearts varied from 220 to 380 grams. Approximately one-haIf were negative grossIy and microscopicaIIy, but foca1 necrosis of the myocardium (2 cases), (4 cases), thrombopetechia1 hemorrhages sis of capiIIaries (2 cases), edema of the myocardium (2 cases), and fatty degeneration of the myocardium (one case) were encountered. The abnorma1 hearts showed varying combinations of these mentioned Iesions. The Iungs, with the exception of one case, showed varying degrees of congestion and edema, often accompanied by termina1 bronchitis and bronchopneumonia. The spIeens varied from I I 3 to 605 grams with the average above normal. In genera1 the consistency was soft and the puIp congested and hemorrhagic. In approximateIy one-half the cases evidence of a so-caIIed “toxic splenitis” was encountered: necrosis of stroma ceIIs in the foIIicIes, infiItration of these structures by a few macrophages, and the deposition of fibrinoid materia1 in the meshes of the invoIved foIIicIe. This picture is simiIar to that seen in diphtheria and in some cases of overwheIming streptococca1 sepsis. HyaIinization of foIIicuIar arterioles, seen in one-half the cases, is probabIy not a significant Iesion with regard to ecIampsia. The Iivers were usuaIIy of average norma1 size with occasiona ones weighing 2300 grams. No adequate expIanation was found for the Iargest since no appreciabIe except in one instance fat was present, when the Iiver was aIso greatIy enIarged. SubcapsuIar petechia1 hemorrhages were usually present as smaI1 coIIections of extravasated red ceIIs approximateIy I mm.

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in diameter, unassociated in the majority of cases, with the universaIIy present foca1 necrosis. The latter lesion varied in type,

from case of fatal prreckunpsia compIicated by cardiac asthma and pulmonal-- c~dcmx. Note fragmented, but non-necrotic liver cell columns in periportal distribution cytrnding out into lobule. x 170.

FIG. I. Liver

magnitude and distribution. Similar l-ariations have been pointed out by AcostaSisson in a much larger series of cases. The hepatic arterioIes were thrombosed in 2 of the cases suggesting very strongly a vascuIar pathogenesis of the “eclamptic liver Iesion ” in general and for these 2 cases in particuIar (Figs. 2 and 3). The foci of necrosis were periportal, mid-zona1 or centra1 with occasional combinations of various distributions. Necrosis aIone existed as we11 as necrosis associated with fibrin masses distending sinusoids. The kidneys aImost aIways showed enIargements, a soft consistency and varying degrees of cIoudy sweIIing. The gIomeruIi were usually swoIIen, ischemic, and showed irreguIar thickenings in their capiIIary waIIs due to thickening of the basement membranes, a finding first recorded by Be11 in

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1932. Less constantIy was the swoIIen endotheIium of the gIomeruIi infiItrated with smaI1 numbers of poIymorphonucIear

FIG. 2. Liver from a case of fatal ecIampsia without convukions. Note thrombosed hepatic arteriole and recent foca1 necrosis of mid-zonal distribution. x 170.

Ieucocytes in the capiIIary Ioops. In onIy one instance were there capiIIary thrombi. The convoIuted tubuIes inconstantIy were the seat of fatty and hyaIine degeneration and rareIy foca1 necrosis. OnIy rareIy were the coIIecting tubuIes invoIved. Three cases of ecIampsia were compIicated by pre-existing renaI disease; nameIy, one of vashydronephrosis and 2 of progressive cuIar nephritis (arterioIoscIerosis). The adrenaIs showed petechia1 hemorrhages in approximateIy one-haIf the cases, associated in one instance with necrosis and fibrin thrombi in the cortex. The uterus in over haIf the cases showed cornua1 and subserosa1 hemorrhages, usuaIIy biIatera1. This is of interest when it is recaIIed that a simiIar though more marked Iesion occurs in fuIminating toxic separation of the pIacenta. Then too, patients with preecIampsia and ecIampsia have

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separation of their normaIIy pIacentas more frequentIy than pregnant patients. The generic

FIG. 3. Liver from case of fatal ecIampsia with convukions. Note periporta1 necrosis associated with fibrin thrombi in associated sinusoids. There is necrosis of mid-zona1 region beyond. x 170.

reIationship between these forms of toxemia and toxic separation of the pIacenta is further shown by the fact that both these forms of toxemia may rareIy continue to biIatera1 symmetrica cortica1 necrosis of the kidneys. The brain in these cases of fata ecIampsia was usuaIIy the seat of a variabIe degree of congestion and edema, a finding noted by a11 observers. However, 3 of these cases showed no appreciable change of this IntracraniaI hemorrhage was a nature. cause of death in 2 of this series of I I cases and was present to a lesser degree in a third. These fata cerebra1 hemorrhages were in cases of pre-existing cerebra1 arterioIar scIerosis. FocaI lesions which have been described as occurring in the brains of ecIamptic patients (Diamond, 1936) were not noted. It must be stated, however,

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that a detaiIed neuropathoIogica1 study of these brains was not performed. Since these focal lesions are reported as rare and of gIia1 proIiferative nature, it is quite possible they were overIooked. Likewise, search for ganglion ceI1 changes were made but were not found aIthough such Iesions are reported together with aseptic meningitis and microgIia1 changes. BEHAVIOR

OF

THE

NEPHROPATHIES

AND

TREATMENT I. Essential hypertension (Group A I) benign and maIignant. Great difference in behavior of patients with essentia1 hypertension may be observed both in different patients apparentIy with the same degree of disease and in the same patient in different pregnancies. We have certain impressions with regard to differences of behavior depending on age of patient, and occurrence in clinic as opposed to private practice, but nothing reaIIy to substantiate these impressions. I beIieve we must have greater experience with the Iong time study of such patients, especiaIIy the “ maIignant ” since some of those considered group, “malignant” on earlier study seem so far not to have proved so. Treatment at present must foIIow ruIe of thumb indications as they appear. 2. Nephritis (Group A II). Our Iack of experience with acute gIomeruIar nephritis (or with its recognition) permits us to accept at present Dieckmann’s4 concIusions regarding it, and to attempt more frequent diagnosis on the basis of his findings. True chronic gIomeruIar nephritis with pregnancy has impressed us by its reIative rarity or the rarity with which we have been abIe to diagnose it. Since the chronic form may present varying amounts of renaI damage with exacerbations of renal insufficiency, it gives rise to many diagnostic diffrcuIties. This is particuIarIy true if first observed after the twentieth week of pregnancy. Many patients with this disease have compIete compensation of renaI function. However, with the added

