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SUCCESSFUL PREGNANCY UNDER TREATMENT FOR MALIGNANT HYPERTENSION
508
uptake by the perfused liver (Laguna
et al. 1956) may be interest in this connection. Cirrhotic patients behaved similarly to control subjects. In some patients we found a higher fasting value of urinary pyruvate. This has been reported elsewhere in severe liver failure (Amatuzio and Nesbitt 1950, Thompson 1956). According to our results, it is due to a depression of the tubular reabsorption of pyruvate. In conclusion, we can say that intravenous administration of fructose interferes with the metabolism of the renal tubules. This leads to an increase in the excretion of pyruvate, inorganic phosphate (Hoenig et al. 1958), and perhaps of other metabolites. Further studies are required, to assess the clinical importance of these observations.
of
some
Summary Infused intravenously, fructose increases the renal excretion of pyruvate. Glucose does not do this. The increased renal excretion is mainly due to depression of the tubular reabosorption of pyruvate. In most cases it ceases within an hour of the administration of the sugar. Its extent depends on the infusion-rate. REFERENCES
Amatuzio, D. S., Nesbitt, S. (1950) J. clin. Invest. 29, 796. Bonsnes, R. W., Taussky, H. (1945) J. biol. Chem. 158, 581. Enoki, Ch., Mukaiama, H. (1952) Igaku to Seibutsugaku 25, 80. Friedemann, T. E., Haugen, G. E. (1943) J. biol. Chem. 147, 415. Hoenig, V. (1957) Vnitřní lék. (czech) 3, 588. Schück, O., Fischer, O., Hoenigová, J., Patová, V. (1958) Acta med. scand. (in the press). Laguna, J., Chagoya, Q. F. B. V., Pardo, E. (1956) Rev. invest. clin., Mex. 8, 51. Leuthardt, F. (1956) Therapiewoche, 6, 343. Mendeloff, A. J., Weichselbaum, T. E. (1953) Metabolism 2, 450. Miller, A. T., Jr., Miller, J. O., Jr. (1949) J. appl. Physiol. 1, 614. Pletscher, A. (1953) Helv. med. Acta, 20, 100. Renold, A. E., Thorn, G. W. (1955) Amer. J. Med. 19, 163. Sasaki, H. (1950) Folia. endocrin. jap. 26, 73. Slavík, K., Michalec, C. (1949) Chem. listy 43, 102. Smith, C. H. Jr., Ettinger, R. H., Seligson, D., Lightcap, S. (1953) J. clin. Invest. 32, 273. Thompson, R. H. S. 57th general meeting of the Association of Clinical Pathologists, London, October, 1956. —
SUCCESSFUL PREGNANCY UNDER TREATMENT FOR MALIGNANT HYPERTENSION PRISCILLA KINCAID-SMITH B.Sc., M.B. W’srand, M.R.C.P., D.C.P. KRIS SOMERS W’srand, M.R.C.P.
M.B.
J. C. MCCLURE BROWNE B.Sc., M.B. Lond., F.R.C.S., F.R.C.O.G. From the
Departments of Medicine and Gynœcology and Obstetrics, Postgraduate Medical School of London
So far as we are aware, no report has yet appeared of a successful pregnancy in a patient in whom malignant hypertension has been controlled with hypotensive drugs. We report a patient with a fourteen-year history of severe hypertension who gave birth to a surviving premature infant after two previous episodes of malignant hypertension, one four years and the other fourteen years ago.
