554

ECLAMPSIAA Short Review of Recent Trends

By LESLIE B. PATRICK, M.B., Ch.B., F.R.C.S.Ed., F.R.C.O.G.Senior Consulting Surgeon, Jessop Hospital for Women, Sheffield

In Britain, the frequency of eclampsia hasdiminished steadily during the last 20 years, asjudged by the Registrar General's mortality ratesfor the hypertensive toxaemias of late pregnancy.In the City of Sheffield there were ten deaths dueto eclampsia 1936-I945, and four deaths 1946-1955. In consequence few obstetricians havehad the opportunity to make a concentrated studyof the newer methods of treatment. The carefulante-natal care which is given to almost everypregnant woman has shifted the emphasis to thetreatment of early pre-eclampsia and chronichypertension. Such cases adequately treatedrarely deteriorate to the extent of developingeclampsia, though fits do occasionally occur inpatients with only mild pre-eclampsia. Fulminat-ing cases, where there has been no obvious signeven a few hours before, and cases occurring morethan 48 hours after delivery, are also rare.There is no standard definition of imminent

eclampsia, though most obstetricians would agreewhen confronted with an individual case. Theominous symptoms of headache, visual dis-turbances, vomiting, epigastric pain, oliguria, and.rarely slight jaundice are well known but not alwayspresent. A raised blood pressure, albuminuriaand oedema are usually present but again there areexceptions. It is difficult to know the mostimportant single feature in a case of pre-eclampsiawhich is likely to progress to eclampsia. It isprobable that the level of hypertension is the mostimportant; a systolic blood pressure of I60 mm.Hg. is often accepted, and Norman Morris (I955)has stressed that o00 mm. Hg. is the importantdiastolic level.

EtiologyIt is not possible in the compass of this article to

discuss fully the theories of the cause of pre-eclampsia, but in view of the promise shownrecently by the use of hypotensive drugs in treat-ment, it may be useful at the risk of simplificationto examine how the method fits in with existingtheory.

It has been shown by Kellar and Sutherland(I941), that the hypertension of pre-eclampsia isproduced by a humoral agent, though the hyper-tension can be influenced by neurogenic means.For many years the placenta has been suspected asthe source of the' toxin.' Young (I914 and 1942)believes that autolytic products formed in redinfarcts of the placenta are the cause, but it isdoubtful if infarcts are commoner in eclampsiathan in normal pregnancy.More recently attention has focused on

ischaemia of the placenta causing anoxia of themulti-functional trophoblast leading to degenera-tive changes, which may influence the pre-eclamptic process. The mechanism by whichischaemia is produced has been discussed byseveral authors including Becker (1948), Bastiaanseand Mastboom (I950). Pre-eclampsia is com-moner in conditions where relative ischaemia ispresent, hydramnios, multiple pregnancy, primi-parity, obesity, essential hypertension and severematernal anaemia. Wettley (1938) found ahypoplastic uterine vascular system at autopsy inabout one quarter of cases of eclampsia. It isknown that blood oestrogens are at a low level inpre-eclampsia suggesting premature senility of theplacenta, or a hypoplastic vascular supply to theuterus in pregnancy may lead to an inadequatesupply of steroid hormones from the placenta forthe normal development of the uterine vessels.Bastiaanse and Mastboom sum up as follows:'toxaemia could be caused by any disturbance inthe normal relationship of the volume of bloodcarried to the placenta per unit of time, and thequantity of placental tissue. Toxaemia is thendependent on an absolute or a relative insufficientblood supply to the placenta .. In this way thetoxaemia of late pregnancy is a sign of insufficientadjustment of the mother's organism, especiallyher vascular system to the demands of pregnancy.In other words, the toxaemia of late pregnancy isa disease of insufficient adaptation.'Brown and Veall (I953), by measuring the rate of

radio-active sodium clearance from the placental

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November 1956 PATRICK: Eclampsia 555

