POSTGRAD. MED. J. (1966), 42, 188

THE DIAGNOSIS AND MANAGEMENT OFHYPERTENSION IN PREGNANCY

C. KEITH VARTAN, F.R.C.S., F.R.C.O.G.British Hospital for Mothers and Babies, Woolwich.

WHEN one uses the terms normotension andhypertension one must realise that the dis-tinction between the two is arbitrary andartificial. We know that the blood pressurereadings rise slightly with increasing age andscales of acceptable figures have been drawnup. Thus Pickering suggests the following:-Age 20-24 Systolic 100-130 Diastolic 60-85 mm.Hg.Age 25-29 ,, 102-130 ,, 60-85Age 30-34 ,, 105-135 ,, 60-88Age 35-39 ,, 105-140 ,, 65-90A gentle rise in the diastolic pressure over aperiod of 20 years, yet all within normal range.It is also acknowledged that variations occurin the same individual throughout the day andcan be affected by a variety of circumstances.Nevertheless the obstetrician is so well awareof the dramatic variations which take placein pregnancy that he must of necessity drawarbitrary lines between normal and raisedpressures and further subdivide the raised intomild and severe elevations in order that hemay observe what happens and learn how todeal with them.

There are a great many different possiblecauses of hypertension in pregnancy.

It may be secondary to phaeochromocytoma,or coarctation of the aorta or it may 'be a'legacy of acute or chronic nephritis, or be apart of Cusghing's syndrome and all of thesewill have to 'be considered if the hypertensionis severe, say 170/100 and upwards when thepatient first presents. These disorders are rarehowever and for the most part all we can sayis that a certain number of women have anelevation of their blood pressure above ourarbitrary standard of normality, without therebeing any discoverable cause -for it. It maybe familial or have'been acquired in childhoodpossibly by undiagnosed pyelonephritis. Mostobservers acknowledge that about 10% ofwomen are with these reservations classifiableas being hypertensive, and further that anadditional 15% will develop their hypertensionin pregnancy. These two groups are usuallydesignated 'chronic hypertension' and 'pre-eclampsia'.

Browne (1956) believes that pre-eclampsiaunmasks a familial tendency to hypertension.Robert Platit (1958)'s classic case of hyper-tension in identical twins, one a multipara andone a nullipara supports this. Epstein (1964)however went further than this and showedthat pre-eclampsia actually predisposed tohypertension. Gibson and Platt (1959) similarlyfound higher blood pressure readings 4 yearsafter pre-eclamptic pregnancies, than wouldhave been expected.A leader writer in the British Medical

Journal (1965) concluded his summary of'Pregnancy Toxaemia and Hypertension' withthe question 'Are words and their meaningsobscuring the truth?' Again in the same journal(1961) 'A misnomer can hardly ever beeradicated. In this same field the archaic andconfusing terminology of the so-called'toxaemias of pregnancy' 'has persisted overthe years though it has done little other thanprovide this aspect of obstetrics with an auraof obscurity'. Pickering has recom;mended ithatthe term 'toxaemia of pregnancy' 'be abolished.Lance Townsend '(1959) concurs.

In the author's view pre-eolampsia is acutehypertension. In some cases it unmasks achronic hypertensive tendency, in others itproduces it. The terms pre-eclampsia andtoxaemia are ripe for eradication.

DiagnosisIf we are to compare the normotensive with

the hypertensive we must adopt an arbitraryand personal standard. I personally use thefigures of 130/70 which were suggested byF. J. Browne in the 1930's. He is supportedin this by Hahn (1952) who reported a meanreading of 117/67 at the age of 15 in anextensive study of schoolboys and 'by Robinsonand Brucer (1939) reporting on blood pressurereadings from 11,000 persons and stating thatthe normal range of the systolic blood pressurewas from 90-120 'mm. Hg., and of diastolicpressure 60-80 mm. Browne's 'figure is neitherright nor wrong but it is realistic for in twoextensive studies of antenatal patients the author