Case-report February, 1942, at the antenatal clinic at University College Hospital, a woman aged 22 was found to be hyperIn
tensive in the twentieth week of her first pregnancy, her blood-
being 220/140 mm. Hg. Malignant hypertension was diagnosed because of bilateral papilloedema and retinitis. Abdominal hysterotomy was done at twenty-six weeks. In pressure
September, 1942, she was admitted to the London Hospital for investigation of the hypertension. Immediately before admission she had had frequency of micturition, dysuria, and lumbar pain. Her blood-pressure varied between 190/130 and 215/140 mm. Hg, but she showed no other abnormality, and the papillcedema and retinitis noted in February had completely regressed. Renal function was normal, apart from persistent albuminuria. A culture of urine yielded a scanty growth of Staphylococcus albus and a moderate growth of coliform bacilli. In 1945 the patient consulted the gynxcological department at the Westminster Hospital, being anxious to undertake a further pregnancy. Her blood-pressure was 210/140 mm. Hg, her blood-urea level 40 mg. per 100 ml., and an intravenous pyelogram normal, but her urine contained protein 100 mg. per 100 ml. In September, 1946, when she miscarried a macerated foetus at 26 weeks, her blood-pressure was 230/180 mm. Hg. In 1951, at the age of 31, she attended the gynaecological department at Hammersmith Hospital. Her blood-pressure was 210/140 mm. Hg, and her optic fundi showed arterial narrowing but no retinitis. Her urine was now, for the first time, free from albumin; her blood-urea level was 21 mg. per 100 ml., and the specific gravity of her urine ranged from 1.002
to
1.020.
She next presented at the ophthalmic clinic of the Hospital in December, 1952, complaining of blurring of vision for a month. Bilateral papillcedema with hxmorrhages and exudates was noted, and she was admitted to a medical ward. An additional relevant fact in her history was the absence of any hypertensive disease in her family. In addition to the visual difficulties she had had breathlessness on exertion and ankle swelling for two weeks and two attacks of paroxysmal nocturnal dyspnoea. She was dyspnoeic, her pulse-rate was 120 and blood-pressure 230;160 mm. Hg. A presystolic triple rhythm was noted, and she was in congestive heart-failure; soon after admission she had an attack of acute pulmonary cedema. Radiography of her chest showed considerable left ventricular hypertrophy, which was confirmed by electrocardiography. An unusual feature was a prolongation of the P-R interval . (024, sec.), which has been present intermittently on subsequent records. A transient albuminuria was present while the patient was in heart-failure. Her blood-urea level was 21 mg. per 100 ml., and isosthenuria was present. She improved rapidly on treatment with subcutaneous hexamethonium bromide together with digoxin, diuretics, and a low-salt diet. She was stabilised on subcutaneous hexamethonium bromide 60 mg. thrice daily, which reduced the blood-pressure to 110/70 mm. Hg in the erect position an hour after the injection. On this treatment papillcedema resolved completely in two months. A year later the cutaneous
patient’s
pentolinium
treatment was
60 mg. thrice
daily
changed to suba satisfactory
with
hypotensive
response. In 1955 reserpine (’ Serpasil’) 01 mg. three times a day was added to the treatment, and during follow-up from December, 1952, to June, 1956, the patient remained subjectively extremely well. Radiological and electrocardiographic evidence of left ventricular hypertrophy persisted.
