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PubMed1975

Treatment of pre-eclampsia and eclampsia as a hypoperfusion syndrome.

A therapeutical program in pre-eclampsia and eclampsia is presented. The results in 10 patients suggest that the same basic program as is used in the hypoperfusion syndrome can be used in pre-eclampsia and eclampsia: Chlorpromazin to combat vasoconstriction and dilate the vascular bed. Plasma expanders, plasma, albumin and glucose with electrolytes to fill up the dilated vascular bed and restore the tissue perfusion. Buffers to combat acidosis, oxygen to combat hypoxemia, hypertonic Mannitol to mobilize edema. Furosemide to force diuresis.

Acidosis↗
PubMed1993

Phenytoin prophylaxis in severe pre-eclampsia and eclampsia.

OBJECTIVE: To determine plasma phenytoin levels and seizure outcome in women given phenytoin for seizure prophylaxis in severe pre-eclampsia and eclampsia. DESIGN: Prospective observational study comparing two phenytoin loading regimens. SETTING: Two UK teaching hospitals. SUBJECTS: Sixty-seven consecutive women with severe pre-eclampsia and five with eclampsia. INTERVENTIONS: The first 29 women were given a 15 mg/kg intravenous loading dose of phenytoin. The next 43 received 17.5 mg/kg. All were given 500 mg phenytoin 12 h after completion of the loading dose and then 250 mg every 12 h for four doses. MAIN OUTCOME MEASURES: Total plasma phenytoin levels at 30 min, 6 h and 12 h after loading dose, 6 h after first maintenance dose and on days 2 and 3 of maintenance therapy; eclamptic seizures after starting phenytoin. RESULTS: Mean plasma phenytoin levels were higher at 30 min and 6 h after the 17.5 mg/kg loading dose. Nine of 29 (31%) phenytoin levels 30 min after the loading dose were above the therapeutic range in the 15 mg/kg group compared with 26/38 (68%) in the 17.5 mg/kg group (P < 0.01). Six of 27 (22%) phenytoin levels 12 h after the loading dose were subtherapeutic in the 15 mg/kg group compared with 2/38 (5%) in the 17.5 mg/kg group (P < 0.05). Three women, two in the 17.5 mg/kg group, developed seizures after starting phenytoin. All three had plasma levels within the therapeutic range. CONCLUSIONS: Compared with a loading dose of 17.5 mg/kg, loading with 15 mg/kg phenytoin was associated with a lower incidence of high plasma levels at 30 min but a higher incidence of subtherapeutic levels at 12 h. Seizures occur in 2 to 3% of pre-eclamptics despite apparently therapeutic phenytoin levels.

Adult↗
PubMed2004

T594M mutation of the epithelial sodium channel beta-subunit gene in pre-eclampsia and eclampsia in Black South African women.

The possible role of the beta-subunit of the epithelial sodium channel T594M polymorphism in hypertensive disorders of pregnancy has not been examined. This study compared Black South African women with pre-eclampsia (n= 204), early onset pre-eclampsia (n= 67), eclampsia (n= 120) and gestational hypertension (n= 78) with 338 women from the same ethnic group who had full-term normotensive pregnancies, for the presence of the T594M polymorphism. The variant allele was detected in 1.7% to 3.8% of the various patient groups and in 3.6% of the control group reflecting no significant difference. These results suggest that the T594M polymorphism in the sodium channel beta-subunit is not associated with the pathogenesis of pre-eclampsia or gestational hypertension.

Black People↗
PubMed2004

Nitric oxide, lipid peroxides, and uric acid levels in pre-eclampsia and eclampsia.