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VARTAN: Hypertension in Pregnancy

has found twice that 900/, of women presentat the booking clinic with 'figures below 130/70.By using 'this standard then the patients

are divided into normotensive ;(900/,) andhypertensive (10%). Of the former group afurther 15% will develop hypertension, oedemaand proteinuria. These are usually calledpre-eclamptic, though in my submission thosewho develop these signs for the first time inpregnancy are acute hypertensives. Similarlya patient with established hypertension whodevelops oedema and proteinuria is usuallysaid to have developed pre-eclampsia whereasshe has really developed an exacerbation ofher hypertension. It is important to get nomen-clature right. Eden (1906) introduced the termtoxaemia to explain how -the patient was beingintoxicated by the waste products of foetalmetabolism added to her own, and the advicegiven was "to promote the free action of thevarious organs of excretion". At one period inhistory the Dublin School was famous for itsgastric and colonic lavage as the treatment forsevere 'toxaemia'. James Young devoted muchtime in an attempt to discover toxins in thered infarcts of the placenta which are nowacknowledged to be part of an impairedplacental circulation, in turn probably causedby an impaired myometrial circulation(Browneand Veale, 1953). The word "pre-eclampsia"was intended to draw the attention of thepractitioner to the fact that albuminuria ofpregnancv, as it was originally called, was aserious condition and might lead on toeclampsia. Yet it rarely does lead on toeclampsia and many cases of eclampsia arenot preceded by albuminuria. The term pre-eclampsia appears in the 7th edition of Edenand Holland's Manual of 'Midwifery (1931).If we could come to regard these artificiallyseparated conditions, pre-eclampsia and chronichypertension, as acute and chronic hyper-tension we would bring them closer togetherand perhaps even give them a commonaetiology.

AetiologyIt was shown by Pollak (1956) that 'pre-

eclampsia' had a specific renal lesion.McCartney (1964) investigated 14 primigravidaeclinically diagnosed as having 'pre-eclampsia'by means of renal biopsy, and found 5 to havechronic glomerular nephritis, 2 nephrosclerosisand 2 to have normal renal histology; 5 hadthe 'toxaemic glomerular lesion' described byPollak, and they state that the 'toxaemic

glomerular lesion differs significantly from allother'categories of patients'. 'It is characterisedby constricted glomerular capillary lumina,caused primarily by increase in the cytoplasmof the glomerular endothelial cells'. Pollakobserved that this change, unlike other renalpathology, was reversible. On this evidence thekidney is ischaemic in acute hypertension, andthe question to be answered is why? Sophian's(1953) suggestion is that the uterus resists beingstretched and that the ischaemia is producedrefiexly. To some extent iSophian too has 'beena victim of his own nomenclature in coiningthe phrase 'Utero-Renal Reflex' for many haveshown, amongst them Benjamin and Craig(1961), that it can occur in advanced extra-uterine pregnancy. But why not? The tubeis morphologically part of the uterus. Theauthor has also observed all the manifestationsof acute hypertension, as a post-operativecomplication where much blood had spilled intothe peritoneal cavity. Perhaps "renal-reflex"would have been a better term. Acute hyper-tension is virtually the prerogative of theprimigravida. 37 out of 45 primigravidae withmultiple pregnancy in the author's seriesdeveloped acute hypertension, a very highproportion. Increasing suppression of urine isa 'feature of the disorder, as is the diuresis whichfollows delivery. The work of Browne andVeal on the myometrial blood flow and ofDixon, Browne and Davey (1963) on thechorio-decidual circulation lends support to tb'-concept that the uterus is tense. Furthermorethe blood pressure falls after delivery and it isacknowledged to fall when the baby is dead,and liquor production presumably ceases andliquor is in fact concentrated. What is not yetacknowledged is that the blood pressure fallsand proteinuria diminishes when the baby isdying in utero, but if this is a valid observation,and I believe it to be so, then we have an easyclinical method of telling when the baby'slife is in jeopardy, always provided that thepatient has not been given hypotensive drugsand diuretics which may produce the samepicture, yet without affecting the outcome.Why some 15% of apparently normal women

should have a uterus which is unable to fulfilits function without causing renal ischaemiais another problem. Duncan, Baird andThompson (1952) calls this state of affairs'physiological failure' and hints at deficienciesin the nutritional and general health of thepatients 'not merely during pregnancy butalso during growth and adolescence'.