Successful Pregnancy In June, 1956, at the
age of 37, the patient was found to be six-weeks pregnant. As she was most anxious to continue with the pregnancy, and as her blood-pressure was easily controlled, it was decided that she should continue under close supervision. She was given a high-protein low-carbohydrate low-salt diet, and strict attention was paid to her weight. She was seen at weekly intervals, and much variation was notedin her response to hypotensive drugs, together with a definite decrease in dosage requirements. The total daily pentolinium dosage was decreased from 180 to 120 mg.; but even with this reduction readings of 95/60 mm. Hg were noted an hour after the injection. In view of possible impairment of the placental
509 circulation she was admitted at the fifteenth week of pregnancy. She was transferred to oral mecamylamine 10 mg. b.d., together with the previous dosage of reserpine. She continued her weekly attendances at the antenatal clinic. Her weight, which at the beginning of pregnancy was 151 lb., remained almost stationary. She was last seen at this clinic when twentynine weeks pregnant. Her blood-pressure in the erect position was 170/120 mm. Hg, and in the recumbent 200/140 mm. Hg. She had no oedema, and her weight showed a sudden drop of 2 lb. 4 oz. from that of the previous week. She felt perfectly well but was admitted for observation. Two days later she had a sudden onset of colicky lower abdominal pain and a vaginal hxmorrhage of about 300 ml. The foetal heart was still heard. She went spontaneously into labour eight hours later and gave birth spontaneously to a
healthy male infant weighing 4 lb. 1 oz. The placenta followed rapidly with about 200 ml. of blood-clot; it weighed 1 lb. 2 oz. and had obviously been involved in an accidental haemorrhage. The patient’s blood-pressure after delivery was 170/125 mm. Hg in the supine position. Over the next month a gradual increase in mecamylamine dosage to the present daily total of 45 mg. was necessary. The baby was discharged when at the age of 36 days, weighing 5 lb. 10 oz. and has remained fit and well. Discussion
The pregnancy
produced a live baby in spite of two of malignant hypertension. The first of these occurred during pregnancy in 1942 and reverted to benign hypertension, judged by retinal changes, after termination of the pregnancy. Malignant hypertension was again diagnosed in 1952 and responded to hypotensive drugs, on which the patient has been maintained until previous episodes
now.
The original hypertensive episode in 1942 must be regarded as chronic hypertension and not as a pregnancy toxxmia, because of severe hypertension at the twentieth week of pregnancy. Albuminuria persisted for "
"
at least seven months after termination of the pregnancy. This albuminuria is of considerable interest because the urine at present is free from albumin, as it has been on numerous examinations in the past fifteen years. Albuminuria is almost universal in malignant hypertension (Ellis 1938, Kincaid-Smith et al. 1958), and its absence here probably indicates that the vascular changes of malignant nephrosclerosis had not yet developed when hypotensive therapy was instituted in 1952. The subsequent favourable course and normal renal function support this hypothesis. The aetiology of the hypertension in the present case is by no means clear. The rarity of essential malignant hypertension in this age-group (Platt 1948, Kincaid-Smith et al. 1958) caused us to seek some renal or other cause. The dysuria and positive urine culture in 1942 introduced the possibility of chronic pyelonephritis as a causal factor. This condition is notoriously difficult to diagnose; but, in the absence of any further positive evidence, and with repeated normal intravenous pyelograms and urine deposits, we think it unlikely. Investigation has provided no other evidence of any underlying cause of the hypertension. Pregnancy was clearly the precipitating factor in 1942. Irrespective of the cause of malignant hypertension this condition carries a very poor prognosis, most patients dying in three months. Survival beyond two years is exceptional in untreated cases (Kincaid-Smith et al. 1958). A slight fall in the blood-pressure after the abdominal hysterotomy in 1942 was associated with disappearance
of the papilloedema and retinal exudates in seven months. The second episode of malignant hypertension, in 1952, responded readily to hypotensive drugs. Few data are available for the prognosis of malignant hypertension in pregnancy, but death from urasmia may certainly occur within a short period in spite of termination of the pregnancy (Heptinstall 1953, Currens et al. 1956, KincaidSmith et al. 1958). Termination of this pregnancy was at first contemplated in view of the past history and the well-known risks to the mother. Because of the patient’s insistence, however, it was decided to continue the pregnancy under close
supervision. Young (1952) showed that hexamethonium bromide accumulates in the amniotic fluid of animals. Morris (1953) reported deaths from paralytic ileus in two of ten infants where hexamethonium bromide had been used as a hypotensive agent during pregnancy; he consequently advised that hexamethonium should be withheld at least twenty-four hours before delivery. Because of its diffusibility we expected mecamylamine to produce similar effects in the foetus and had therefore intended to discontinue it a week before cxsarean section at thirty-four weeks. Spontaneous premature labour prevented these precautions, but in spite of full doses of mecamylamine until the time of delivery and the excretion by the infant of 0 53 mg. of mecamylamine, no paralytic ileus or other com-
plications developed. Although commonly the child in cases of hypertension is smaller than usual for the period of gestation, in this case, with an undoubted gestation period of twenty-nine weeks and two days, the infant was unusually large, suggesting that hypotensive treatment had influenced favourably the placental ischxmia known to be associated with maternal hypertension (Browne and Veall 1953). The decreased pentolinium requirements between the eleventh and fourteenth weeks of the pregnancy interested us because of the known physiological fall in the blood-pressure which takes place in the second trimester (Browne and Browne
1955). In view of the
success reported here, there may be give hypotensive drugs such as mecamylamine extensive trial in similar cases. An integral part
reason to a more
of the management should be the maintenance of the erect posture as much as possible instead of the traditional rest in bed.