The aim was to study the role of nitric oxide (NO), lipid peroxides (LPX), and uric acid in pre-eclampsia and eclampsia. Plasma levels of NO metabolites (nitrite+nitrate), malonyldialdehyde (MDA), and uric acid and erythrocyte MDA levels were compared between normal pregnant, pre-eclamptic, and eclamptic pregnant women in third trimester. Student's t-test was used for statistical evaluation. Plasma NO metabolites levels were higher in eclamptic group (35.7 +/- 16.5 micromol/liter, p < 0.05) but not in pre-eclamptic group (22.1 +/- 10.8 micromol/liter) than control group (18.8 +/- 6.9 micromol/liter). Plasma MDA and uric acid concentrations were higher in preeclamptic (4.4 +/- 1.7 nmol/ml, p < 0.05; 0.45 +/- 0.11 mmol/liter, p < 0.05, respectively) and eclamptic (5.8 +/- 1.9 nmol/ml, p < 0.05; 0.47 +/- 0.12 mmol/liter, p < 0.05) groups compared with control group (3.0 +/- 1.3 nmol/ml; 0.35 +/- 0.06 mmol/liter). Erythrocytes MDA concentrations were higher only in eclamptic group (174.4 +/- 62 nmol/gHb, p < 0.05) than control group (139.2 +/- 49.5 nmol/gHb). These results suggest that NO, LPX, and uric acid are important factors in the pathogenesis of pre-eclampsia and eclampsia, and that NO production and LPX are directly related to the severity of disease.

Adult↗
PubMed2003

Absence of Factor V Leiden, thrombomodulin and prothrombin gene variants in Black South African women with pre-eclampsia and eclampsia.

It has been suggested that gene aberrations may contribute to vascular endothelial dysfunction of pre-eclampsia in Caucasian and Japanese women. This study was undertaken to examine the association between pre-eclampsia in Black Zulu speaking South African women and the Factor 5 Leiden mutation. 100 patients with pre-eclampsia comprised the study group. The control group comprised 110 normotensive pregnant women of the same population group. Genotyping was performed to detect the G or A allele at residue 506 of the Factor V gene, and the C or T allele at residue 455 of the thrombomodulin gene. Our findings demonstrate that these particularly genetic loci are of little use in disease association studies for pre-eclampsia in homogenous Zulu speaking Africans.

Adolescent↗
PubMed1997

Severe pre-eclampsia and eclampsia: a broad overview with discussion of the nursing care required for the eclamptic patient.

Severe pre-eclampsia and eclampsia are conditions which are rarely seen in A & E departments today. Although the percentage of patients suffering from these conditions is extremely small, the author has been involved in the care and treatment of two patients with this severe complication of pregnancy. A lack of clear guidelines on this subject was the motivation which prompted further study. This paper covers definitions of pre-eclampsia, eclampsia, history, incidence, risks and pathophysiology. The main discussion is the nursing care and treatment of the eclamptic patient in the acute phase of the condition. The author hopes that by the end of this paper it is evident that all health care professionals should be aware of this dangerous condition and know the appropriate treatment to give to ensure the best quality of care possible.

Emergency Nursing↗
PubMed2006

Relationships between maternal plasma leptin, placental leptin mRNA and protein in normal pregnancy, pre-eclampsia and intrauterine growth restriction without pre-eclampsia.

Leptin, an adipocyte hormone involved in energy homeostasis, is important in reproduction and pregnancy. Questions yet to be addressed include the source of higher leptin during pregnancy and its relationship to pregnancy outcome and fetal growth. The objective of this study was to investigate the relationship between placental leptin gene expression, placental leptin protein concentration and maternal plasma leptin concentration among control pregnant women, women with pre-eclampsia and women with growth-restricted infants. We also investigated the relationship between placental leptin expression and the placental expression of enzymes involved in cellular lipid balance: fatty acid translocase (CD36), carnitine palmitoyltransferase I (CPT-1B) and lipoprotein lipase (LPL). Placental leptin expression, placental protein and maternal plasma concentration were higher in pre-eclampsia than in controls but not in women with growth-restricted infants. Placental leptin expression and placental protein were higher in the preterm pre-eclamptic subjects, whereas maternal leptin was higher in the term pre-eclamptic subjects. The placental gene expression of CD36, CPT-1B and LPL were not different among the groups. This study suggests that despite similar failed placental bed vascular remodelling in pre-eclampsia and intrauterine growth restriction (IUGR), leptin gene expression is higher only in preterm pre-eclampsia.

Adult↗
PubMed1999

[Neurological spectrum of pre-eclampsia and eclampsia].