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Ioad of pregnancy, certain degrees of kidney faiIure may be produced, The more severe forms are usuaIIy recognized earIy in pregnancy, and appropriateIy treated. Patients with minima1 or subcIinica1 chronic gIomeruIar nephritis may not show evidences of renaI insufhciency until after the twentieth week of pregnancy. In these patients the differentia1 diagnosis between chronic gIomeruIonephritis and preeclampsia appears to us on occasion to be impossibIe as the problem now stands (vide supra). OnIy in the foIIow-up of these patients can the uItimate diagnosis be made. It is our impression that the miIder cases of chronic gIomeruIonephritis often progress to a successfu1 termination of pregnancy. However, we wouId aIso emphasize that there is an occasiona patient in this group who may for the first time, Iate in pregnancy, show severe renaI insuffIciency with uremia, manifested by convulsions has and/or coma. That such a patient occasionaIIy been mistakenIy diagnosed as an ecIamptic there can be no doubt. We have seen one such case at autopsy. The management of chronic gIomeruIar nephritis compIicating pregnancy depends on meeting indications as they arise; the degree of renaI impairment checked at times against the duration of the pregnancy and estimated size of the baby in an effort to obtain a Iiving child. It is my impression that as a genera1 principIe it is wiser to take the smaIIest possibIe chiId that seems to have a chance to survive than to try to Iet it grow Iarger in utero because of the tendency to intrauterine death. This is the reverse of my point of view concerning the baby per se in essential hypertension. I have no evidence to support this contention, and this feeling is not shared by some of my associates. PracticaIIy, it works itself out in my mind, irrespective of the finer points of diagnosis, that it is safer from the point of view of intrauterine death to carry a patient with reratively high hypertension and low albumin than with reIativeIy Iarge amounts of aIbumin and Iow hypertension.

3 IO

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FocaI gIomeruIar nephritis is onIy a compIication of the pregnant state in pregnant women with septic endocarditis. We have seen one such case at autopsy. PYELONEPHRITIS

Reference to Peters’13J4,26 work has aheady been made. For many years I had observed at infrequent intervaIs a group of “pyelitistoxemia” cases of bad prognostic import without the slightest notion of cause and effect reIationship, considering them simpIy as coincidenta mixed types. The importance of his work in this fieId cannot be overestimated. It is comparabIe to that of those other internists, Corwin and Herrick and TiIIman,17Js for cIarifying the reIationship of the other nephropathies to the ecIamptic state. EIsewhere we have said of this group, Under the inflammatory nephritides we wouId add pyelonephritis which may occur in the acute and chronic form. From many sources attention is being caIIed to this type of kidney pathoIogy in the production in Iater Iife of hypertension which is many times associated with kidney faiIure. As a complication of pregnancy, doubtIess, too IittIe attention has been paid to it in the past, and we wouId emphasize the need for more carefu1 study of this group of cases with a view to a cIearer understanding of the reIationship between urinary tract infection and the “kidney of pregnancy.” So-caIIed pyeIitis is a frequent compIication of pregnancy, antepartum and postpartum. It seems certain that a number of these patients deveIop, or have developed, prior to the appearance of the “ pyelitis ” an infection of the true kidney parenchyma, which in certain instances has resuIted in permanent renaI damage. In the acute stage of pyeIonephritis, the cIinica1 course may simuIate severe pyelitis with or without renal failure which is usuaIIy transient. The amotint of permanent kidney damage is quite variabIe as it enters the chronic stage. Here the differential diagnosis from chronic gIomeruIonephritis is difficult. The presence of infectious eIements in the urinary sediment in chronic pyelonephritis in contrast at the same time to the meagre or absent hematuria and casts is most important. PyeIography may be

of Pregnancy

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193,

of some assistance. The routine kidney function tests and bIood chemistry are of value to determine the amount of kidney impairment. The treatment of pyeIonephritis in pregnancy shouId be to empty the uterus on faiIure of the patient to improve from an attack of “pyeIitis of pregnancy” within a reasonabIe time after the estabIishment of treatment by medica and genitourinary methods. That the condition may be extraordinarily dangerous in the present and in the future seems probabIe. Degenerative Nephropathies, i.e. Nephrosis. We believe that the diagnosis of nephrosis during pregnancy is an extremeIy hazardous one. Certain findings in this disease may be found in the norma pregnant patient, namely, high choIestero1 vaIues with Iowering of the serum proteins of the bIood, and the occurrence of doubIe refractory Iipoid bodies in the urine. Our experience with chronic nephrosis in pregnancy has been practicaIIy ni1. Such cases in the past as we have so diagnosed were probabIy, according to our definition (I) chronic gIomeruIar nephritis without renaI faiIure or (2) chronic gIomeruIar syndrome” nephritis in the “nephritic stage if they were observed before the twentieth week of pregnancy; or if they were observed after this (3) preecIampsia grade I. The question of chronic nephrosis and of acute nephrosis (Iipoid) is discussed by Dieckmann in an articIe previousIy mentioned.4 GROUP

B

I. Preeclampsia Grade I. We have defined this heading for cIassification purposes to cover cases in which there is no evidence of disease apart from pregnancy, which show hypertension and/or albuminuria without other signs or symptoms. 2. Preeclampsia Grade II. The same together with some or a11 the signs and symptoms commonly attributed to the preecIamptic state. 3. Eclampsia. The same as preecIampsia gra.de II but with convuIsions in addition, or occasionaIIy without convuIsions

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when such a patient dies in coma, and shows at autopsy a “shock”) identica1 with ecIampsia.

(or after findings

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A ntc.ric3nJournal 01 Surgrrv

3’1

very rarely, fuIminating-without warning. Since this is true, a weekly urine examination and a bIood pressure and Cons*

J Siam /;;\

,Iw*bxt, . Bf

&+-ma_

E~~Sqrni?FLIPS Tr~~~~$'i

DIAGRAM

II.The edamptic

I have made prior reference to the Group PreecIampsia Grade I and shaI1 omit it in further discussion in this paper. The cases either prove to be something eIse, remain as such, or go on to PreecIampsia Grade II. PreecIampsia Grade II and EcIampsia we beIieve to be the same disease except in degree (vide supra “ PathoIogy “). Signs and Symptoms. The we11 known signs and symptoms of reIative hypertension, aIbuminuria, edema, especiaIIy of the face, sudden weight gain, bIurring of vision, nausea and vomiting, constitute premonitory signaIs and sufficient cause whenever possibIe to hospitalize the patient. Increased respiratory depth, torpor and irritability, mental or motor, constitute the final danger signaIs. Epigastric pain, convulsions, coma, and death within thirty-six to forty-eight hours too frequentIy constitute the termination of the ecIamptic state. It is important to note that this condition progresses at different rates of speed, I.e., sIowIy in a matter of days or even weeks, rapidIy in a matter of hours, or

i

,;:"c'c I

state.

weight record every two weeks is the minimum requirement for proper prenata1 care. Even then, some “quick cases” wiI1 get off to a long start before detection. We have come to fee1 that borderIine diastoIic pressure, 90 to 100, is an important prognostic sign. If a patient shows any of these signs or symptoms and cannot be hospitaIized for observation because of economic reasons, a daiIy urine specimen and bIood pressure reading every other day constitute the minimum requirement. It is wise to consider the ecIamptic state in toto because on its usua1 behavior depends the rationaIe of the treatment of preecIampsia. EcIampsia is caused by pregnancy. It is a disease self-limited by the termination of its cause either by feta1 death or deIivery or both. Frequently the mother dies before these eventu;Iities occur. Sometimes she dies afterwards from a proIongation of the effect of the cause. EcIampsia is usuaIIy a rather sIow to appear (sometimes more abrupt) cuImination of a progressive state characterized by a