Summary A successful pregnancy ensued in
patient in whom malignant hypertension hypotensive drugs. Hypotensive drugs, particularly mecamylamine, should be given a more extensive trial in severe hyperwas
a
controlled with
tension in pregnancy. We are grateful to Prof. J. McMichael, under whose care this patient was treated from 1952 until 1956; Dr. J. P. M. Tizard, who supervised the management of the premature infant; Dr. Donald Hunter and the departments of obstetrics and gynaecology at the Westminster and University College Hospitals for details about the patient’s previous hospital admissions; and Dr. M. D. Milne for estimating the mecamylamine excreted by the premature infant. REFERENCES
Browne, F. J., Browne, J. C. M. (1955) Antenatal and Postnatal Care. 8th ed., London. Browne, J. C. M., Veall, N. (1953) J. Obstet. Gynœc. Brit. Emp. 60, 141. Currens, J. H., Reid, D. E., Newell, J. L. (1956) J. Amer. med. Ass. 161, 1232.
Ellis, A. (1938) Lancet, i, 977. Heptinstall, R. H. (1953) J. Path. Bact. 65, 423. Kincaid-Smith, P., McMichael, J., Murphy, E. A. (1958) Quart. J. Med. 27, 117. Morris, N. (1953) Lancet, i, 322. Platt, R. (1948) Quart. J. Med. 17, 83. Young, I. M. (1952) J. Physiol. 116, 4P.
uptake by the perfused liver (Laguna
et al. 1956) may be interest in this connection. Cirrhotic patients behaved similarly to control subjects. In some patients we found a higher fasting value of urinary pyruvate. This has been reported elsewhere in severe liver failure (Amatuzio and Nesbitt 1950, Thompson 1956). According to our results, it is due to a depression of the tubular reabsorption of pyruvate. In conclusion, we can say that intravenous administration of fructose interferes with the metabolism of the renal tubules. This leads to an increase in the excretion of pyruvate, inorganic phosphate (Hoenig et al. 1958), and perhaps of other metabolites. Further studies are required, to assess the clinical importance of these observations.
of
some
Summary Infused intravenously, fructose increases the renal excretion of pyruvate. Glucose does not do this. The increased renal excretion is mainly due to depression of the tubular reabosorption of pyruvate. In most cases it ceases within an hour of the administration of the sugar. Its extent depends on the infusion-rate. REFERENCES
Amatuzio, D. S., Nesbitt, S. (1950) J. clin. Invest. 29, 796. Bonsnes, R. W., Taussky, H. (1945) J. biol. Chem. 158, 581. Enoki, Ch., Mukaiama, H. (1952) Igaku to Seibutsugaku 25, 80. Friedemann, T. E., Haugen, G. E. (1943) J. biol. Chem. 147, 415. Hoenig, V. (1957) Vnitřní lék. (czech) 3, 588. Schück, O., Fischer, O., Hoenigová, J., Patová, V. (1958) Acta med. scand. (in the press). Laguna, J., Chagoya, Q. F. B. V., Pardo, E. (1956) Rev. invest. clin., Mex. 8, 51. Leuthardt, F. (1956) Therapiewoche, 6, 343. Mendeloff, A. J., Weichselbaum, T. E. (1953) Metabolism 2, 450. Miller, A. T., Jr., Miller, J. O., Jr. (1949) J. appl. Physiol. 1, 614. Pletscher, A. (1953) Helv. med. Acta, 20, 100. Renold, A. E., Thorn, G. W. (1955) Amer. J. Med. 19, 163. Sasaki, H. (1950) Folia. endocrin. jap. 26, 73. Slavík, K., Michalec, C. (1949) Chem. listy 43, 102. Smith, C. H. Jr., Ettinger, R. H., Seligson, D., Lightcap, S. (1953) J. clin. Invest. 32, 273. Thompson, R. H. S. 57th general meeting of the Association of Clinical Pathologists, London, October, 1956. —
SUCCESSFUL PREGNANCY UNDER TREATMENT FOR MALIGNANT HYPERTENSION PRISCILLA KINCAID-SMITH B.Sc., M.B. W’srand, M.R.C.P., D.C.P. KRIS SOMERS W’srand, M.R.C.P.