circulation have shown that in pre-eclampsia andchronic hypertension the rate of maternal bloodflow is about one-third of the normal maternalplacental blood flow. Morris et al. (1955) carriedthis work farther by measuring the uterine bloodflow in normal and in pre-eclamptic pregnancies.They found that the effective blood flow is abouthalf the normal in mild, and only quarter thenormal in severe pre-eclampsia, and that it issomewhat decreased in twin gestation. They alsomeasured the effect of exercise upon the uterineblood flow and found that in normal patients it isalmost halved, and in pre-eclamptic patients it isreduced by about one-third. This is of greatsignificance as it is a common observation that thepatient who begins to show signs of pre-eclampsiahas been ' overdoing it' and conversely the mildcase often settles with bed rest. It is also acceptedthat rest prevents or delays the onset of pre-eclampsia in the chronic hypertensive. Morris(I955) also states that. from his observations thereduction in uterine blood flow appears to bedirectly related to the increase in diastolic bloodpressure; an increase of io mm. Hg. is associatedwith a clearance rate which is only half that of thenormal. In 84.1 per cent. of 63 eclamptics thediastolic blood pressure was Ioo mm. or over.In the Jessop Hospital, of 82 consecutive cases ofeclampsia in which there was a record of thediastolic blood pressure before the onset of fits82.9 per cent. had a diastolic blood pressure ofioo mm. Hg. or over.Thus it seems reasonable to assume that the

hypertension characteristic of pre-eclampsia isproduced by arteriolar spasm probably caused by ahumoral agent derived from an anoxic placenta.In the kidney this leads to glomerular changeswhich cause albuminuria, and a reduced filtrationrate.

Neurogenic factors may also play a part in renalpathology. Sophian (I953) has presented experi-mental evidence that the resistance of the uterus tostretching causes a utero-renal reflex producingischaemia of the type described by Trueta.

Endocrine factors are concerned in salt andwater retention. Hawker in a personal com-munication to Kellar (I955) believes that anti-diuretic hormone is increased during pregnancybut that its effects are held in check by an enzymederived from the placenta; and that a failure ofthis enzyme leads to the presence of active A.D.H.in the plasma of the severe pre-eclamptic. Lloydet al. (I952) and Hughes et al. (I954) have shownthat adrenal steroids are considerably increased insevere pre-eclampsia above that found at the samestage of normal pregnancy. It is well known thatadrenal steroids cause sodium retention; andthere is evidence that the adrenal cortex elaborates

a secretion which can maintain hypertension.The primary cause of the increase of adrenalsteroid in pre-eclampsia is not known.McCall (I949) has shown that Cerebral Vascular

Resistance is increased in pre-eclampsia, probablydue to vasospasm; yet the body maintains anadequate cerebral blood flow. However, cerebraloxygen metabolism is significantly depressedduring the coma of eclampsia.Theobald (I955) has stressed the importance of

dietetic deficiencies and mechanical factors (TheNutritional-Mechanical Hypothesis). The geo-graphical distribution, the decrease in frequencyfollowing better ante-natal care including diet, andthe occurrence of eclampsia three or four days afterdelivery lend support to this view.

Probably many factors are involved in theetiology of pre-eclampsia. Fatigue super-imposedupon and caused by mechanical factors associatedwith pregnancy, and sometimes nutritional de-ficiencies and developmental uterine vasculardefects may produce anoxia of the trophoblastwhich in turn by a humoral mechanism causes thewidespread changes associated with vasoconstric-tion and hypertension. In puerperal eclampsia,which is difficult to explain by any theory, is thereproof that no trophoblastic tissue remains in theuterus or possibly elsewhere ?

Mechanism of the Production of FitsAll cases of pre-eclampsia do not progress to a

stage of convulsions, and it is not clearly under-stood why some patients are more prone to con-vulsions than others. Stern and Burnett (i954)have enumerated the factors, any one of whichmay sensitize the patient: (i) A state of nervoushyperexcitability associated with the presence ofcerebral oedema. (2) An excessive retention ofsodium ions causing increased neuronal excita-bility. (3) A state of hypertension. The fitbeing a manifestation of hypertensive encephalo-pathy. Spasm of the central arterioles mayinitiate a convulsion. (4) A predisposition to fitsshown by cerebral dysrhythmia.