In this connection the geographical distribu-

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190 POSTGRADUATE MEDICAL JOURNAL March, 1966

tion of eclampsia in the British Isles is interest-ing. It is highest in Aberdeen, four times ashigh as in London. The incidence falls in factquite steadily from north to south. Perhapsthis is accounted for by variation in thestandards of living from North to South whichcould contribute to this variable physiologicalfailure.

There are of course a great many othersuggestions concerning the aetiology of'toxaemia.' In fact it is called the disease oftheories. Space does not permit me to go intothese seriatim. Sophian (1958) however has re-viewed them in Excerpta Medica giving 142references and anyone anxious to cover thisaspect of the disorder is referred to this paper.Symptoms and ManagementThe orthodox symptoms of hypertension in

pregnancy are well known but Katharina Dalton(1957) drew attention to the fact that only7% of toxaemia patients were free from suchminor disturbances as lethargy, headache,

irritability and depression. The managementconsists in organising regular ante-natal visitsand also in ensuring that the patient co-operates.At these visits the patient's weight and herblood pressure are recorded and the urinetested. The hypertensive is advised to rest.In some areas free home-help services areavailable to enable them to do this. A sedativemay be prescribed to ensure sleep. A drop inthe blood pressure readings during the mid-pregnancy months is a good prognostic signhowever high the initial reading may be.Admission to hospital is necessary if protein-uria occurs; some may be admitted for hyper-pyesis and oedema without proteinuria. Patientsare admitted for rest and observation and forsuch treatment as may be called for. The restis absolute for the first few days during whichtime the pressure will fall to its basal level.This is presumed to be due to the improvedrenal circulation. Now the patient is allowedup for part of the day. The effect if any onher pressure will be noted and acted upon.

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c,",-,--ILA FIG 1.--Chart showing a steady rise in both systolicand diastolic ibloo,d pressures and an increase inproteinuria. A chart of good ,prognosis.

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March, 1966 VARTAN: Hypertension in Pregnancy 191

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FIG. 2.--Chart showing a stationary level of both systolic and diastolic blood pressures and amore or less even level of proteinuria. A chart of the ul'timately, "small for dates"live babv.

The observations are of the systolic anddiastolic pressures. These are recorded at thesame times every day. The quantity of albumenin the urine is recorded. An Esbach's urino-meter reading every 24 hours is accurateenough for this purpose. The urinary outputis also recorded daily. The weight is recordedonce a week and the foetal heart is auscultatedas often as necessary.

Broadly speaking the charts will show oneof four trends, after the initial settling hasoccurred.

1. The pressures may gradually rise togetherwith the quantity of albumen passed. (Fig. 1.)

2. The condition may be static and therecord a horizontal one. ,(Fig. 2.)

3. The pressures may first rise then fall.(Fig. 3.)

4. The records may show a fall from thestart.On Sophian's theory these can be interpreted

thus. 1. The baby is growing, and liquor pro-duction is normal. The uterus is being increas-ingly stretched. 2. The baby is not growingthough it is alive. Ultimately it will be seento be 'small for dates'. 3. and 4. mean thatthe baby is dying, the liquor is not beingproduced, is in fact being absorbed and thetension in utero is lessening.

This is why with reservations I personallyadvocate no hypotensive drugs Ibeing given,or diuretics either. Furthermore Dixon andothers have shown that hypotensives do notaffect the choriodecidual blood flow. Agar,Barrett and Exley (1958) noted the failure ofganglion-blocking agents to produce improve-ment, and noted fatal ileus in a prematurebaby probably attributable to the mecamyla-mine which had been given. In fact all observersstate that hypotensive drugs do not improvethe prognosis for the child. Watt and Philipp(1960) recording five cases of intra-uterinedeath while their patients were being givendiuretics noted that the blood pressure hadfallen and the oedema had lessened and theycame to the conclusion that 'two valuablesigns of toxaemia of pregnancy are minimisedor lost while the toxaemic process continues.'MacGillivray, Hythen, Taggart and Buchanan(1962) showed that sodium diuretics had littleeffect on the progress of the disease. Morerecently, however, methyldopa has been shownto be beneficial in some series (see Hamilton,p. 195).

