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PubMed2001

Pregnancy complicated by pre-eclampsia-eclampsia with HELLP syndrome.

OBJECTIVE: To determine the incidence of, and assess the relationship between liver enzymes and platelet counts with the severity of HELLP (hemolysis elevated liver enzymes and low platelet count) syndrome, and describe incidences of serious maternal complications. MATERIALS AND METHODS: Retrospective descriptive study of patients with pre-eclampsia-eclampsia complicated by HELLP syndrome that occurred over a 3-year period in Panama. The primary outcome included: platelet count; serum aspartate aminotransferase; serum alanine aminotransferase; symptoms and complications among class 1, 2, and 3 HELLP. RESULTS: There were 558 pregnancies complicated by severe pre-eclampsia and 26 by eclampsia. The incidence of HELLP syndrome among women with severe pre-eclampsia in our population was 12% and among women with eclampsia was 34.6%, (P<0.0008); with a total incidence of 16%. Epigastric pain, visual symptoms and hematuria increased with the severity of HELLP syndrome. Hematuria was the fourth symptom, but was significantly (P=0.002) associated with class 1 HELLP. There were significant differences in the platelet count, and liver enzymes among the classes of HELLP syndrome. Abruptio placentae, acute renal failure and disseminated intravascular coagulation were the most frequent maternal complications. There were two maternal deaths. CONCLUSIONS: This study supports the theory that HELLP syndrome is associated with increased maternal morbidity and mortality. Our data suggest that certain subgroups of patients with class 1 HELLP syndrome ('classic or true HELLP') are at increased risk for serious maternal complications, including those with: platelet counts below 50000/microl; lactic dehydrogenase> or = 2000 IU/l; aspartate aminotranferase> or = 500 IU/l; alanine aminotransferase> or = 300 IU/l; and hematuria.

Adult↗
PubMed2001

Placental nitric oxide synthase (NOS) activity and nitric oxide (NO) production in normal pregnancy, pre-eclampsia and eclampsia.

OBJECTIVES: To measure nitric oxide synthase (NOS) activity and total nitrites levels (as an index of nitric oxide 'NO' production) in placental villous homogenate of normal, pre-eclamptic and eclamptic pregnant women. DESIGN: Two groups were studied cross-sectionally: late pregnant women with pre-eclampsia and eclampsia (n=31) and normal pregnant women (all late) as controls (n=32). Two tissue blocks of whole placenta, each 1 x 1 x 1 cm, were collected at delivery and assayed for NOS activity and total nitrite levels. SETTING: Department of Obstetrics and Gynecology, Assiut University Hospitals, Egypt. METHODS: Placental tissues were homogenized and villous homogenates were assayed for NO production by Griess reaction which measures the combined oxidation products for NO (nitrites and nitrates) after reduction with nitrate reductase. NOS activity was determined by measuring NO synthesis by tissue extracts spectrophotometrically using the oxidation of oxyhemoglobin to methemoglobin by NO. RESULTS: Placental villous homogenates of pregnancies complicated by pre-eclampsia and eclampsia had significantly higher NOS activity and total nitrites levels compared with those of normal pregnancy [for NOS (P<0.0001) and for total nitrites (P<0.001)]. CONCLUSIONS: (1) Placental NOS activity and NO production are significantly increased in pre-eclampsia and eclampsia than those of normal pregnancy; this increase was directly related to the severity of this disorder. (2) Such increase possibly represents a physiologic adaptive response to overcome the increased placental vascular resistance and to minimize platelet and leukocyte adhesion to the surface of placental villi or within the intervillous spaces.

Adult↗
PubMed2003

Emergency management of eclampsia and severe pre-eclampsia.

Eclampsia and severe pre-eclampsia are rare, but potentially life-threatening conditions that emergency physicians must be able to diagnose and treat promptly, because initial presentations to the ED are real possibilities. The treatment of the major complications of this disorder, hypertension and seizures, have been the focus of much research. Magnesium sulphate is now the first line agent for acute treatment and prophylaxis of seizures in eclampsia and pre-eclampsia. Severe pre-eclampsia should be treated with magnesium to prevent progression to eclampsia. Severe hypertension requires treatment with an intravenous antihypertensive agent familiar to the clinician. No single antihypertensive has been proven to be better than another, although in Australia, hydralazine is probably the initial intravenous agent of choice. Routine use of invasive haemodynamic monitoring and volume expansion is not recommended and consultation with obstetric colleagues is essential.