Rowntree (I923) has caused fits in dogs by pro-ducing cerebral oedema, but oedema is not alwayspresent in eclampsia. Tatum (1954) has shownthat there is a significant increase in sodium ionsin the oedema fluid in pre-eclampsia, but there isno increase in the serum. The effect of thissodium retention may be due to the production ofoedema rather than to an increase in neuronalexcitability. Damage to capillary walls and insome patients hypoproteinaemia may be otherfactors which produce oedema. Increased adrenalcortical activity in pre-eclampsia and its effect onsodium retention has already been noted. Hyper-tensive encephalopathy may occur in the absence

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556 POSTGRADUATE MEDICAL JOURNAL November 1956of oedema. Browne (1950) has suggested thatoedema and hypertension are complementary,convulsions arising if there is much oedemawithout hypertension or marked hypertensionwithout oedema. The immediate cessation ofconvulsions as a result of adequate hypotensivetherapy suggests that hypertensive encephalopathyplays a major part in the production of fits.

Dysrhythmia is found in about I2 per cent. ofthe normal population and in 90 per cent. ofepileptics between fits. It has been found in ahigh percentage of eclamptics. This led to theassumption that fits occurred in patients withcerebral dysrhythmia. James (I955) has pointedout that this concept of eclampsia would mean thatall cases of severe pre-eclampsia showing cerebraldysrhythmia should be dealt with radically andpromptly. He recorded the encephalograms of51 eclamptics from a few months to 14 years afterthe attack, and 52 patients with pre-eclampsia wererecorded as controls. Forty-three per cent. of theeclamptic tracings were abnormal and 28.8 percent. of the controls. He concluded that hefound no statistical support to the view thatelectroencephalography would be of direct valuein the choice of treatment in cases of pre-eclampsia;but thinks that repeated tracings on the samepatient would be worth while. Thus suggestingthat an observed change in cerebral rhythmwould indicate the probability of convulsions.

Pathological Lesions in EclampsiaThe lesions of eclampsia vary greatly in degree,

and, according to different authors, greatly infrequency. There is also some confusion becauseit is not always stated whether a pre-existingnephritic lesion was present. Naked-eye examina-tion of the kidneys may show a pale cortex andcongested medulla; the liver shows subcapsularhaemorrhages and scattered haemorrhages in thesubstance of the organ. In about one-third ofcases cerebral lesions may be visible to the nakedeye. These may be frank haemorrhages orpetechial haemorrhages into the grey or whitematter or the basal ganglia.There is some dispute concerning the patho-

genesis and the actual nature of the lesions as seenmicroscopically. In the liver the characteristiclesion consists of periportal haemorrhage withfibrin deposition and degeneration of the sur-rounding liver cells. Sheehan (I950) thinks thatthe renal lesion is essentially in the glomeruli; theendothelial cells of the capillary loops beingswollen and laying down a network of fine fibrils.The epithelial cells over the loops are also swollen.He thinks the basement membrane is notthickened. The main afferent vessel in the stalkof the glomerular tuft shows similar endothelial

fibril formation, whereas the afferent arterioleleading to the tuft is not affected. There is littlechange in the convoluted tubules, but the collect-ing tubules usually show obstruction by casts.Sheehan considers that the lesions may be due tointermittent spasm in the afferent arteriole or inthe glomerulus and that they may develop in afew days.Govan (1954) reports changes in the kidneys

comparable to those found in eclampsia in womendying during pregnancy or childbirth from causesunrelated to eclampsia.McKay et al. (I953) consider that eclampsia,