3 I2

American Journal of Surgery

KeIlogg-Toxemias

usuaIIy definite train of signs and symptoms known as preecIampsia. The course of most cases may be simpIy iIIustrated for the sake of our argument as is shown diagrammaticaIIy in Diagram II. Davis and Harrar27 state, “We find statisticaIIy that the sooner the woman comes to deIivery after her first convuIsion, the better are her chances of recovery.” Most authors find postpartum ecIampsia gives the Iowest mortaIity. In the Boston Lying-In HospitaI28 series antepartum ecIampsia had a mortaIity of 33.6 per cent, in intra and postpartum ecIampsia combined it was about 17 per cent. In our experience then antepartum ecIampsia is about twice as dangerous as the other types. MaternaI mortaIity in ecIampsia at the Boston Lying-In HospitaI since Ig 15 has never been Iess than 20 per cent under four different methods of treatment, three of them definiteIy conservative, in approximateIy I73 cases occurring in I68 patients. It was 26.6 per cent if we combine emergency and cIinic cases and severe and miId (Eden cIass&cation) cases. “The mortaIity was highest in the smaI1 group with known preceding hypertensive disease or nephritis, 61.5 per cent, intermediate in the patients with unknown past history 28.1 per cent, and Iowest in the group with ecIampsia known to be uncompIicated by preceding vascuIar or renaI disease 10.3 per cent.“28 I reviewed two series of 400 cases of “toxemia.” The mortaIity in the 25 per cent and 8 per cent convuIsive cases in the respective series was practicaIIy the same, nameIy, 25 per cent in each. The materna1 mortaIity in the non-convuI,sive cases was 2.5 per cent. From these figures certain opinions may be deduced. That we have saved no ecIamptics by altering our treatment of ecIampsia since the days Iong ago when accouchement for& was abandoned. That such women sick with severe “toxemia of pregnancy” as we have saved have been saved by stopping the progress of the disease before ecIampsia supervened by interruption of pregnancy. That when the

of Pregnancy

FEBRUARY, 193,

toxemic crosses the convuIsion Iine on the diagram (Diagram II), if she is in our hands, her chance of dying jumps from 2.5 per cent to 25 per cent. This is not to say that the convuIsions in themseIves are responsibIe for the muItipIied risk, it is onIy to say that they serve as an exceIIent index usuaIIy of the destruction aIready wrought by the disease. It is cIear that certain factors other than treatment enter into reported mortaIity of ecIampsia. These are: veracity of the reporter, seIection of reported cases and Iength of series, severity of the disease possibIy different in different pIaces and at different times in the same pIace, and time of hospitaIization. In any event, except in highIy seIected cases and those reported by men obviousIy taIking about something different from our sort is aIways of ecIampsia, the mortaIity appreciabIy greater in eclampsia than in preecIampsia. Since I use the convuIsion as an index of the severity of the disease and since the mortaIity muItipIies by ten for us or (three or five or seven for others) after convuIsions appear, and since remova of the products of conception is the first step in checking the condition because pregnancy is the soIe sure etoIogica1 factor, I concIude that I wiI1 attempt to empty the uterus of each case of preecIampsia before the patient has convuIsions. The first point to consider apropos of this is how to decide when to interfere. Reference to the diagram of the disease (Diagram II) regarded as a progressive whoIe shows, (as iIIustrated by the four point arrow) that patients either improve, stand stiI1 or grow worse in signs and symptomatoIogy under observation and treatment. As indicated by the position of the Iines broken for emphasis in my opinion torpor and irritabiIity, menta1 but especiaIIy physica1, best exempI&ed by the finger vaguely scratching at an itchy nose, index the Iast point at which one can interfere with a good chance that the patient wiI1 never cross the “convuIsion Iine.” In summary: I interfere on progressive signs and symptoms irrespective of the baby, especiaIIy

N17u SERIES Vol.. XXXV,

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KeIlogg-Toxemias

if I observe the preconvuIsion and precoma signaIs of irritabihty and torpor. The treatment of preecIampsia shouId be as radicaI as the treatment of ecIampsia shouId be conservative. I now discuss different features of the various medica treatments appIied to preecIampsia and what may be expected of them. I have the impression but am not sure that aside from a11 other cIassif?cations there are two distinct of preeclampsia, varieties from the point of view of medica These are preecIampsia of treatment. negIect and preecIampsia deveIoping in In those of negIect spite of good care. rather often good resuIts may be expected by hospitaIization and medica treatment. In those deveIoping in spite of good care, except usuaIIy for a transitory improvement, I have come to fee1 IittIe of permanent recovery can be expected from hospitaIization and medica treatment as a ruIe, and that the condition usuaIIy progresses aIong the Iines of the chart with varying degrees of speed. This point shouId never be Iost sight of in the history; based on it the noted usua1 transitory improvement in the cases deveIoping under good care may be utiIized, as soon as the subsequent down turn begins as a wise moment for interference of whatever sort seIected. The patient is thus “peaked” for obstetrica1 intervention. Many of the stapIe items in different wideIy accepted conservative methods of treatment when appIied to preecIampsia seem to me objectionabIe on the grounds that they tend to mask the very signs on which the prognosis of impending convulsions depend. On occasion, certain of them apparentIy precipitate the convuIsion. Morphia in any quantity produces torpor and its aftermath may be irritabiIity-thus the two cardina1 signs of impending convuIsions are faIseIy produced by its use in preecIampsia. Headache may resuIt from its use. Magnesium suIphate in quantity and concentrated given by mouth shouId and often does produce vomiting; 0nIy true preecIamptic vomiting

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American

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possesses prognostic significance. Thus the value of this sign may be destroyed by the free use of epsom saIts. Seven to fifteen watery movements each twenty-four hours is not conducive to rest and peace of mind so stressed as an essentia1 part of the “conservative treatments.” Epsom saIts in the frequentIy used causes Iarge amounts distention and an irritabIe bowel and perhaps a bowe1 more pervious to microorganisms if for any reason the patient comes to Iaparotomy. HirschfeIder2!j states that there is a cIinica1 syndrome of high pIasma magnesium accompanied by somnoIence or coma, and that this may be induced in patients with renal insufficiency by the ora administration of one or more purgative doses of epsom saIts and that many cases of coma in patients with renaI insuffIciency diagnosed uremic coma, may be simpIy magnesium coma induced by epsom saIts purgation. He states further: “Our experiments on animaIs showed that animaIs whose pIasma magnesium was onIy sIightIy raised (to .5 mg. or more) were much more sensitive than norma animaIs to ordinary doses of morphine.” Starvation and its kin the miIk diet shouId substantiaIIy increase the sometimes existing tendency to acidosis (or “reIative aIkaIinity “) common to a certain group of these cases. This indeed is readiIy controIIed by the gIucose needIe. NeedIes are an irritant and an exasperating psychoIogica1 prick to the not so sick feeIing patient with preecIampsia. The stomach tube may disturb the patient. ApparentIy, convulsions may be brought on by colonic irrigation. In short, certain common items used in the so-caIIed “ conservative treatments” of ecIampsia seem to me for these reasons to be objectionabIe when used in preecIampsia. I prefer to put the patient to bed in a singIe room, insure good sIeep in quantity, give a Iight mixed saIt free diet, move the boweIs adequateIy in a gentle manner from above and beIow, use baIanced ffuids, or if the patient is edematous, Iess intake than output, shut out reIatives and friends, watch her constantly by per-