Sedatives are allowed if the patient is fretfulor sleeping poorly in her new surroundings,but they do not affect the progress of thedisorder.

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192 POSTGRADUATE MEDICAL JOURNAL March, 1966

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FIG 3.-Charts showingthe reversal of !thetrend of systolic anddiastolic pressures inthe week precedingthe still birth. (In alleharts, solid blocksindicate albumenm.g. 1 litre).

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March, 1966 VARTAN: Hypertension in Pregnancy 193

In-patients are given a diet of 125 g. ofprotein daily, low carbohydrates and no addedsalt. Chronic hypertensives may be allowedhome after a period of rest but the acutehypertensive is too unpredictable and must bekept under vigilant observation till delivered.The reservations mentioned above refer to

the severer degrees of hypertension, say 180/110 to 210/120 which may be encountered,often around the thirtieth week. Here the chanceof obtaining a live baby is very remote. If thenthe patient develops symptoms such as con-fusion, visual disturbance or headache, shemust be given hypotensive drug therapy toprevent a cerebro-vascular accident. For thispurpose methyldopa 1-2 g. daily is suitable.Intra-uterine death not infrequently occurs inthese cases.The goal is to get the patient near enough

to term to be able to terminate the pregnancy,for this is exacerbating her blood pressure.This is to be balanced against the risk of losingthe baby from prematurity. In practice thethirty-eighth week is a reasonable target.Pregnancy may of course have to be terminatedvery much earlier, often as early as 29 or 30weeks, in acute hypertension. In this case thebaby will almost certainly be lost, but thepatient's recovery will be more complete thanif the acute process has been allowed to dragon. The risk of the same thing happening asecond time is fortunately minimal.

Caesarean section should not be practisedunless the baby has a good chance of survival.A stillbirth is easier for the mother to acceptthan a neo-natal death, and a premature babyhas probably as good a chance of survival bornnaturally, as it does when born by section.Low amniotomy is therefore performed, andif necessary a syntocinon drip infusion can beset up. If this seems to exacerbate the pressurethen a hypotensive e.g. mag. sulph. 10 ml. ofa 20% solution can be given.

After delivery the blood pressure must berecorded frequently until the patient has hadher diuresis. Hypotensives have an importantrole at this stage in preventing post-partumconvulsions.

Convulsions (eclampsia) are believed to becaused by spasm of the cerebral arterioles.This has been produced experimentally byfeeding salt to rats with hypertension. It isnot proposed to deal in detail with the manage-ment of these cases. Most are preventable byvigilant ante-natal supervision, and by promptamniotomy. If they do occur then heavy seda-tion is advocated and delivery probably by sec-

tion as soon as the condition is under control. Ifthe patient is in labour delivery can be awaited,with emphasis on keeping the patient's airwayclear and supplying oxygen to prevent anoxia.After delivery the severe renal ischaemia mustbe visualised. Diuresis will almost certainlyoccur spontaneously but if there is anxietyan infusion of 25% dextrose can be of help.As to prognosis, most investigations have

shown thatt there is a quantitative relationshipbetween blood pressure and infant mortality,and that the risk increases when proteinuriaappears. When the diastolic pressure is below100 the foetal wastage is little higher thannormal. Landesman (1955) gave these figures:For mild hypertension (140/90 to 179/99)1.7°/% but for more severe degrees (180/100and over) 23%. He further states that with'super-added pre-eclamptic toxaemia' thefigures are 16.4% and 28%. This emphasiseswhat has been said earlier that the prognosisis worse in acute than in chronic hypertension.As to the prognosis in the woman, Gladys

Dodds states that the outlook for futurepregnancies in hypertensive women is favour-able below the age of 30, but becomes lessgood after the age of 35. This contributionshould 'be read in full. In fact those interestedin further reading should study all of the papersin the 'Symposium on non-toxaemic Hyper-tension in Pregnancy' which contains contribu-tions from over 50 authors amongst whom aremost of the important contributors to this veryinteresting subject.