Antihypertensive Agents↗
PubMed2001

Increased plasma hyaluronan in severe pre-eclampsia and eclampsia.

Pre-eclampsia is a serious multi-system disorder with general endothelial disease, often with a component of hepatic dysfunction. The pathogenesis of preeclampsia is not fully understood, and no specific diagnostic tests are available for early and reliable diagnosis, or for monitoring of the disease process. Hyaluronan is an extracellular matrix polysaccharide present at low concentrations in plasma. Normally, it is rapidly eliminated from the blood by the liver. Increased concentrations of circulating hyaluronan are seen in conditions with impaired hepatic function such as liver cirrhosis, and hyaluronan concentrations have previously been used to evaluate hepatic function in other diseases. In the present study, 11 pregnant women admitted to the intensive care unit with severe pre-eclampsia or eclampsia were studied. As control 31 healthy pregnant women, 18 undergoing vaginal delivery and 13 caesarean section, were included. Plasma hyaluronan was measured before and after delivery. Increased concentrations of plasma hyaluronan were found in the pre-eclampsia group both before (171 (75-586) microg/L (p<0.01)) and after delivery (215 (124-768) microg/L (p<0.001)) (median and inter-quartile range), as compared to both caesarean section (13 (7-28) microg/L before and 28 (18-48) microg/L after delivery) and vaginal delivery healthy controls (12 (8-24) microg/L before and 30 (13 63) microg/L after delivery). In the control groups, a small increase in plasma hyaluronan was seen after delivery, after both caesarean section (p<0.05) and vaginal delivery (p<0.01). In conclusion, plasma hyaluronan is increased in severe pre-eclampsia and eclampsia. The cause of the increase is unknown.

Adult↗
PubMed1971

Coagulation and fibrinolytic systems in pre-eclampsia and eclampsia.

The coagulation and fibrinolytic mechanisms were investigated in a group of patients with severe pre-eclampsia and eclampsia and the findings were compared with those of healthy women in late pregnancy. In patients with pre-eclampsia the following significant differences were found: (1) greater depression of plasma fibrinolytic activity (euglobulin lysis time) than in normal pregnancy, (2) a higher level of inhibitor to urokinaseinduced lysis, (3) increased levels of serum fibrin degradation products, and (4) reduced platelet counts.In patients with eclampsia a progressive increase of the level of serum fibrin degradation products was found over the three days following eclamptic seizures. No such increase occurred after grand mal seizures in late pregnancy. The findings in this study support the view that intravascular clotting is taking place in pre-eclampsia and that this disturbance of the balance between coagulation and fibrinolysis may be localized to certain areas of the vascular compartment, particularly the placental and renal circulations. Fibrin deposition in the maternal vessels supplying the placenta would impair the placental blood flow, which may explain the placental insufficiency which occurs in pre-eclampsia. Likewise fibrin deposition in the renal vasculature will result in glomerular damage and proteinuria. Hypertension may be related to the renal ischaemic changes or a compensatory response to the presence of fibrin deposition in the vascular compartment. This evidence of intravascular fibrin deposition raises the question of the possible therapeutic value of antithrombotic agents to inhibit the clotting process. On a theoretical basis such treatment might be expected to improve blood flow to the placenta and thereby fetal growth.

Adult↗
PubMed2005

Use of parenteral magnesium sulphate in eclampsia and severe pre-eclampsia cases in a rural set up of Bangladesh.

This was a quasi-experimental interventional study to see the role of injection magnesium sulphate in eclampsia and severe pre-eclampsia patients at community level in a rural set up before referral to the hospital. This study was conducted on 265 cases of eclampsia and severe pre-eclampsia over a period of six months from July 2001 to December 2001. Among 265 cases, 133 were in intervention group who had received loading dose of injection magnesium sulphate before referral and the rest 132 were in non-intervention group, had not received injection magnesium sulphate before admision in hospital. The number (mean +/- SD) of convulsion before treatment in intervention and non-intervention groups were 4.7 +/- 2.64 & 6.86 +/- 2.97 respectively. Recurrence of fits observed more in non-intervention group and the difference was statistically significant (p<.001). Mean (+/- SD) time taken to regain full consciousness was 12.0+9.6 and 17.4+7.4 hours in the intervention and non-intervention group respectively (p<.05). Control of convulsion by loading dose of 10 gm of injection magnesium sulphate was achieved in 94.0% of the intervention group and 74.0% in non-intervention group. There was only 3(2.3%) maternal death in study group whereas in non-intervention group maternal death was 14(10.4%) and the difference was highly significant (p<.005). Fourteen (13.7%) babies were still born in intervention group and 21(20%) in non-intervention group. The difference was statistically highly significant (p<.001). Remarkable achievements were obtained through use of magnesium sulphate at the community level at rural setting among the eclampsia and severe pre-eclampsia cases.