M.B.
J. C. MCCLURE BROWNE B.Sc., M.B. Lond., F.R.C.S., F.R.C.O.G. From the
Departments of Medicine and Gynœcology and Obstetrics, Postgraduate Medical School of London
So far as we are aware, no report has yet appeared of a successful pregnancy in a patient in whom malignant hypertension has been controlled with hypotensive drugs. We report a patient with a fourteen-year history of severe hypertension who gave birth to a surviving premature infant after two previous episodes of malignant hypertension, one four years and the other fourteen years ago.
Case-report February, 1942, at the antenatal clinic at University College Hospital, a woman aged 22 was found to be hyperIn
tensive in the twentieth week of her first pregnancy, her blood-
being 220/140 mm. Hg. Malignant hypertension was diagnosed because of bilateral papilloedema and retinitis. Abdominal hysterotomy was done at twenty-six weeks. In pressure
September, 1942, she was admitted to the London Hospital for investigation of the hypertension. Immediately before admission she had had frequency of micturition, dysuria, and lumbar pain. Her blood-pressure varied between 190/130 and 215/140 mm. Hg, but she showed no other abnormality, and the papillcedema and retinitis noted in February had completely regressed. Renal function was normal, apart from persistent albuminuria. A culture of urine yielded a scanty growth of Staphylococcus albus and a moderate growth of coliform bacilli. In 1945 the patient consulted the gynxcological department at the Westminster Hospital, being anxious to undertake a further pregnancy. Her blood-pressure was 210/140 mm. Hg, her blood-urea level 40 mg. per 100 ml., and an intravenous pyelogram normal, but her urine contained protein 100 mg. per 100 ml. In September, 1946, when she miscarried a macerated foetus at 26 weeks, her blood-pressure was 230/180 mm. Hg. In 1951, at the age of 31, she attended the gynaecological department at Hammersmith Hospital. Her blood-pressure was 210/140 mm. Hg, and her optic fundi showed arterial narrowing but no retinitis. Her urine was now, for the first time, free from albumin; her blood-urea level was 21 mg. per 100 ml., and the specific gravity of her urine ranged from 1.002
to
1.020.
She next presented at the ophthalmic clinic of the Hospital in December, 1952, complaining of blurring of vision for a month. Bilateral papillcedema with hxmorrhages and exudates was noted, and she was admitted to a medical ward. An additional relevant fact in her history was the absence of any hypertensive disease in her family. In addition to the visual difficulties she had had breathlessness on exertion and ankle swelling for two weeks and two attacks of paroxysmal nocturnal dyspnoea. She was dyspnoeic, her pulse-rate was 120 and blood-pressure 230;160 mm. Hg. A presystolic triple rhythm was noted, and she was in congestive heart-failure; soon after admission she had an attack of acute pulmonary cedema. Radiography of her chest showed considerable left ventricular hypertrophy, which was confirmed by electrocardiography. An unusual feature was a prolongation of the P-R interval . (024, sec.), which has been present intermittently on subsequent records. A transient albuminuria was present while the patient was in heart-failure. Her blood-urea level was 21 mg. per 100 ml., and isosthenuria was present. She improved rapidly on treatment with subcutaneous hexamethonium bromide together with digoxin, diuretics, and a low-salt diet. She was stabilised on subcutaneous hexamethonium bromide 60 mg. thrice daily, which reduced the blood-pressure to 110/70 mm. Hg in the erect position an hour after the injection. On this treatment papillcedema resolved completely in two months. A year later the cutaneous
patient’s
pentolinium
treatment was
60 mg. thrice
daily
changed to suba satisfactory
with
hypotensive
response. In 1955 reserpine (’ Serpasil’) 01 mg. three times a day was added to the treatment, and during follow-up from December, 1952, to June, 1956, the patient remained subjectively extremely well. Radiological and electrocardiographic evidence of left ventricular hypertrophy persisted.