Preeclampsia is a disorder specific to pregnancy which can affect all maternal organs. Cerebral involvement with the occurrence of convulsions is the defining factor for eclampsia. The most prominent signs of cerebral dysfunction include headache, hyperreflexia, visual disturbances, confusion and/or altered state of consciousness. Patients usually recover completely however some patients remain disabled due to cerebrovascular damage. Intracerebral and subarachnoidal hemorrhage are severe however rare complications of eclampsia. TCD investigations regularly find vasospasm in all great cerebral arteries. Reversible hypodense lesions in the white matter on early CT-scans and increased signal intensities on T2-weighted MRT images indicate local edema. The etiology of preeclampsia and eclampsia remains unknown and its current pathophysiology is still hypothetical. The clinical picture may best be explained by an endothelial dysfunction with increased vascular sensitivity to circulating pressure agents as well as by a structural endothelial lesion with fluid loss from the intravascular compartment.

Adult↗
PubMed1996

Correlated plasma elastase and sera cytotoxicity in eclampsia. A possible role of endothelin-1 induced neutrophil activation in preeclampsia-eclampsia.

The activation of neutrophils was studied in preeclampsia (n = 10) and eclampsia (n = 20) compared to normotensive controls (n = 10) and nonpregnant essential hypertensives (n = 10). Plasma elastase levels were raised in preeclampsia (0.53 +/- 0.32 microgram/mL, P < .002) and eclampsia (1.26 +/- 0.8 microgram/mL, P < .001) respectively compared to normal pregnancies (0.032 +/- 0.009 microgram/mL). The plasma elastases were more elevated in eclamptic cases compared to essential hypertensive (0.53 +/- 0.27 microgram/mL; P = .01) patients. We analyzed the correlation among elastase values, systolic (SBP), mean blood pressures (MBP), endothelin-1 (ET-1) levels and sera cytotoxicity (as measured by fura-2 release from human umbilical venous endothelial cell culture) in eclamptic cases. SBP and MBP were significantly correlated with plasma elastase levels in preeclampsia (r = 0.67, 0.63, respectively; P < .03) and eclampsia (r = 0.49, 0.49, respectively; P < .02). ET-1 levels were correlated with SBP (P = .003) and MBP (P = .001) and corresponding elastase levels (r = 0.606, P < .003) in eclamptic patients. Doses of 10, 25, and 50 pmol/mL of ET-1 increased elastase release in human neutrophil cultures dose and time dependently. Cytotoxicity of eclamptic sera correlated (P < .001) to the corresponding plasma elastase values. Therefore, this study suggests that neutrophil activation and ET-1 induced neutrophil activation occurs in this disease.

Adult↗
PubMed1995

Possible dietary measures in the prevention of pre-eclampsia and eclampsia.

The recurring theme when considering the various dietary manipulations that have been advocated in the prevention of pre-eclampsia is of dietary deficiencies and excesses that appear to be associated with the disease. However, whether these deficiencies and excesses cause, or arise as a consequence of, pre-eclampsia has frequently not been established. Advocates of dietary theories of the aetiology of the disease have tended to base their claims upon uncontrolled clinical trails and inadequate research investigations. With very few exceptions, the better-designed studies have failed to show any effect of dietary supplementation or restriction on the incidence of pre-eclampsia. While certain manipulations, for example calcium and n-3 fatty acid supplementation seem intriguing and merit further study, potentially harmful effects of other manipulations, namely weight restriction (Campbell Brown, 1983), salt restriction (Robinson, 1958) and magnesium supplementation (Lamm et al, 1988), have been demonstrated. The persistent tendency for the medical profession to provide dogmatic and often conflicting advice, and to advocate rigorous intervention, is thus culpable. Until the appropriate research is performed in a less haphazard fashion, with all interventions performed in the context of controlled trials, no dietary intervention can be advocated.

Diet, Sodium-Restricted↗
PubMed2004

Evidence of parvovirus B19 infection in patients of pre-eclampsia and eclampsia with dyserythropoietic anaemia.

