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Placental growth retardation caused 84 fetal and neonatal deaths per 100,000 births. Its frequency increased as mothers' diastolic blood pressure levels increased, an effect augmented by proteinuria. The perinatal deaths also increased with advancing maternal age, anemia, and poverty. Maternal weight gains were low in the involved pregnancies, and the fetuses and neonates who died had a pattern of growth retardation characteristic of fetal undernutrition. Microscopic abnormalities in the decidua and placenta were characteristic of inadequate perfusion of the placenta from the uterus. They included fibrinoid changes in the arteries and arterioles of the decidua, villous cytotrophoblastic hyperplasia, and an obliterative endarteritis in fetal stem arteries of the placenta.
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PMID:Causes and consequences of placental growth retardation. 62 66

Several methods were used in an attempt to produce preeclampsia in the pregnant rat. Desoxycorticosterone acetate plus increased NaCl intake produced hypertension, proteinuria, rapid weight gain, convulsions, decreased litter size, decreased offspring weight, increased fetal and maternal mortality, and renal lesions similar to those seen in human preeclampsia. Injection of placenta in Freund's adjuvant produced mild blood pressure elevation and proteinuria in the pregnant rat. Rabbit antirat placenta serum produced hypertension in the pregnant rat but not in the nonpregnant rat. Liver congestion and renal glomerular congestion were observed in both pregnant and non-pregnant rats. Pregnancy in the rat reduced hypertension produced by applying a Goldblatt clamp prior to breeding. Uterine ischemia produced by wrapping the uterus in cellophane produced mild blood pressure elevation and proteinuria. A vitamin-E-deficient diet that contained substantial amounts of partially perioxidized, polyunsaturated fatty acids produced morphological lesions in the pregnant rat similar to those seen in human preeclampsia, but hypertension, edema, and proteinuria were absent. None of the maneuvers was effective in producing a complete model of human preeclampsia, but they do provide material for study that could answer somebasic questions about preeclampsia.
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PMID:The rat as a model for preeclampsia. 100 52

The aetiology of pregnancy-induced hypertension (PIH) is at present unknown. Epidemiological data lead us to assume, that two main mechanisms could be responsible for the development of PIH. They are not well understood in their complexity, but result in the same pattern of signs and symptoms: Oedema, proteinuria and hypertension. 1. "Goldblatt-Phenomenon" in the uterus, as a result of a disturbed maternal immune response to the cytotrophoblast, followed by the reduction of uterine blood flow and the liberation of vasoactive substances from the placenta. 2. Renal factors, especially in elderly women, result in a manifestation of nephrotic diseases during pregnancy. No screening methods are at the present time available to diagnose PIH in advance. It is therefore necessary, to look at typical clinical manifestations, i.e. the development of hypertension. It is also important to estimate the weight gain and the occurrence of oedema before rising blood pressure demonstrates a general vasoconstriction in the maternal vascular system. The basic therapeutical concept is to reduce the peripheral vascular resistance, to prevent maternal complications and to reduce the uterine vascular resistance to improve foetal oxygenation. In many cases an improvement of the oxygen supply to the foetus is not possible, since irreversible alterations of the uterine arterial vascular bed have already taken place. For the treatment of PIH, different drugs are available which act on different targets. In cases of special medical history, the early application of magnesium and acetyl salicylic acid (ASA) should be included in the therapeutical concept of prophylaxis.
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PMID:["Goldblatt phenomenon of the uterus" and latent kidney disease as the cause of pregnancy-induced hypertension--epidemiology and therapeutic consequences]. 193 79

A researcher reviewed the January 1984-December 1986 birth and obstetrical records at the University of Nigeria Teaching Hospital in Enugu. During this period, the incidence rate for abruptio placentae was .44% (81/18,215). 56 of these cases were considered mild and 25 were severe. 15/81 cases did not have adequate antenatal care. 49.4% of the cases were in the 26-30 year old age group. The higher the parity of the women the higher the percentage of those with abruptio placentae, e.g., 3.7% for primigravidas and 33.3% for parity or = 5. The leading symptoms included tender uterus (87.7%), abdominal pain (85.2%), and vaginal bleeding (54.3%). Other symptoms included hypertension, shock, and proteinuria. Vaginal delivery accounted for 80.3% of the abruptio placentae births, while cesarean section accounted for 12.4%, vacuum extraction 3.7%, and breech delivery 3.7%. 91.4% of the patients required a blood transfusion with an average of 3 pints of blood/patient. 22.2% of the patients experienced severe postpartum hemorrhage as a result of uterine atony, coagulation failure, or puerperal sepsis. The perinatal mortality rate stood at 58%. None of the 15% of mothers who had severe abruptio placentae had a live infant. 16% of the infants were premature. Since most of the referred patients either did not have any antenatal care or had inadequate antenatal care, it appears that an appropriate measure to reduce the gravity of abruptio placentae would be a wider distribution of excellent antenatal and obstetric management in the rural areas.
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PMID:Abruptio placentae at the University of Nigeria Teaching Hospital, Enugu: a 3-year study. 280 22