cortical necrosis and pituitary necrosis, show to avarying degree a common histological pattern.They stress the presence of multiple fibrin thrombiin the afferent arterioles and in the glomerular stalk,in the periportal blood vessels of the liver, in theafferent vessels of the pituitary stalk and in otherorgans. They failed to demonstrate these fibrinlesions in a case of uncomplicated toxaemia whodied as a result of spinal anaesthesia, but did findlesions typical of eclampsia in patients dying frombacterial infections with no evidence of pre-existing toxaemia. They suggest that these wide-spread lesions are an exhibition of the generalizedShwartzman reaction* and postulate that thepreciptating agent is a substance derived from theplacenta.They stress the idea, quoting Sheehan for

support, that there are two closely related but notidentical lesions with sufficient differences towarrant considering them separately; the firstordinary pre-eclampsia, a prolonged functionaldisturbance with little histological change and thatmainly in the kidney; the second, an acute patho-logical disturbance usually developing in patientswho have the first.

Place for Caesarean SectionApart from the case that fails to go into labour

after induction there is no place for caesareansection in eclasmpsia. Stroganoff taught that themembranes should be ruptured if the patient hadthree or four fits after the commencement oftreatment, and it may be necessary to rupture themembranes after the fits have been controlled. Itis probably true to say that today the continuanceof fits after treatment would indicate that thetreatment is inefficient.

*The generalized Shwartzman reaction is producedin non-pregnant animals by giving a ' preparing ' dose ofcertain toxins intravenously, followed by a second' provoking' dose intravenously. This second in-jection produces a reaction in many organs similar tothat found in eclampsia, cortical necrosis, etc. Inpregnant animals the generalized Shwartzman reactionhas been observed to occur without the 'preparing'injection.

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Some consider that caesarean section should bedone on the fulminating case of pre-eclampsiawhich does not respond to treatment. Also insevere pre-eclampsia there would appear to beanother place for caesarean section. In theJessop Hospital out of 193 cases of toxaemia inwhich a surgical termination of pregnancy wasdone, 51 were less than 36 weeks pregnant. Of these51, caesarean section was done 14 times andartificial rupture of the membranes 37 times.Three caesarean section infants and x surgicallyinduced infants were lost. In the 142 cases ofinduction over 36 weeks only five infants died.

Examination of the cause of death of infantsunder 36 weeks shows:-

51 cases under 36 weeksCaesarean Section 14. Foetal deaths 3:

Atelectasis 2, Broncho Pneumonia i.Surgical Induction 37. Foetal deaths 11;

Intra-cranial haem 5; I.C.H. No P.M. i; Intra-uterine death after A.R.M. 4; Prolapsed Cord i.The noticeable fact is that the deaths following

caesarean section are all due to post-natal condi-tions, and the deaths following surgical inductionare almost all due to intrapartum conditions, and,therefore, might have been avoided by caesareansection.

Examination of the case histories of the surgicalinduction group under 36 weeks did not show anysignificant difference in the length or severity oftoxaemia between those with live babies and thosewith dead. But the dead babies were almost allunder 4 lb. and the live babies were almost all over4 lb. On the other hand, of babies under 4 lb.delivered by caesarean section most survived.

This suggests that caesarean section should bedone on cases where severe toxaemia hasdeveloped comparatively early and is tending tobecome worse despite treatment-cases oftenabout 32 to 34 weeks, and in all cases where thebaby appears to be less than 4 lb. in weight.These babies are liable to intra-cranialhaemorrhage.There is support for this; Dieckmann and

Brown have shown that the toxic baby of ,000o g.(2 lb. 2 oz.) to 2,000 g. (4 lb. 4 oz.) has a betterchance of survival if delivered abdominally.New methods of treatment may reduce the

incidence of prematurity, but if it becomesnecessary to terminate the pregnancy while thefoetus is less than 4 lb., the above argument wouldstill stand.

TreatmentBecause the etiology is not known the treatment

of eclampsia has varied considerably even inrecent years. Attempts to eliminate toxins gaveplace to sedation or a combination of both, and

now hypotensive drugs are being used with thepromise of improved results.