Parvovirus B19 (PVB19) infection can induce transient anaemia in patients with increased erythropoiesis. However, the dynamic change within the bone marrow after PVB19 infection is not well understood. Increased erythropoiesis is a physiological phenomenon in puerperital women. Nevertheless, anaemia as a result of PVB19 infection in puerperital women has never been reported. We report one patient with eclampsia and two patients with pre-eclampsia who had transient, severe anaemia during the puerperital period because of PVB19 infection. Viral genomes were detected in the peripheral blood during the anaemic period by polymerase chain reaction and became undetectable after the anaemia was resolved. Viral genomes and protein could also be detected in bone marrow by in situ hybridization and immunohistochemical staining, respectively. Serial aspiration cytology of bone marrow showed severe dysplastic change involving erythroid precursors with a few apoptotic cells at the initial onset of anaemia, markedly increased apoptotic cells that was confirmed by the increased expression of activated caspase 3, around the nadir of anaemia, and a normal marrow picture without features of apoptosis after recovery from anaemia. Our data indicates that PVB19 infection can induce transient, severe dyserythropoietic anaemia in puerperital women with pre-eclampsia/eclampsia and the pathogenetic mechanism may probably involve the induction of apoptosis following PVB19 infection.

Adult↗
PubMed2000

[Alterations of cerebral hemodynamics in pre-eclampsia and eclampsia].

Clinical and pathophysiological aspects of preeclampsia and eclampsia have been found to be responsible for the majority of maternal mortality, but the exact role of them is still unknown. It is conceivable that altered cerebral hemodynamics and autoregulation is responsible for the neurological complications. The background of the cerebral processes is still not clarified. Authors summarize the changes of cerebral circulation which develop during preeclampsia and explanations for cerebral hemodynamic alterations during normal, preeclamptic and exclamptic pregnancies are discussed. They conclude that there is no accurate method for predicting eclampsia. Cerebral hemodynamical studies are only helpful in better understanding the pathophysiological background of preeclampsia-eclampsia syndrome at present.

Cerebrovascular Circulation↗
PubMed1978

[Pros and cons in the therapy of hypertensive gestoses. I. Pre-eclampsia and eclampsia].

The authors report on the modern trends and the pro and contra in treatment of pre-eclampsia and eclampsia. Ambulatory therapy is only allowed in mild preeclampsia by rest, high-protein lowcaloric diet and mild sedation. Also during the stationary therapy diuretics should be commonly avoided. As sedative drugs magnesium sulfate, diazepam, clomethiazole and barbiturates are recommended. Antihypertensive drugs are given when the blood pressure exceeds 180/110 mm Hg. Favoured drugs are hydralazine, methyldopa and beta adrenergic substances. For the treatment of eclampsia well tried standardized methods with few drugs as magnesium sulfate and when necessary barbiturates and hydralazine are mentioned, furthermore, the combination with new therapeutic managements as the osmo onco-therapy and the modern anaesthetic technics. There is agreement that in severe preeclampsia induction of labor should be performed before term. The indication for that is facilitated by the modern perinatal diagnostics.

Antihypertensive Agents↗
PubMedDate not supplied

[The role of nutritional factors in pre-eclampsia and eclampsia].

Preeclampsia and eclampsia are very important health problems because they are the main contributors to maternal and perinatal morbidity and mortality. These disorders are unique in pregnancy and are characterized by oedema, proteinuria and hypertension. they occur in 0.5% to 30% of all pregnancies, primarily in primigravidas, after the 20-th week of gestation. Preeclampsia and eclampsia are diseases of undetermined cause. Many different factors might play an important role in the development of these diseases. One of them is nutrition. Recent studies have emphasized the possible role of general nutritional deficiency or imbalance of several specific nutrients in the aetiology of the disease. Deficiency of a variety of nutrients has been reported in patients with preeclampsia. The obtained results are contradictory and further study is necessary. Nevertheless, some evidence is highly suggestive of a relationship between nutritional status and the onset or progress of the disease. The article reviews the study that correlates the role of several nutritional elements with the pathophysiology of preeclampsia and eclampsia: proteins, lipids, calcium, vitamin D, sodium, magnesium and zinc. The evidence that supports or rejects the role of each of these nutrients is presented. In this way a guideline for general nutritional counseling in the prenatal period that will promote a healthier pregnancy, is offered.

Eclampsia↗
PubMed1988

The significance of proteinuria in pre-eclampsia; proteinuria associated with low birth weight only in pre-eclampsia.