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KeIIogg-Toxemias

sonalIy taken frequent bIood pressure readings and daiIy or bidaiIy persona1 urine observations suppIemented if possibIe by Esbach estimation of albumin, and trust to interference with the pregnancy on the grounds noted when and if it becomes necessary. I cannot see that it is the wisest course to treat any patient by a routine since each patient’s reaction differs to the same treatment. StiII Iess can I see the wisdom of permitting interference after an arbitrary interva1 of so many hours unsuccessfu1 medica treatment, since each patient “peaks” at a different time. In the instance of a preecIamptic patient entering a hospita1 apparentIy nearing convuIsions, distinct differences of authoritative opinion exist concerning the wisdom of immediate obstetrica interference as against paIIiative treatment for a period of time by conservative methods used in estabIished ecIampsia (pIasmapheresis or venesection, intravenous magnesium suIphate, morphia, etc.). There is much to be said on both sides. In defense of immediate intervention are the mortaIity figures quoted against anteparturn ecIampsia and in favor of the intra and postpartum variety. In defense of paIIiative treatment are two outstanding facts, (I) that the patient is a poor risk for intervention and it in itseIf may precipitate convuIsions, and (2) that briIIiant results on occasion are seen to foIIow pIasmapheresis or venesection, or magnesium suIphate intravenousIy or intramuscuIarIy, or in Iesser degree other conservative measures, in that the patient rapidIy improves and continues to do so. I am of the opinion that in principIe paIIiative treatment for a not set number of hours but unti1 the patient is “peaked” (or continues steadiIy to improve) is best. A study of my own cases shows that I have aImost aIways foIIowed this practice. On occasion, however, so certain has it seemed to me that the patient wouId deveIop ecIampsia that I have intervened forthwith in an attempt to force her into the intra or postpartum group with its better mortaIity. Such patients do not aIways deveIop ecIampsia; whether as a

of Pregnancy

FEBRUARY, 1937

resuIt of intervention or because they were not fated to is arguabIe. At times, I have had a feeIing that intervention with its usua1 accompanying drop in bIood pressure had (with immediate subsequent treatment) prevented ecIampsia. This point is a nice one and shouId not yet be argued too dogmaticaIIy. I have considered specificaIIy why interference is wise and when it is wise. We must now consider how it is best accompIished. This involves my persona1 experience. In my very beginnings it was stiI1 the custom to assembIe the Staff and take turns with the meta diIator to divuIse the cervix. The resuIts of this require no comment. From that we took to the Voorhees bag and when I graduated from the hospital I was firmIy convinced that the answer for a11 “toxemic” interference Iay in that soft instrument. After seven years experience with the bagged, conica1, untaken-up, partiwith accompanying aIIy dilated cervix manual diIatation, high forceps and version, torn cervices, bIeeding, and sepsis, I gave up the use of the Voorhees bag for induction in preecIampsia. I abandoned vagina1 hysterotomy after a short tria1 because of its Iimitation of appIication, its occasiona technica diffIcuIties, the reIativeIy Iong time I took at it and a high septic rate with it in our hospita1 at that time, and without trying muItipIe cervica1 incision because it did not appea1 to me, I adopted the pIan of emptying the uterus of a progressing case of preeclampsia, with anything Iess than the most favorabIe cervix (and these when I feIt convuIsions were imminent), by abdomina1 hysterotomy. Time, experience, and the reIativeIy successfu1 use of rupture of the membranes as opposed to the use of the bag for induction of Iabor has somewhat modified this practice-to what extent wiI1 be apparent. It can be said with certainty that the indiscriminate use of abdomina1 hysterotomy for preecIampsia wiI1 give worse resuIts in a Iong series of cases than rupture of the membranes with (or without if possibIe) the guarded use of a Iow pressor principle oxytocic. OnIy by careful attention to anaIgesics and anesthetics, to tech-

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nique, and to the hour by hour treatment of the underIying condition is abdomina1 hysterotomy a wise procedure even in selected preecIamptics. I think no sensibIe man chooses to enter the abdomen to deliver a patient who is obviousIy a poor surgica1 risk. A patient with bIood pressure of 200, soIid albumin, edema, frequentIy fat, is a poor surgica1 risk. The fact that forty-eight times I have done abdominal hysterotomy (about 23 per cent of a11 my sections) on somewhat such cases mereIy I have means that forty-eight times thought, in the Iight of my own and observed experience, that it was the best way out of a bad situation. I have aIways had misgivings. This does not mean that I section a11 cases of preecIampsia in whom I deem interference wise. In what I estimate to be considerabIy more than twothirds of the cases, circumstances of the mother in reIation to other Iive chiIdren and her condition and the state of the cervix permit me to induce the patient from below with the idea, especiaIIy if the baby is premature, of getting a normaI, nonoperative deIivery. In some instances, the patient fortunateIy goes into spontaneous Iabor whiIe under treatment and is then left strictIy aIone. The baby of a primipara diagnosed as a “ preecIamptic ” may be of extraordinary importance to its fami1.y in that it may be the patient’s onIy opportunity to have a chiId. This because in many instances of the sort, it is not possibIe to predict the fina situation of this mother in respect to the nephropathies, and on this depends in large part her prospects for other babies. So, too, in murtiparae who have Iost one or more babies in previous pregnancies associated with “toxemia” the baby may be of vast importance. However, it must be borne in mind that abdomina1 hysterotomy in preecIampsia does not guarantee a Iiving baby, especiaIIy if it be premature. CIifford30 has shown a 45 per cent mortahty in infants under five pounds in cesarean sections done for this condition; a mortaIity of 27 per cent in the infants in this group that weighed from four to five pounds.

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These figures are from the cIinic of the Boston Lying-In HospitaI. With regard t 0 maternal mortality figures in genera1 on abdominal hysterotomy in preecIampsia we have the foIIowing at hand: PIass 31 has shown recentIy a 6 per cent materna1 mortaIity in 67 sections for preecIampsia done throughout Iowa in 1930-1932. Smith32 of Boston reports a simiIar series of 57 cases with a materna1 mortaIity of 5.3 per cent. On the other hand, the writer, paying especia1 attention to anesthesia with the omission of a11 preoperative medication and a technique of operation which exposes the baby to practicaIIy no anesthetic and the mother to very IittIe, has performed 48 sections for severe preeclampsia with the death of a singIe mother, a rate of about 2 per cent. Of the babies in this series, 13 weighed between four and five pounds and were al1 discharged we11 from the hospital Babies under four pounds, 8 in number, were al1 thirty weeks or less and a11 died. Babies over five pounds, 27 in number, a11 Iived but one. The mother of this baby had preIiminary medication incIuding morphine forty-five minutes before operation. It may be added that 4 of the 48 preecIamptics deveIoped ecIampsia. The patient who died was in this group. She was an emergency patient who had been sick for four weeks before entering the hospita1. She had a plasmapheresis after deIivery with a Iow pressure, had to be transfused foIIowing it, remained in coma and died. Autopsy findings were such that it might be argued that she wouId probabIy have died irrespective of the method of treatment. Figures and comment on this series foIIows: PARITY