Acute Disease↗
PubMed1998

Circulating vascular cell adhesion molecule-1 in pre-eclampsia, gestational hypertension, and normal pregnancy: evidence of selective dysregulation of vascular cell adhesion molecule-1 homeostasis in pre-eclampsia.

OBJECTIVE: Our purpose was to investigate circulating levels of vascular cell adhesion molecule-1 in the peripheral and uteroplacental circulations during normotensive and hypertensive pregnancies. STUDY DESIGN: This prospective observational study involved 2 patient groups. Group 1 consisted of 22 women with pre-eclampsia and 30 normotensive women followed up longitudinally through pregnancy and post partum. There were an additional 13 women with established gestational hypertension. Group 2 consisted of 20 women with established pre-eclampsia and 19 normotensive control subjects undergoing cesarean delivery. Plasma levels of vascular cell adhesion molecule-1 were measured in blood drawn from the antecubital vein (group 1) and from both the antecubital and uterine veins (group 2). Data were analyzed by analysis of variance. RESULTS: In group 1 vascular cell adhesion molecule-1 levels did not change significantly throughout normal pregnancy and post partum. Women with established pre-eclampsia had increased vascular cell adhesion molecule-1 levels compared with the normotensive pregnancy group (P = .01). Vascular cell adhesion molecule-1 levels were not elevated in women with established gestational hypertension. In group 2 significantly higher levels of vascular cell adhesion molecule-1 were detected in the uteroplacental (P < .0001) and peripheral (P < .0001) circulations of pre-eclamptic women by comparison with normotensive women. In the pre-eclamptic group there was a tendency toward higher vascular cell adhesion molecule-1 levels in the peripheral circulation than in the uteroplacental circulation (P = .06). In contrast to vascular cell adhesion molecule-1, circulating levels of E-selectin and intercellular adhesion molecule-1, other major leukocyte adhesion molecules expressed by the endothelium, were not different in pre-eclamptic and normotensive pregnancies. CONCLUSION: Established pre-eclampsia is characterized by selective dysregulation of vascular cell adhesion molecule-1 homeostasis. This event is not an early preclinical feature of pre-eclampsia, does not persist post partum, is not a feature of nonproteinuric gestational hypertension, and is not observed with other major leukocyte adhesion molecules. Induction of vascular cell adhesion molecule-1 expression in pre-eclampsia may contribute to leukocyte-mediated tissue injury in this condition or may reflect perturbation of other, previously unrecognized, functions of this molecule in pregnancy.

Adult↗
PubMed2005

An audit of the use of magnesium sulphate in severe pre-eclampsia and eclampsia.

Over the last decade there has been an increase in the use of MgSO4 for the prevention of seizures in women with severe pre-eclampsia or eclampsia. At the Rotunda Hospital it is regularly used for this purpose. The aim of this study was to audit the use of MgSO4 at the hospital, to determine whether the drug was being used according to the hospital's protocol and to observe its effectiveness in the prevention of eclampsia in our population. A retrospective chart review over the two years from 1/1/2000 to 31/12/2001 was undertaken. Outcome measures assessed were; Patient selection, Administration of the drug - whether recommended protocols were adhered, Effectiveness of therapy for seizure prophylaxis, Maternal and neonatal outcomes. There were 12,910 deliveries at the Rotunda hospital over this period of time. Fifty of these women were treated with MgSO4 (0.4%). Patient selection was appropriate in all cases. The correct loading dose of MgSO4 was administered in all cases, however MgSO4 levels were recorded in only 30 (60%) of women. There were no seizures in the treated group. Two women presented with seizures (one was antenatal the other post-natal period), both were treated with MgSO4. There were no maternal or neonatal mortality. Seventy two percent (36) of these women were delivered by lower segment caesarean section. The mean gestation at delivery was 36 weeks (range 28-41 weeks). Thirty eight percent (13) of babies required admission to the neonatal intensive care unit. The mean birth weight at delivery was 2.54 kg (range 1.11-3.68 kg). MgSO4 use in the Rotunda hospital appears to be safe and effective for the prevention of seizures in women with severe pre-eclampsia or eclampsia. Serum MgSO4 levels were only recorded in 60% of patients and the hospital's protocol was not adhered to regarding monitoring of patients on treatment. This needs to be addressed.