To examine the significance of proteinuria in pre-eclampsia, we studied 87 nulliparous patients in whom pre-eclampsia was diagnosed clinically and whose blood pressure and urine findings returned to normal after delivery. There was no difference in the gestation at diagnosis, highest systolic and diastolic blood pressures before treatment/delivery, or the number given antenatal hypotensive therapy between patients with proteinuria (group A, n = 46) and without proteinuria (group B, n = 41). Group A patients had higher plasma urea concentration (p less than 0.02), but similar creatinine and urate concentrations to group B patients. Group A patients had a higher rate of induction of labour (p less than 0.04) and Caesarean section before labour (p less than 0.04), and the mean gestation at delivery as well as the birth weight were less (p less than 0.03 and p less than 0.004, respectively). The results suggest that proteinuria in pre-eclampsia is associated with more severe fetal involvement and growth retardation only, but not with an increased severity of the maternal condition such as hypertension and a higher plasma urate concentration.

Blood Pressure↗
PubMed1981

Placental protein 5 (PP5) in severe pre-eclampsia and eclampsia.

Circulating methods of placental protein 5 (PP5) were studied in patients with severe preeclampsia and eclampsia. Elevated PP5 levels were frequently observed in the eclampsia group. This elevation may be due to disturbance in endogenous coagulation mechanisms at the placental site.

Eclampsia↗
PubMed1996

-Obstetric prognosis after pre-eclampsia, eclampsia or HELLP syndrome-.

Preeclampsia, eclampsia and the HELLP syndrome are serious pregnancy complications associated with increased maternal and perinatal mortality and morbidity. The question of subsequent pregnancy outcome in these patients is of great importance for the patient and the obstetrician. The risk of recurrence of hypertensive complications during subsequent pregnancy is related to the time of the onset and the clinical signs of hypertension during the first pregnancy. Patients having hypertensive pregnancies should be examined for chronic hypertension, kidney disease and other internal diseases. The recurrence risk is for preeclampsia between 19.5% and 25.9% and for eclampsia between 21.9% and 46.8%. Patients developing the disease early in pregnancy and with chronic hypertension are at higher risk. For the HELLP syndrome the risk of recurrence is between 3% and 5%. These patients should be considered to be at increased risk for obstetric complications in subsequent pregnancies and close perinatal care is indicated in subsequent pregnancies.

Eclampsia↗
PubMed1996

Thrombelastography changes in pre-eclampsia and eclampsia.

We have measured platelet count, bleeding time and thrombelastography (TEG) variables and the correlation between these variables in 49 pregnant patients presenting with pre-eclampsia or eclampsia. Eighteen patients (37%) had a platelet count < or = 150 x 10(9) litre-1 and seven (14%) had a platelet count < or = 100 x 10(9) litre-1. Bleeding time was prolonged > 9.5 min in 13 (27%) patients and the TEG was abnormal in four (8%). The TEG variables, k time and maximum amplitude (MA) had a strong correlation with platelet count (k time-platelet count < or = 150 x 10(9) litre-1, r = -0.68, P = 0.003, platelet count < or = 100 x 10(9) litre-1, r = -0.84, P = 0.02; MA--platelet count < or = 150 x 10(9) litre-1, r = 0.72, P = 0.001, platelet count < or = 100 x 10(9) litre-1, r = 0.78, P = 0.04). There was no correlation between bleeding time and thrombocytopenia (platelet count < or = 150 x 10(9) litre-1, r = -0.18, ns; platelet count < or = 100 x 10(9) litre-1, r = 0.09, ns). There was no correlation between bleeding time and any measured TEG variable. Of the 10 (20%) patients with an adequate platelet count (> 100 x 10(9) litre-1) but prolonged bleeding time, the TEG was normal, suggesting adequate haemostasis. An MA of 53 mm, which is the lower limit for normal pregnancy, correlated with a platelet count of 54 x 10(9) litre-1 (95% confidence limits 40-75 x 10(9) litre-1). Although the number of patients with severe thrombocytopenia was small, a platelet count of 75 x 10(9) litre-1 should be associated with adequate haemostasis.

Anesthesia, Conduction↗