29

19

Primiparae .\lultiparae as follows: 12 Para II 2 Para III 3 Para 1v I Pal-a” I Para VI

48 Previous

19 muItiparae

Dead

Baby.

had a history

EIeven of the of a dead baby

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KeIIogg-Toxemias

in one or more previous pregnancies. Two other essentia1 primiparae gave a history of very earIy miscarriages. Previous Eclampsia. Five of the 19 muItiparae gave a history of ecIampsia in a previous pregnancy. One had had it twice before. Previous Toxemia. Nine other muItiparae gave a history of toxemia in a previous pregnancy. In two others, this was suspected but couId not be estabIished. Eclampsia in Subsequent Pregnancy. One patient deveIoped ecIampsia in a subsequent pregnancy. In her first pregnancy, I sectioned her in consuItation at short eight months with a five pounds, fourteen ounce baby. In her second her physician carried her nearIy to term with more pronounced symptoms and an eight pounds, eight ounce baby. She had six convulsions beginning nineteen hours after delivery and recovered. Recent figures from the New York Lying-In HospitaI are of interest in connection with this discussion. From 1932 through August, I 936, I 3 I preecIamptics and 26 ecIamptics were treated without materna1 mortaIity. ApproximateIy 30 per cent of the preecIamptics had pregnancy artificiaIIy interrupted. Of these interruptions, 22 were by Voorhees bag, bougie or artificia1 rupture of the membranes in about equa1 numbers. Sixteen had cesarean section but onIy I I of these were done primariIy for preeclampsia. It may thus be seen that in that hospita1 to date, twothirds of the artificia1 interruptions of pregnancy were done from below and onethird from above. In the preecIamptic series 9 babies weighing four pounds or more were stiIIborn, deadborn or neonata1 deaths, approximateIy 7 per cent. It is further interesting to note that the ratio between preecIampsia and ecIampsia in this series is 5 :I. This is quite different from the ratios reported in the origina series of 801 cases occurring in the Johns Hopkins HospitaI in the six years ending May I, 1929. In that series, preecIampsia was given 9.2 per cent and ecIampsia

of Pregnancy

FEBRUARY, *93,

per cent of the whoIe series. The present figures from the New York Lying-In HospitaI correspond more cIoseIy to our experience and fit in better with the idea of the quaIitative identity of the two conditions.33 So it may perhaps be concIuded that abdomina1 hysterotomy done with specia1 precautions, for special reasons, incIuding one’s own interpretation of what constitutes that mirage-Iike entity “the favorabIe cervix” has a pIace in the treatment of preecIampsia. But as a warning to enthusiasts for this procedure stands the apparentIy inevitabIe yearIy Iist in each state’s materna1 mortaIity statistics, “ToxemiaCesarean Section-Peritonitis,” and the opinion of sound, conservative obstetrics epitomized in the words of Irving. He says, “Cesarean section is rareIy justified in preecIamptic toxemia and is frequentIy an admission on the part of the obstetrician that his haste to evacuate the uterus has obtained the upper hand of his common sense and resourcefuIness ” unIess the patient has some other indication for section or is a primipara with a Iong rigid cervix. He says, “Patients so treated are just as IikeIy to have ecIampsia as those on whom Iabor has been induced.“3 One condition in pure preecIampsia deserves specia1 mention. TeeI, Reid and Hertig34 in a paper entitled “Cardiac Asthma and Acute PuImonary Edema as CompIications of Non-ConvuIsive Toxemia of Pregnancy” made a study of 6 patients with this syndrome and reached the foIIowing concIusions: (I) Six case histories are presented in which severe non-convuIsive toxemia of pregnancy was compIicated by sudden paroxysms of dyspnea accompanied by acute puImonary edema. In 5 of these cases the patient suffered from a simpIe preecIampsia without preceding hypertension or nephritis. (2) The attacks a11 came on in patients at bed rest under treatment, and cIoseIy resembIed cIassica1 cardiac asthma. (3) The immediate prognosis for patients who develop this symptom-compIex is grave. If they survive 12.5

and the early puerperium, the deliver? ultimate outIook as regards chronic cardiovascular and renaI disease seems to be good. (4) Left ventricuIar faiIure may be an important factor in the precipitation of these attacks of “cardiac asthma” in patients with severe preecIampsia. It may also pIay a dominant roIe in the production of acute puImonary edema in ecIampsia. The fact that a number of our preecIamptic patients recovered indicates that such Ieft ventricuIar faiIure is not necessariIy an agonal phenomenon. (5) If overIoading of the Ieft ventricIe pIays a roIe in the production of acute puImonary edema in certain of the severe and fata cases of preecIampsia some caution shouId be and eclampsia, exercised in the use of methods for rapid mobiIization of edema fluid in patients with severe toxemias of pregnancy as we11 as eclampsia. It might aIso be advisabIe to digitalize a11 ecIamptics and those patients with se\-ere toxemia over thirty years of age. It was my good fortune to deliver 3 of the recovered patients studied in this report, and to see one of these through a subsequent norma deIivery eight years later. Since such patients are reported rareI?; my cIinica1 impression of them may be recorded. They are muItiparae with obstetrica histories negative for “ toxemia.” They are in the thirties. They have immediate histories of proIonged preeclampsia, (1, 4, 2, 2, 5 weeks) with or without treatment. They have marked albuminuria, variabIe hypertension, marked edema, variabIe bIood uric acid (3 to 4.71, N.P.N. usuaIIy not elevated (27-46). In the 3 that I saw the symptoms of preeclampsia were so marked that I feIt interruption shouId have been done on genera1 principIes prior to the attack of cardiac failure. These cases for treatment must be distinguished from essentia1 hypertension with cardiac faiIure. Since the preecIampsia has been unsuccessfuIIy treated in these patients the only treatment Ieft is to empty the uterus. Common sense, and my experience with this smaI1 number of cases

indicates that treatment of the cardiac condition with morphia (?) and rapid digitalization should precede obstetrical intervention but that there should be no deIay once the patient is improved, since she may die in a repetition of the first attack and the underIying cause persists. As a matter of fact, this was accompIished in the 3 patients twice by rapid abdomina1 hysterotomy, and once in a three hundred pound woman by bougie and pack. These patients were very sick not onIy at the time of cardiac faiIure but in and around the period of deIivery. One was unquestionabIy operated without sufficient time for the treatment of the cardiac condition to be whoIIy effective. Aside from this, the most important practica1 considerations brought out by this study are (I) that too rapid mobiIization of edema fluid in preecIampsia is perhaps not without danger and (2) a probable expIanation of the way in which most ecIamptics die. Treatment of Eclampsia. It is the generaIIy accepted opinion that some one or other of the so-caIIed conservative routine methods of treating the ecIamptic state once the patient has deveIoped convuIsions (or coma) gives far better results than active obstetrical intervention. Further it is generaIIy stated that cesarean section is, next to the Iong abandoned accouchement for&, the method of treatment attended by the worst resuIts. Yet, one discovers that in most of the accepted routines, some form of interference is permitted after so many hours or days of conservative treatment if improvement is not noted or the patient grows worse; and in studying many series of ecIamptics treated ConservativeIy, on occasion the method of interference used appears to be cesarean section, so that we must concIude that it has a pIace, rareIy at Ieast, in the treatment of eclampsia also, after faiIure of conservative treatment. Late figures, quoting PIass again, show that of 84 cesarean sections done for eclampsia in Iowa in 1930-1932, 16 died, a mortality rate of 19 per cent. If we compare this materna1 mortaIity of ecIampsia treated by