Case reports are presented on 2 patients to show the importance of following up apparently false positive results of pregnancy tests. In case 1, a 25-year-old woman was admitted to the hospital with severe breathlessness in September 1987. After she had stopped using oral contraceptives (OCs) in 1985 her periods were irregular and on 4 occasions the results of pregnancy tests bought over the counter were positive. She was twice referred for ultrasound examinations, but the uterus was empty each time. In April 1987, dysfunctional uterine bleeding was diagnosed; she was treated with clomiphene. She then experienced intermittent pleuritic chest pain and breathlessness on exertion. In early September she was admitted with acute breathlessness and chest pain. A further pregnancy test was positive; results of laparoscopy of the pelvis were normal. A radioisotope ventilation-perfusion lung scan showed multiple filling defects in the left lung and no perfusion to the right. A presumptive diagnosis of choriocarcinoma was made with the syndrome of tumor growing in the pulmonary arteries. In case 2, a 32-year-old woman was admitted to the hospital in March 1988 with acute lower abdominal pain. A pregnancy test was positive, and she underwent laparoscopy for suspected ectopic pregnancy. A macroscopic tumor was found on the surface of the right ovary and a right salpingo-oophorectomy was performed. A subsequent histological examination showed choriocarcinoma. The 2 cases reported show the importance of seeking a definitive explanation for a false positive result of a pregnancy test. If the test has been performed correctly and proteinuria and drug interference, for instance, are ruled out, then a raised human chorionic gonadotropin concentration, particularly in young women, is virtually certain. In most cases this will be due to a pregnancy that ends in a 1st trimester abortion, but in a small minority it will be due to the hormone producing a tumor such as choriocarcinoma.
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PMID:Don't ignore a positive pregnancy test. 284 5

Continuous wave Doppler studies were carried out on both uterine arteries in 71 pregnant women from the twentieth week of gestation onward. Analysis of the waveform included the systolic/diastolic ratio and the presence or absence of a diastolic notch. In the current study, these ratios from 31 women with left/right systolic/diastolic difference, (between left and right uterine arteries) were compared with those of women having normal ratios. A normal left/right systolic/diastolic ratio difference of 0.3 with SD of 0.3 was found. When the left/right difference was plotted against the left/right averaged systolic/diastolic ratio, a correlation coefficient of 0.7 was noted (p less than 0.001). Significant outcome differences were noted between normal and abnormal left/right difference systolic/diastolic ratios in the perinatal parameters of gestational age at delivery, fetal weight, pregnancy-induced hypertension, proteinuria, and intrauterine growth retardation. Divergent uterine artery ratio findings are a result of one artery being the dominant supplier to the placenta. The majority of women with an elevated systolic/diastolic ratio seem to have divergent uterine blood supply to the uterus and placenta. These data suggest that errors in placentation site contribute to the development of preeclampsia and growth retardation in the fetus.
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PMID:Uterine artery Doppler velocimetry: the significance of divergent systolic/diastolic ratios. 268 59

Toxemia was induced in 13 of 20 pregnant ewes by the stress of a change in environment and food deprivation late in pregnancy. Of the toxemic ewes, eight developed prominent neurological findings with convulsions, motor weakness, and blindness, whereas five ewes developed azotemia without neurological signs. Proteinuria and azotemia occurred in all but one of the toxemic animals. Seven animals did not develop clinical or laboratory evidence of toxemia. Hypertension did not occur with the onset of toxemia but all toxemic animals showed glomerular changes by light and electron microscopy. These abnormalities, which were similar to those seen in human preeclampsia, included endothelial cell swelling, focal reduplication of the basement membrane, and fusion of the epithelial cell foot processes. The toxemia could not be attributed to changes in hematocrit, plasma glucose, Na, Cl, CO(2), K, Ca, fibrinogen, arterial pH, lactate, or pyruvate concentrations. Cardiac output fell only in ewes with prominent neurological signs. Plasma renin rose strikingly in animals developing toxemia, without change in substrate concentration. In contrast to human and other species, sheep uterus and amniotic fluid contained no detectable quantities of renin. Thus in response to stress the pregnant ewe develops a toxemia which in the absence of hypertension has clinical and pathological similarities to human preeclampsia.
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PMID:Toxemia of pregnancy in sheep: a clinical, physiological, and pathological study. 538 29