REFERENCESAGAR, H., BARRETT, C. T. H., and EXLEY, K. A.

(1958): Experiences with Mecamylamine inHypertensive Complications of Pregnancy, J.Obstet. Gynaec. Brit. Emp., 65, 378.

BENJAMIN, F. and CRAIG, C. J. T. (1961): UterineDistension and Pre-Eclamptic Toxaemia, Obstet.Gynaec. Brit. Cwlth., 68, 827.

BROWNE, F. J. and SHENMACK, D. R. (1956):Chronic Hypertension following Pre-EclampticToxaemia. The Influence of Familial Hypertensionon its Causation, J. Obstet. Gynaec. Brit Emp.,63, 677.

BROWNE, J. C. McD. and VEALE, N. (1953): TheMaternal Placental Blood Flow in Normotensiveand Hypertensive Women, i. Obstet. Gynaec.Brit. Emp., 60, 141.

DALTON, KATHARINA (1957): Toxaemia of PregnancyTreated with Progesterone during the SymptomaticStage, Brit. med. J., ii, 378.

DIXON, H. G., BROWNE, J. C. Mc., DAVEY, D. A.(1963): Chorio-decidual and Myometrial BloodFlow, Lancet, ii, 369.

DODDS, GLADYS, H. (1950): Symposium on Non-Toxaemic Hypertension in Pregnancy, p. 200.London: J. & A. Churchill.

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DUNCAN, ETHEL H. L., BAIRD, D., THOMPSON, A. A.(1952): The Cause and Prevention of Stillbirthsand First Week Deaths, J. Obstet. Gynaec. Brit.Emp., 59, 183.

EPSTEIN, F. H. (1964): Late Vascular Effects ofToxaemia of Pregnancy, New Engl. J. Med., 271,391.

GIBSON, G. B., and PLATT, ,R. (1959): Incidence ofHypertension after Pregnancy Toxaemia, Brit.Med, J., ii, 159.

HAHN, L. (1952): The Relation of Blood Pressureto Weight, Height and Body Surface Area inSchoolboys aged 11 to 15 years, Arch. Dis. Childh.27, 43.

LANDESMAN, R. (1955): Foetal IMortality in EssentialHypertension, Obstet. and Gynec., 6, 354.

LEADING ARTICLE (1965): Brit. med. J., i, 738.LEADING ARTICLE (1965): Brit. med. J., ii, 1007.MCCARTNEY, C. P., SPARGO, B., LORINCZ, A. B.,LEFEBURE, Y. and NEWTON, R. E. (1964): RenalStructure and Function in Pregnant Patients withAcute Hypertension, Amer J. Obstet. Gynec., 90,579.

MACGILLIVRAY, I., HYTHEN, ;F. E., TAGGART, N. andBUCHANAN, T. S. (1962): The Effect of a SodiumDiuretic on the Total Exchangeable Sodium andTotal Body Water in Pre-eclamptic Toxaemia,Obstet. Gynaec. Brit. Cmwlth., 62, 438.

PLATr, R. (1958): Chronic Hypertension followingPre-eclamptic Toxaemia, J. Obstet. Gynaec. Brit.Emp., 65, 385.

POLLAK, V. E. (1956): 'Report on the First RossObstetric iResearch Conference. Univ. ChicagoSchool of Medicine.

ROBINSON, S. C. and BRUCER, M. (1939): Range ofNormal Blood Pressure. A Statistical ClinicalStudy of 11,383 Persons, Arch. intern. Med., 64,409.

SOPHIAN, J. (1953): Toxaemia of Pregnancy. London:Butterworth.

SOPHIAN J. (1958): The Aetiology of Toxaemia,Excerpta med. (Amst.) Sect. II No. 1.

TOWNSEND, L. (1959): High Blood Pressure inPregnancy. Melbourne: University Press.

WATr, J. D. and PHILLIPP, E. E. (1960): OralDiuretics in Pregnancy Toxaemia, Brit. med. J.,1, 1807.

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