It need hardly be said that rest and salt restric-tion and adequate nutrition are likely to remainbasic factors in prevention.Sedation

Nursing. During treatment by sedation goodnursing is essential and it is best to have the patientin a single room. It is not necessary for the roomto be darkened but the patient should be protectedfrom stimulation of the senses by sudden changesin the intensity of light, sound, or touch. If thereis pulmonary oedema the comatose patient shouldnot be left lying in one position for long, andshould be protected from injury during fits. Theairway must be kept free.

Treatment by sedation is associated with thename of Stroganoff. It aims at lowering thepatient's perception of stimuli and neuronalexcitability, thus stopping fits. If fits are allowedto continue the patient's condition usuallydeteriorates rapidly. Stroganoff induced heavysedation with morphine, chloral hydrate, andchloroform in addition for any manipulation suchas catheterization or vaginal examination. Latermagnesium sulphate replaced chloral hydrate andchloroform was replaced by other less toxicanaesthetics. Sodium pentothal, paraldehyde andother sedatives are also used successfully but allhave some disadvantages. McCall (1952) hasshown that heavy sedation, especially by the intra-venously administered barbiturates, depresses theoxygen metabolism of the brain. Sedation hasto be deep and patients with eclampsia often haverespiratory difficulty and diminished cough reflex.Broncho-pneumonia is a common complication.Collins (1955) recommends tracheotomy in caseswhere there is great respiratory difficulty. Itfacilitates the removal of bronchial secretions andthe administration of oxygen. Vomiting is some-times persistent with danger of inspiration ofthe vomitus; gastric suction is then necessary.

Chloroform is generally condemned because ofits toxicity but in our experience when it isproperly administered with ample air or oxygen,as an adjuvant to other forms of sedation, and onlyfor short intervals to facilitate manipulations suchas catheterization or vaginal examination, thematernal mortality is no higher than when otheranaesthetics are used. In the Jessop Hospital inthe ten years I940 to 1949, there were I 15 cases ofeclampsia with six maternal deaths, and of theseo10 cases were given chloroform with four maternaldeaths; the other two patients who died did notreceive chloroform. This maternal mortality ratecompares favourably with other records for thattime. Morphine is in every doctor's bag, and is

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most useful when eclampsia occurs in the patient'shome, yet it has a depressive effect on renalfunction (Kraushaar et al. 1949), and depressesmaternal and foetal respiration. Magnesiumsulphate acts as a depressant of the central nervoussystem and blocks muscular contraction producedeither by electrical stimulation or by drugs, butanimals are rendered unconscious before themuscles lose their ability to respond to stimulation.Through its central action the blood pressure islowered (Goodman and Gilman 1945).The results of sedative treatment in I,o7I cases

collected by Stern and Burnett, excluding Avertin,showed an overall maternal mortality of 7.56 percent. and in 840 cases the foetal mortality was29.17 per cent.The methods of sedative treatment are numerous

and it is not proposed to give details here.The use of Avertin or of hypotensive drugsalone or combined with basal sedation appear to bereplacing the Stroganoff treatment.Bromethol, 'Avertin'Treatment with Bromethol (Avertin) was re-

introduced by Dewar and Morris (I947) and themethod has been adopted in many hospitals. Thepublished results are better than by other sedativemethods. Working in a region which included alarge rural area they found that patients, after theinitial dose, could be transported long distances tohospital: no patient developed fits in the ambu-lance. Bromethol appears to be a powerful anti-convulsant. The improved results may be due toits hypotensive effect in combination with itssedative effect. The blood pressure drops by anaverage of 55 mm. Hg. after its use.The initial dose is about 0.0875 ml. per Kg. of

body weight of the concentrated bromethol fluid.This can be repeated if there are signs of restless-ness but it is usually three hours after the first dosebefore a second dose is necessary. A third or laterdose should not be given within a period of threehours following the preceding dose. More thansix doses should not be given. In preparing eachdose for rectal administration the manufacturersinstructions must be followed closely. It is madeup into a 3 per cent. solution in distilled water at4o0C. and must then be tested with congo red toexclude breakdown products, which cause pro-ctitis. If the rectal injection is given slowly thepatient will usually retain it. The drug takeseffect in about 20 minutes.