318

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cesarean section all over one state, which perhaps imphes in some instances at Ieast a Iack of detaiIed care, with the figures given earher in this essay from an individua1 series treated in a variety of ways but practicaIIy a11 “conservative,” we find that these cases treated by section give equaIIy good resuIts as our “under observation” group and twice as good resuIts as the “emergency group.” No fair concIusion can be drawn from these comparative statistics for a variety of reasons. The purpose of stressing them here is to emphasize that method of treatment and method of deIivery in ecIampsia are two, on the whoIe, separate propositions though they sometimes interIock. The question of method of deIivery resolves itseIf into adding the least possibIe insuIt to an aIready heaviIy damaged body. From a practica1 point of view no deIivery at aI1, or norma delivery when possibIe, does the Ieast mischief. How much more ecIampsia a given patient wiI1 take and Iive, and how a given doctor views this aspect of the question is an individua1 matter, and no routine can be laid down that meets the requirements of a11 cases. This is justifiabIe criticism of a11 “routine conservative treatment.” Constant observation, treatment incIuding rest, and individuaIized action depending on the resuIts of these, wiI1 give the best resuIts in ecIampsia. Among the untoId number of remedies for and treatments of ecIampsia, two deserve specia1 mention. It has been shown that a reIativeIy smaI1 proportion of ecIamptic deaths resuIt from cerebra1 hemorrhage, perhaps IO per cent to 15 per cent. Such deaths are apt to occur in eIderIy women, probabIy with hypertension background. A few survive to die of Iung or other sepsis. The rest die of, or with, edema of the Iungs or brain, or both. The typica moribund ecIamptic is cIinicaIIy a cyanotic woman with wet lungs and running fluid from the mouth-the head lowered for drainage. As aIready stated, TeeI, Reid, and Hertig2* have shown that a few preeclamp-

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tics exhibit acute left ventricular faiIure, seemingIy the resuIt of the proIonged hypertension of the preecIampsia and not associated either with chronic nephritis or chronic heart disease. It seems IikeIy that the wet Iung moribund ecIamptic is in the same state for the same reason. From the frequent findings of cerebra1 edema at autopsy and the common cIinica1 observation of edema of the Iungs, it may be Iaid down as a sound principIe that any treatment which may increase edema is unsound. Hence, the theory of baIanced fluids or dehydration by stiI1 more fIuid Iimitation35,36 in the ecIamptic state deserves special consideration. Since it is known that the damaged kidney wiI1 excrete onIy what Auids its condition aIIows, more fIuids than this amount taken in must increase edema. If it is true on the above reasoning that increased edema is bad, then it may be reasoned that any agent which tends to reduce edema, within the Iimits aIready suggested, is good. It seems to me the use of magnesium suIphate intravenousIy or intramuscuIarIy most directIy fuIfiIIs this requirement. Stander states that 6 grams of the drug may be given in twenty-four hours provided not more than 20 C.C. of a IO per cent soIution are administered at a singIe dose. HirschfeIder, previously quoted in respect to mouth administration of epsom saIts in preecIampsia,2g specificaIIy states intravenous or intramuscuIar magnesium suIphate in the customariIy used doses is not open to the same objections as by mouth because the reIativeIy smaI1 dose does not resutt in dangerous concentrations of magnesium in the bIood. Lazard37 reports 225 cases treated by intravenous magnesium suIphate with a gross mortaIity of 13.3 per cent.* Schwarz and Dorsett38 of St. Louis (1930) report 186 cases of ecIampsia treated basicaIIy with intramuscuIar or intravenous magnesium suIphate with a maternal mortaIity of 7 per cent. McCord of AtIanta reports good * Lazard, Persona1 Communication, 328 cases, gross mortahty 12.8 per cent, corrected mortality approximateIy g per cent.’

Nt>w IEI
VOI..

XXXV,

No.

2

KelIogg-Toxemias

results by this method. Most impressive to me in American reports is the work of Rucker3” of Richmond. He has so treated I 27 consecutive ecIamptics40 with 6 deaths, a mortaIity of Iess than 3 per cent. He says of these cases (and publishes the findings of each case), “ In onIy two cases was I unabIe to stop convuIsions.” And further to show that his mortality is not a corrected one, “Of the six deaths that occurred in the 127 cases of the uItraconservative group, two were not treated uItraconservativeIy, two died of infections after the ecIampsra had subsided and onIy two were truIy ecIamptic deaths treated in the manner described.” Added weight is given to these results by comparison with two previous series in his own hands. Active intervention gave him a 31.6 per cent mortaIity. Morphine, venesection, gastic Iavage, coIonic irrigation and treatment otherwise conservative gave a 25.9 per cent mortaIity. In summary, I beIieve the treatment of ecIampsia, on the basis of necropsy findings and statistics in our present state of ignorance of the cause consists of magnesium suIphate intravenousIy, Iimitation of IIuid and not too rapid dehydration, rapid digitaIization and rest. By rest I mean Iack of continuous treatment and the use of the barbiturates if magnesium suIphate intravenousIy faiIs to insure quiet. Sharp individuaIization in method and time of delivery, without deviation from the mother’s interests for those of a probIematica1 baby, is necessary. No routine appIied either to medica or obstetrica treatment wiI1 give the best resuIts. I think that on occasion such divergencies from the suggested principIes as eIimination, morphia, plasmapheresis or venesection, gIucose solution exceeding the output, and even abdominal hysterotomy, wiI1 offer the individua1 patient the best chance. As in preecIampsia, a11 obstetrica manipuIations must take into account the matter of anesthesia-no anesthesia at aI1, i.e., IocaI must, at Ieast in theory and can frequentIy in practice, be used. SpinaI is debatabIe in pregnancy. Short gas oxygen with a

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very smaI1 amount of ether if necessary has in my hands seemed to do no harm in spite of theoretical objections. It s my conviction that the most popuIar so-caIIed conservative routine treatments of ecIampsia have been widely adopted and extoIIed not because of any great intrinsic merit. They are harmless relative to the method of abrupt and shocking jntervention which preceded them. They have lowered mortaIity in large measure by aboIishing this. Most items used in routines of treatment have a pIace at times in the treatment of this or that patient with ecIampsia to meet a given cond, tion and to be abandoned when the object has been accompIished. It seems absurd to treat a patient by posting on the waI1 a bIanket order for so much of this or that at such an hour irrespective of the way the patient responds. And more absurd when none of the therapy is specific. The cardiovascuIar and renaI sequels of preecIampsia and ecIampsia need extended study. What proportion of the group of patients showing these changes subsequent to the ecIamptic state got them as a resuIt of the toxemic pregnancy aIone is far from cIear. The oIder literature on the subject is familiar, some of it not convincing. For a recent consideration of the matter, in which certain fundamenta1 conditions are Iaid down for determining the truth regarding this question, the reader is referred to a paper by Tee1 and Reid.“b The behavior of patients in subsequent pregnancy has been recently considered by S. KjeIIand Mordre of 0~10” as foIIows: TI.e author deaIs with the much discusse,d question of the prognosis with respe~ct to subsequent pregnancies and parturitions in patients who had suffered from eclampsia previousIy. The materia1 comprises 61 cases of subsequent pregnancies and deIiveries in 48 ecIampsia patients, a11 of whom formerry had been treated in the gynecoIogica1 department of the Xiks-HospitaI in 0~10. Nine of these patic:nts were pregnant but free from symptoms. As to the rest the situation was