Successful Pregnancy In June, 1956, at the
age of 37, the patient was found to be six-weeks pregnant. As she was most anxious to continue with the pregnancy, and as her blood-pressure was easily controlled, it was decided that she should continue under close supervision. She was given a high-protein low-carbohydrate low-salt diet, and strict attention was paid to her weight. She was seen at weekly intervals, and much variation was notedin her response to hypotensive drugs, together with a definite decrease in dosage requirements. The total daily pentolinium dosage was decreased from 180 to 120 mg.; but even with this reduction readings of 95/60 mm. Hg were noted an hour after the injection. In view of possible impairment of the placental
509 circulation she was admitted at the fifteenth week of pregnancy. She was transferred to oral mecamylamine 10 mg. b.d., together with the previous dosage of reserpine. She continued her weekly attendances at the antenatal clinic. Her weight, which at the beginning of pregnancy was 151 lb., remained almost stationary. She was last seen at this clinic when twentynine weeks pregnant. Her blood-pressure in the erect position was 170/120 mm. Hg, and in the recumbent 200/140 mm. Hg. She had no oedema, and her weight showed a sudden drop of 2 lb. 4 oz. from that of the previous week. She felt perfectly well but was admitted for observation. Two days later she had a sudden onset of colicky lower abdominal pain and a vaginal hxmorrhage of about 300 ml. The foetal heart was still heard. She went spontaneously into labour eight hours later and gave birth spontaneously to a
healthy male infant weighing 4 lb. 1 oz. The placenta followed rapidly with about 200 ml. of blood-clot; it weighed 1 lb. 2 oz. and had obviously been involved in an accidental haemorrhage. The patient’s blood-pressure after delivery was 170/125 mm. Hg in the supine position. Over the next month a gradual increase in mecamylamine dosage to the present daily total of 45 mg. was necessary. The baby was discharged when at the age of 36 days, weighing 5 lb. 10 oz. and has remained fit and well. Discussion
The pregnancy
produced a live baby in spite of two of malignant hypertension. The first of these occurred during pregnancy in 1942 and reverted to benign hypertension, judged by retinal changes, after termination of the pregnancy. Malignant hypertension was again diagnosed in 1952 and responded to hypotensive drugs, on which the patient has been maintained until previous episodes
now.