Stern and Burnett collected I49 cases treated bythis method and found the maternal mortality tobe 4.03 per cent. and the foetal mortality, 32.58per cent.

Hypotensive DrugsExtracts of veratrum viride have been used in

eclampsia for many years in conjunction with othertreatment, but the side effects were dangerous, andit was regarded as a desperate remedy. Veratrone,a purified extract containing many alkaloids, wasintroduced in I940. Stern and Burnett havecollected from the literature reports of 498 caseswith nine maternal deaths, a mortality of I.8I percent. This is a considerable improvement uponany other group collected from various sources.It should be noted that the hypotensive effect ofthe drug was relied upon without resort to sedativedrugs, though Stern and Burnett in their owncases gave Mag. Sulph. as well.

In comparing mortality figures it is well toremember that eclampsia appears to be less severein recent years. The mortality figures for sedativetreatment are improving. In the Jessop Hospitalthe maternal mortality 1938 to 1946, was 9.17 percent. of I09 cases and I947 to 1955, it was 3.8 percent. of 78 cases treated by magnesium sulphateCases treated by hypotensive drugs are all recentcases.

ProtoveratrineRecently, Puroverine, an extract of veratrum

album has become available. It contains onlytwo closely related alkaloids, protoveratrine A andB, the chemical difference between them being ofa minor nature. They are present in a constantratio of 2:1. These alkaloids are said to be foundonly in veratrum album. Since the first reports ofthe use of Puroverine in severe pre-eclampsia andeclampsia are encouraging, a brief summary ofits clinical and pharmacological properties isuseful.

I. A reduction in arterial blood pressureassociated with peripheral vasodilatation is in-duced by reflex mechanisms the most importantafferent receptors being in the region of the leftcoronary artery. The efferent pathway is notknown.

2. It induces bradycardia which can be abolishedby atropine without a significant reduction in thehypotensive effect. It reduces cardiac work.

3. There is a digitalis-like action on the de-compensated heart.

4. The peripheral vascular resistance of thekidney is reduced. Provided the decrease inblood pressure is gradual, renal blood flow is notdecreased. If the blood pressure falls too rapidlyrenal blood flow is transiently reduced.

5. A decrease in the cerebral vascular resistance.6. A reduction in peripheral resistance in fore-

arm and foot.7. The uterine blood flow in pre-eclampsia is

increased two or three times Morris (1955).An advantage of treatment by hypotensive

drugs is that the nursing is simplified because the

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November 1956 PATRICK: Eclampsia 559

patient remains fully conscious and co-operativeand there is no tendency to pulmonary embarrass-ment. Krupp et al. (I956) stress the need toadapt the dosage to the requirements of eachpatient. They aim at reducing the blood pressureto about I40/90 in severe cases and they noticethat albuminuria and oedema steadily decline afterthe commencement of treatment. Basal medica-tion given to all cases is 0.5 to I mg. of protovera-trine orally every two to four hours until the bloodpressure falls to the desired level. The usualmaintenance dose is 0.5 mg. every four hours. Incases of severe pre-eclampsia and eclampsia, inaddition to the basal dose, they give o.1 to 0.5 mg.protoreratrine intravenously in ,000o c.c. of5 per cent. dextrose in water at a rate of 30 dropsper minute. The rate of infusion is increased ifthe blood pressure has not fallen to the desired levelwithin 30 minutes. If within another 30 minutesthe blood pressure is still not responding o. I mg ofproveratrine is given slowly over a period of twominutes directly into the infusion tube. Thisinjection is repeated as often as is necessaryto maintain the blood pressure at the desired level.It is necessary to record the blood pressurefrequently.Toxic manifestations can usually be controlled

easily. Bradycardia responds to atropine andhypotension to ephedrine. If vomiting is trouble-some it may be necessary to reduce the dose but itcan usually be relieved by aluminium hydroxidemixture.