320

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as foIIows: Among 52 pregnancies ending with parturition 30 were compIicated by recidivations of pregnancy intoxications, as albuminuria, ecIampsism and ecIampsia in 18,5 and 7 cases respectiveIy. The severity of the recidivation was sIight in I I cases, medium in 5 cases and serious in 14 cases. One death occurred due to the premature detachment of a normaIIy situated pIacenta (abruptio pIacentae). As to the chiIdren definite information was avaiIabIe in 4g cases; 36 were aIive and viabIe, 28 of whom were mature; 2 premature but viabIe chiIdren died one and onehaIf days after birth; and I I were stiIIborn, whereof one was mature and 7 were viabIe, but most were macerated. The author strongIy emphasizes that the interruption of the new pregnancy (abortus provocatus) in most of the cases is not necessary. The question has to be soIved individuaIIy in each case, and he mentions a number of factors which he thinks to be of significance for the purpose (e.g. the blood pressure). This ends the consideration of those diseases which we have chosen to pIace in our cIassifIcation. For the sake of compIeteness certain other aIIied conditions may be spoken of in a brief and cIinica1 way. My experience with acute yeIIow atrophy in pregnancy has been smaI1; the cases so far as I know have died, except for two with saIvarsan Iiver. I have seen patients diagnosed as ecIampsia and as pernicious vomiting who were jaundiced, and I have seen 2 or 3 of these recover. It may be that the diagnosis shouId have been acute yeIIow atrophy, but how to make it unIess the patient dies, puzzIes me. In practice, I have always taken the attitude that a pregnant woman jaundiced had better be Ieft aIone ObstetricaIIy and treated medicaIIy if any basis for medica treatment couId be seen with the idea that if she had acute yeIIow atrophy, she wouId die anyway, whereas, if she had catarrha1 jaundice, she might die of hemorrhage if deIivered before she recovered. The patients with the saIvarsan Iiver that I had the opportunity

of Pregnancy

FEBRUARY,,937

to observe was sent to us from the genera1 hospita1 where they had obtained treatment, for immediate emptying of the uterus. The jaundice disappeared, and each gave birth to a chiId three months Iater. It may be noted that to empty the uterus is not a sovereign remedy for a11 medica iIIs in the pregnant woman. VOMITING

OF

PREGNANCY

The question of whether or not “pernicious vomiting of pregnancy” is “toxemic” is unanswered. The foIIowing resume of the pathoIogy in a smaI1 series of cases autopsied by Hertig at the Boston Lying-In HospitaI is presented as a contribution to this question. The pathoIogica1 Iesions of fata hyperemesis gravidarum have been generaIIy stated to be those incident to starvation. Inasmuch as the cIinica1 and pathologica pictures do vary somewhat, as judged by the 6 cases autopsied in this cIinic during the past tive years, this genera1 ‘statement wouId not seem to be entirely accurate. A brief survey of the pathoIogicaI findings of these 6 cases foIIows together with a specia1 reference to one case of Iate pernicious vomiting whose pathoIogica1 findings were signifIcantIy different from those in the other cases. The onIy possibIe significant heart Iesion in this series was edema of the myocardia1 stroma, occurring in 3 of the cases, including the “atypica1” one. The lungs were uniformIy the seat of a variabIe degree of puImonary congestion, usuaIIy moderate in amount. The spIeen, as in ecIampsia, showed gross softening, congestion and occasiona hemorrhages but in no case did it show evidence of the foIIicuIar fibrinoid Iesion seen in such “toxic states” as ecIampsia, diphtheria or streptococca1 infections. The Iiver change was predominantIy one of a fatty nature, there being fairIy Iarge amounts of fat in the centra1 portion of the IobuIes. Petechial, subcapsular and porta hemorrhages occurred in one-haIf the cases whiIe rare, isoIated, necrotic Iiver ceIIs were found in various parts of the IobuIe. There was no characteristic picture in the kidneys. The 5 earIy vomiters showed onIy old chronic pyeIitis and cIoudy sweIIing or cIoudy sweIIing aIone, but the Iate vomiter showed an entireIy differ-

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KeIIogg-Toxemias

ent picture in the kidney: gIomeruIar thrombosis, fatty degeneration of gIomeruIar epithelium and endotheIium, and foca1 necrosis of convoluted tubules with fatty degeneration thereof. The glomeruli varied from those with ischemia to those which were congested. The adrenaIs in haIf the cases were congested and contained petechia1 hemorrhages. The uterus

negative. The brain was was uniformly examined in onIy 3 cases and was negative twice, slightly edematous but without congestion twice, and edematous but congested once. In only one case (with congestion and edema) was there a toxic encephahtis: i.e., gangIion ceI1 degeneration, sateIIitosis about the ganglion ceIIs, recent capiIIary thrombosis, and perivascular Iymphocytic infiItration. It wouId seem, therefore, that the pathoIogica1 picture in toxic vomiting, at Ieast in our experience, is not as constant as in the other great group of toxemias; nameIy, ecIampsia and its aIIied types. That “toxic” changes in various organs such as the brain (toxic en cephaIitis), kidney (fatty degeneration of tubules and gIomeruIar thrombosis), to a lesser extent the liver (foci of necrosis), is evident from our smaI1 series. It wouId aIso appear that this type of toxemia is more variabIe, pathoIogicaIIy, but that much of the change seen in the average case could be ascribed to starvation and rapid postmortem autoIysis incident to the Iowered aIkaIi reserve associated with vomiting.

This bit of pathoIogy bears out the observed cIinica1 distinction between the common earIy and the rare Iate vomiters. Much is heard of the former, IittIe of the latter. The Iate (24-32 weeks) vomiter is a cIinica1 entity and a dangerous one. She may and usuaIIy has vomited too much or too Iong in earIy pregnancy and then her vomiting has stopped or is onIy occasiona1. More or Iess abruptIy, it has begun again and the patient enters the hospita1 sick and apathetic. In the past, partIy because of the rarity of the condition and partIy because a Iittle more time might give a baby developed enough to Iive, we have Iost these patients by procrastination. Such cases are not to be confused with acute yeIIow atrophy or with vomiting of preecIampsia, and I have aIways been at Ioss to know

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Journal ~1 Surgc.l-v

.American

32’

where to fit them in to the scheme of things. Judging by a comparison of these pathoIogica1 findings, they may be thought to represent a transition stage between earIy pernicious vomiting and the ecIamptic state. Where they uItimateIy fit remains to be seen. Treatment Pregnancy.