The original hypertensive episode in 1942 must be regarded as chronic hypertension and not as a pregnancy toxxmia, because of severe hypertension at the twentieth week of pregnancy. Albuminuria persisted for "
"
at least seven months after termination of the pregnancy. This albuminuria is of considerable interest because the urine at present is free from albumin, as it has been on numerous examinations in the past fifteen years. Albuminuria is almost universal in malignant hypertension (Ellis 1938, Kincaid-Smith et al. 1958), and its absence here probably indicates that the vascular changes of malignant nephrosclerosis had not yet developed when hypotensive therapy was instituted in 1952. The subsequent favourable course and normal renal function support this hypothesis. The aetiology of the hypertension in the present case is by no means clear. The rarity of essential malignant hypertension in this age-group (Platt 1948, Kincaid-Smith et al. 1958) caused us to seek some renal or other cause. The dysuria and positive urine culture in 1942 introduced the possibility of chronic pyelonephritis as a causal factor. This condition is notoriously difficult to diagnose; but, in the absence of any further positive evidence, and with repeated normal intravenous pyelograms and urine deposits, we think it unlikely. Investigation has provided no other evidence of any underlying cause of the hypertension. Pregnancy was clearly the precipitating factor in 1942. Irrespective of the cause of malignant hypertension this condition carries a very poor prognosis, most patients dying in three months. Survival beyond two years is exceptional in untreated cases (Kincaid-Smith et al. 1958). A slight fall in the blood-pressure after the abdominal hysterotomy in 1942 was associated with disappearance
of the papilloedema and retinal exudates in seven months. The second episode of malignant hypertension, in 1952, responded readily to hypotensive drugs. Few data are available for the prognosis of malignant hypertension in pregnancy, but death from urasmia may certainly occur within a short period in spite of termination of the pregnancy (Heptinstall 1953, Currens et al. 1956, KincaidSmith et al. 1958). Termination of this pregnancy was at first contemplated in view of the past history and the well-known risks to the mother. Because of the patient’s insistence, however, it was decided to continue the pregnancy under close
supervision. Young (1952) showed that hexamethonium bromide accumulates in the amniotic fluid of animals. Morris (1953) reported deaths from paralytic ileus in two of ten infants where hexamethonium bromide had been used as a hypotensive agent during pregnancy; he consequently advised that hexamethonium should be withheld at least twenty-four hours before delivery. Because of its diffusibility we expected mecamylamine to produce similar effects in the foetus and had therefore intended to discontinue it a week before cxsarean section at thirty-four weeks. Spontaneous premature labour prevented these precautions, but in spite of full doses of mecamylamine until the time of delivery and the excretion by the infant of 0 53 mg. of mecamylamine, no paralytic ileus or other com-
plications developed. Although commonly the child in cases of hypertension is smaller than usual for the period of gestation, in this case, with an undoubted gestation period of twenty-nine weeks and two days, the infant was unusually large, suggesting that hypotensive treatment had influenced favourably the placental ischxmia known to be associated with maternal hypertension (Browne and Veall 1953). The decreased pentolinium requirements between the eleventh and fourteenth weeks of the pregnancy interested us because of the known physiological fall in the blood-pressure which takes place in the second trimester (Browne and Browne
1955). In view of the
success reported here, there may be give hypotensive drugs such as mecamylamine extensive trial in similar cases. An integral part
reason to a more
of the management should be the maintenance of the erect posture as much as possible instead of the traditional rest in bed.
Summary A successful pregnancy ensued in
patient in whom malignant hypertension hypotensive drugs. Hypotensive drugs, particularly mecamylamine, should be given a more extensive trial in severe hyperwas
a
controlled with
tension in pregnancy. We are grateful to Prof. J. McMichael, under whose care this patient was treated from 1952 until 1956; Dr. J. P. M. Tizard, who supervised the management of the premature infant; Dr. Donald Hunter and the departments of obstetrics and gynaecology at the Westminster and University College Hospitals for details about the patient’s previous hospital admissions; and Dr. M. D. Milne for estimating the mecamylamine excreted by the premature infant. REFERENCES
Browne, F. J., Browne, J. C. M. (1955) Antenatal and Postnatal Care. 8th ed., London. Browne, J. C. M., Veall, N. (1953) J. Obstet. Gynœc. Brit. Emp. 60, 141. Currens, J. H., Reid, D. E., Newell, J. L. (1956) J. Amer. med. Ass. 161, 1232.
Ellis, A. (1938) Lancet, i, 977. Heptinstall, R. H. (1953) J. Path. Bact. 65, 423. Kincaid-Smith, P., McMichael, J., Murphy, E. A. (1958) Quart. J. Med. 27, 117. Morris, N. (1953) Lancet, i, 322. Platt, R. (1948) Quart. J. Med. 17, 83. Young, I. M. (1952) J. Physiol. 116, 4P.