ApresolineApresoline has a potent hypotensive effect,

increases the renal blood flow and the cerebralblood flow. Its effect on the uterine blood flowis not yet known. Its mode of action is probablycentral and is different from other hypotensivedrugs. Side effects are common and increase asthe blood pressure falls but subside when fairlynormal levels are attained (McCall I952).Hexamethoneum

Morris (I955) thinks that the Hexamethoniumcompounds concentrate in the liquor amnii pre-disposing the infant to ileus or pneumonia.Therefore, their use should not be prolonged.Rauwolfia

This group combines a sedative action withhypotension and is useful alone or in combinitionwith other hypotensive drugs, especially inchronic hypertensive states in pregnancy.Summary

Reports indicate that the hypotensive drugs areof great value in the treatment of eclampsia. The

pharmacological action of protoveratrine andApresoline seems to be ideal for the treatment of thehypertensive states of pregnancy-depression ofblood pressure, increase in the cerebral and renalblood flow, and in the case of protoveratrine in-crease in the uterine blood flow. The first reportsare encouraging in regard to the mother, but notas yet in regard to the foetus. If the drugs can betolerated for long without the development ofresistance or unpleasant side-effect, there is hopethat their administration early in the disease bypreventing a decrease in placental blood flow maybe beneficial to the foetus as well, even if they donot alter the fundamental cause of the ischaemia.If placental ischaemia is the initial cause thenindeed we are at the beginning of a new era in thetreatment of pre-eclampsia and eclampsia.

BIBLIOGRAPHYBASTIAANSE, M. A. VAN BOUWDIJK, and MASTBOOM,

J. L. (1950), 'Toxaemias of Pregnancy,' Ciba Foundation:'e Symposium, Churchill, London.BECKER, J. C. (1948), J. Obstet Gynaec. Brit. Emp., 55, 756.BROWNE, F. J. (I950),' Postgraduate Obstetrics and Gynaecology,,

Butterworth & Co. Ltd., London.BROWNE, J. C. McL., and VEALL, N. (1953), J. Obstet. Gynaec.

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Brit. Emp., 54, 4I7.DIECKMANN, W. J., and BROWN, I. (I939), Amer. J. Obstet.

Gynaec., 33, 214.GOODMAN and GILLMAN (I94), ' The Pharmacological Basis

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GOVAN, A. T. D. (I954), J. Path. Bact., 67, 31I.HUGHES, E. C., LLOYD, C. W., JONES, D., LOBOTSKY, J.,

RIENZO, J. S., and AVERY, G. M. (1954), Amer. J. Obstet.e Gynaec., 67, 782.

JAMES, J. R. E. (I955), J. Obstet. Gynaec. Brit. Emp., 62, 704.KELLAR, R. J. (I955), Ibid., 62, 683.KELLAR, R. J., and SUTHERLAND, J. K. (1941), Ibid., 48, 487.KRAUSHAAR, 0. F., BRADBURY, J. T., WANG, Y. K.,and

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and AVERY, G. M. (1952), J. Clin. Invest., 31, Io56.McCALL, M. L. (1949), Surg. Gynaec. Obstet., 89, 7I5.McCALL, M. L. (I953), Amer. J. Obstet. Gynaec., 66, ioIS.McCALL, M. L., and TAYLOR, H. W. (1952), J. Amer. med'

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Lancet, i, 323.ROWNTREE, L. G. (1923), Arch. Intern. Med., 32, I57.SHEEHAN, H. L. (I950), ' Toxaemias of Pregnancy,' Ciba Founda-

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Co. Ltd., London.STERN, D. M., and BURNETT, C. W. F. (1954): J. Obstet.

Gynaec. Brit. Emp., 6i, 590.TATUM, H. J. (I954), Amer. 3. Obstet. Gynaec., 67, I97.THEOBALD, G. W. (I955), 'The Pregnancy Toxaemias,' Henry

Kimpton, London.WETTLEY (1938), quoted by Bastiaanse and Mastboom (1950).YOUNG, J. (1914), Proc. Roy. Soc. Med., 7, 307.YOUNG, J. (I942), J. Obstet. Gynaec. Brit. Emp., 49, 221.

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