A 17-year-old youth was admitted because of proteinuria noted during a routine examination at his high school. His parents and three siblings were living in good health and there was no familial tendency to hypertension and no consanguinity. On physical examination, he was 161cm in height and weighed 43Kg, and his facial expression was female-like. Neither webbed neck nor cubitus valgus was noticed. Severe hypertension ranging from 190/120 to 230/130 was noted. No axillary or pubic hair was present, and the breasts were prepubertal in size. A gynecological examination revealed the presence of labia and vagina. Laboratory findings on admission were summarized as follows: The urine gave a (-)--(+) test for protein, renal function was revealed as normal, serum potassium ranged from 3.2 to 4.2mEq/L, the specimen of arterial blood showed pH 7.421, and an electrocardiogram revealed left ventricular hypertrophy and U wave changes in leads V2, V3, V4. X-rays showed a bone age of 12 years, and chromosome analysis revealed a karyo type of 46,XY. Endocrinological studies confirming the presence of a 17 alpha-hydroxylase deficiency were summarized as follows: 1) Plasma ACTH was markedly elevated. 2) Plasma renin activity was markedly suppressed showing no response to exercise. 3) Plasma progesteron, plasma DOC and plasma-corticosteron were extremely high. In contrast, plasma aldosteron was extremely low. 4) Plasma 17 alpha-OH progesteron and plasma cortisol were markedly reduced. Urinary excretion of 17-OHCS was extremely low. 5) Plasma testosteron and urinary 17-KS were markedly reduced. The patient was treated with 2mg then 1mg dexamethasone daily for half a year. After one month of therapy, the blood pressure was down to 160/100mmHg, and the serum potassium had risen from 3.2mEq/liter to 5.6mEq/liter. Plasma progesteron, plasma DOC, plasma corticosteron and plasma ACTH decreased to a normal level. Subsequently suppressed plasma renin activity elevated to a normal value. After 6 weeks of this treatment, a laparotomy was performed. Ovaries and uterus were absent, but bilateral testes were found at the external inguinal ring. Microscopic examination of the testis showed Sertoli cell adenoma. We have reported here a case of 17 alpha-hydroxylase deficiency with male pseudohermaphoriditism and discussed the endocrinological data and histological findings of the testis.
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PMID:[A case of 17 alpha-hydroxylase deficiency with male pseudohermaphroditism (author's transl)]. 696 32

The pregnancy complication characterized by proteinuric hypertension is called preeclampsia. Preeclampsia, an important cause of maternal and perinatal death, has an onset and progression impossible to predict. Termination of pregnancy is the only cure of preeclampsia. It is indicated when the fetus can survive outside the uterus or when the maternal condition deteriorates to such a condition that continuation would bring greater harm to the mother. The etiology of preeclampsia is unknown. Preeclampsia appears to be linked to abnormal trophoblastic implantation. In normal pregnancies, implantation effects changes in the spiral arteries that supply the intervillous space and fibrin-containing trophoblast, and amorphous matrix replace the endothelium and the internal elastic lamina. These changes do not occur or are limited in pre-eclamptic women. There appears to be a familial tendency to preeclampsia. Impaired formation of blocking antibodies to antigenic sites on the placenta increases the risk of pre-eclampsia. Risk factors are primigravidity, short duration of sexual cohabitation before conception, abundance of trophoblastic tissue (e.g., multifetal and molar pregnancies), and underlying vascular disease as in diabetes. Poor placental perfusion may account for the increase in maternal blood pressure. Preeclampsia can lead to eclampsia, cerebral hemorrhage, coagulopathy, and death. Poor utero-placental circulation retards fetal growth and causes fetal distress and maybe even perinatal death. When the diastolic blood pressure is higher than 110 mmHg, pre-eclamptic women should be administered antihypertensive drugs (e.g., methyldopa, beta-blockers, calcium channel blockers, hydralazine, labetatol, or diazoxide) to prevent maternal complications, but these drugs do not improve utero-placental blood flow nor do they prevent proteinuria. Diuretics should not be administered. Proteinuria indicates that the kidneys have been affected. A large randomized trial shows that aspirin does not effectively prevent preeclampsia. Routine calcium supplementation does appear to prevent it and preterm delivery.
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PMID:Pre-eclampsia. 875 7

A 36-year-old woman, at the 17th week +5 days gestational age, who was already admitted to the nephrology department for gestational hypertension, proteinuria and legs oedema, was admitted to our Institute. About three weeks before her admission to the nephrology dept., the patient presented heart palpitations and exertional dyspnoea related to the first evidence of the legs oedema, weight gain (about 5 kg during only one month) and normal blood pressure values. During the following days, an antihypertensive therapy was made, but hypertensive crisis and strong headache were also persistent. Vulvar oedema was observed, the uterus was moderately contracted and its dimensions were similar to an uterus at the 21st week; beta-hCG serum values were more than 500,000 IU/lt. An echography confirmed the diagnostic suspicion of hydatidiform the presence of a fetus developed as much as the gestational time. beta-hCG serum values increased to 1,200,000 IU/lt; the molar abortion induction was made thru prostaglandins: fetal extrusion occurred after three hours. The placenta was instrumentally extracted and it showed evident hydatidiform moles a uterine curettage. Patient temperature was very high (39 degrees C) in the immediate postoperative period and three hematologic pockets were transfused. After a week, we made a second elective uterine curettage with the extraction of a little quantity of gestational material; the patient was still hospitalised for ten days: during this time there was a progressive decrease of the beta-hCG serum values (last value at discharge: 7,200 IU/lt). The patient had also positive beta-hCG serum values after about one year.
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PMID:[Partial hydatidiform mmole at the 17th week of pregnancy]. 1023 Feb 45


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