of

Pernicious

Vomiting

of

Over the period of my obstetrica1 experience, the treatment of severe vomiting of pregnancy has steadiIy improved. Fewer deaths have occurred and fewer abortions have been necessary to prevent deaths. With added individual attention to these patients and to each of the indications produced by the condition, and Iess resort to routine methods to be carried out by a variety of house physicians, our hospita1 resuIts in the Iast two or three years have shown a marked further improvement. Tube feedings (in the duodenum or the stomach) after sufficient sedation have directIy met the patients’ starvation. In the Iast 59 consecutive cases there have been no deaths and onIy 2 therapeutic abortions, a far better record than in any previous years. Patients that we formerIy wouId have aborted in desperation, many of whom no doubt, would have died, have recovered under this treatment, nor have we seen the patients as formerIy who, though they stopped vomiting, went on to die. Tube feeding permits the immediate administration of the vitamins protective against the neuritis of starvation. This method of treatment, furthermore, keeps down the number of deaths resuIting from reIigious convictions since the question of therapeutic abortion need seIdom be raised. TOXIC

SEPARATION IMPLANTED

OF

THE

NORMALLY

PLACENTA

Regarding this entity, I shaI1 onIy discuss the treatment. The concensus of opinion in America seems to be that the wisest treatment for toxic separation of the pIacenta, baby aIive or dead, unIess the cervix is fuIIy diIated is immediate abdomina1 cesarean

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section coupIed with immediate repIacement of Iost bIood by transfusion. For a Iong time I heId the same opinion and in a smaI1 series of persona1 cases had satisfactory resuIts, with the death of one woman onIy. She proved to have an ecIamptic Iiver at autopsy though she had no convuIsions. However, J. A. Smith32 reported from the Boston Lying-In Hospital on 42 toxic (of 76 cesareans done for separation of the normaIIy impIanted pIacenta) premature separations as foIIows : Since this group of 42 patients shows a mortahty of 21 per cent (9 deaths), they are reported in some detaiI. Roughly, one-third were primiparae. Two patients had convuIsions antepartum and both died. Thirty-six patients were deIivered by the cIassica1 operation with 6 deaths; 2 by the Kerr operation with one death (in this case hysterectomy was done seven hours after deIivery) ; and in 4 cases the Porro operation was done with 2 deaths. Thirty-nine were done under gas-oxygen, ether anesthesia with 8 deaths, 3 under IocaI anesthesia with no deaths, one under spina anesthesia with one death. Three fata cases and 3 recovered cases were transfused at the time of operation. One fata case was transfused on the seventh day and one recovered case on the twenty-eighth day. The essentia1 facts in the 9 fata cases are given briefly beIow. I. Para IX. Nephritis. OIiguria. Died on seventh day in uremia. No autopsy. 2. Para IV. Toxemia without convuIsions. Died suddenIy seven hours after operation without evidence of hemorrhage. PartiaI autopsy showed hemorrhages in Iiver and severe nephrosis. 3. Para II. ConvuIsions. OIiguria. Died on seventh day in coma. 4. Para I. Toxemia without convuIsions. Died on eighth day of peritonitis. Autopsy. 4. Para I. ConvuIsions. Died four hours after operation without evidence of hemorrhage. Autopsy showed Iiver necrosis. 6. Para v. Toxemia without convuIsions. Died in thirty-six hours, anuric, twitching, apparentIy on verge of convuIsions. No autopsy. 7. Para III. Toxemia without convuIsions. S uppression of urine. Died three hours after cIassica1 operation. No autopsy. Diagnosis shock. No externa1 hemorrhage.

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8. Para XII. Toxemia without convulsions. Oliguria. Died on sixth day. Sepsis and uremia. Autopsy. 9. Para v. Toxemia without convuIsions. Laparotomy seven hours after deIivery because of suspected interna hemorrhage which was not found. Uterus removed aIthough there had been IittIe externa1 bleeding postpartum. Died on third day. Autopsy showed acute hepatitis and pregnancy nephrosis. There are three noteworthy facts about this smaI1 group of patients. They have an extremeIy high mortahty; hysterectomy is infrequent, aIthough the opportunity afforded of removing the uterus has often been advanced as an argument for deIivering this type of case by cesarean section; there are no deaths cIearIy due to hemorrhage. There wouId seem to be a reasonabIe doubt as to whether cesarean section is the best method of deIivering these patients.

In connection with Smith’s concIusions, I may say that I have yet to be obIiged to take out a uterus in hysterotomy for toxic separation. With these figures based on a considerabIe experience with the worst type of cases, it was reasonabIe to seek some other method of treatment. The poIicy of doing sections was continued if the baby was in good condition and suffrcientIy advanced in pregnancy to grant its surviva1. Otherwise, tight cervica1 and vagina1 pack and pressure over the fundus in the form of a Spanish windIass (Rotunda treatment) is fohowed by expectancy and treatment of the patient’s condition as she requires. This automaticaIIy resuIts in treating the poor risk patient by the vagina1 route and reserves abdomina1 hysterotomy for patients in reIativeIy good condition with a baby which is of good size and which has shown no marked evidence of feta1 distress. Comparative statistics are perhaps not yet in order, but resuIts to date have been satisfactory. UntiI one sees for himseIf the working out of this procedure, he is sceptica1. PersonaIIy, from the opposite point of view, I am convinced that it is worthy of extended tria1. We know that some of these patients wiI1 die from their toxemia (vide Smith) no matter what is done, but by this method patients do not die of shock and

NFX

II.HIES

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XXXV, No. 2

KeIIogg--Toxemias

the added hemorrhage which is inevitabIy the accompaniment of hysterotomy. A Scotsman from Munro Kerr’s cIinic in Edinburgh, visiting the hospita1 this summer, said that often these patients ceased to bIeed after simpIe rupture of the memdeIivery took bra nes, and spontaneous place without packing, thus reducing the risk of sepsis. About this time I packed such a patient who was in very poor condition from blood 10s~. For twenty-four hours I treated the patient. Labor had not started at the end of this time, and I removed the pack with the idea of repacking. There was no bIeeding so I Ieft the patient as she was. Within the folIowing few hours, she delivered herself spontaneously without hemorrhage either during Iabor and deIi\.crJ- or afterwards. SUMMARY

No conclusions can be drawn from this It constitutes a highIy persona1 paper. picture of the probIems invoIved in “The Toxemias of Pregnancy.” Some progress has been made in the subject in the twenty odd vears that I have viewed it-much more-in the last ten years than in a11 the time before-but it is stiI1 in a far from satisfactory state as proved by the persistence of its materna1 and infant mortaIity rate. Further careful study is needed. PracticaIIy this shouId take the form first of an effort to approach it from a common point of view and with a common terminology, and second, group study shouId invariabIy be conducted by the cIoseIy knit cooperation and effort of obstetrician, internists especiaIIy interested in the cardiorenal aspects of the probIem, and the pathologic, metaboIic and endocrinoIogic Iaboratories. REFERENCES I.

H. J. Williams Obstetrics. Ed. 7. New York, D. Appleton-Century Co., 1936. 2. KELLOGG, F. S. et aI. Recent experience with a new classification of pregnancy complicated by hypertension and aIbuminuria. Am. Jour. Obst. and Gynec. (Feb.) 1937. ST~ASDER,

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