Adolescent↗
PubMed1986

Genetics of hypertension in pregnancy: possible single gene control of pre-eclampsia and eclampsia in the descendants of eclamptic women.

Our report concerns the incidences of pre-eclampsia and eclampsia in 147 sisters, 248 daughters, 74 granddaughters, and 131 daughters-in-law of women who have had eclampsia. The disorder is highly heritable. We have analysed the data in two ways, firstly, as a single gene condition and, secondly, as a multifactorial condition. The observed incidences fit closely with the single gene model with frequency of the putative gene being 0.25. When Falconer's method of estimating heritabilities of discrete characters is used, estimates of 120% (sisters), 88% (daughters), and 105% (granddaughters)--none significantly different from 100%-are obtained. Insofar as possible, our definition of pre-eclampsia corresponds with EPH in the descriptive classification of the Organisation Gestosis and to 'severe pre-eclampsia' in Nelson's classification. The women were delivered in many different hospitals, however, and many records fail to provide all of the essential information.

Eclampsia↗
PubMed1996

Role of magnesium sulfate in seizure prevention in patients with eclampsia and pre-eclampsia.

Eclampsia is a leading cause of maternal mortality. The prevention of seizure activity in pre-eclampsia and recurrent seizures in eclamptic patients is an essential aspect of management. Many drugs with anticonvulsant properties have been used to treat patients with pre-eclampsia and eclampsia. Magnesium sulfate is a significantly better drug than either diazepam or phenytoin for preventing recurrent seizures in eclamptic patients. Magnesium sulfate has diverse cardiovascular and neurological effects and also alters calcium metabolism. Although the drug crosses the placenta and may affect the fetus, these effects are clinically small and fetal morbidity has been shown to be reduced in randomised studies comparing magnesium sulfate to either phenytoin or benzodiazepines. Dosage regimens of magnesium sulfate are empirical. Because adverse effects of this agent are related to toxicity, the establishment of greater efficacy by using higher dosage regimens needs to be tested against a greater risk of adverse effects. The most serious toxicity related to magnesium sulfate use is magnesium sulfate use is neuromuscular blockade that may result in respiratory arrest. Magnesium sulfate is now the drug choice for treating eclamptic patients. However, further studies are required to establish the role of this agent as a prophylactic agent in the prevention of eclampsia.

Anticonvulsants↗
PubMed2000

Magnesium sulfate in eclampsia and pre-eclampsia: pharmacokinetic principles.

Magnesium sulfate (MgSO4) is the agent most commonly used for treatment of eclampsia and prophylaxis of eclampsia in patients with severe pre-eclampsia. It is usually given by either the intramuscular or intravenous routes. The intramuscular regimen is most commonly a 4 g intravenous loading dose, immediately followed by 10 g intramuscularly and then by 5 g intramuscularly every 4 hours in alternating buttocks. The intravenous regimen is given as a 4 g dose, followed by a maintenance infusion of 1 to 2 g/h by controlled infusion pump. After administration, about 40% of plasma magnesium is protein bound. The unbound magnesium ion diffuses into the extravascular-extracellular space, into bone, and across the placenta and fetal membranes and into the fetus and amniotic fluid. In pregnant women, apparent volumes of distribution usually reach constant values between the third and fourth hours after administration, and range from 0.250 to 0.442 L/kg. Magnesium is almost exclusively excreted in the urine, with 90% of the dose excreted during the first 24 hours after an intravenous infusion of MgSO4. The pharmacokinetic profile of MgSO4 after intravenous administration can be described by a 2-compartment model with a rapid distribution (a) phase, followed by a relative slow beta phase of elimination. The clinical effect and toxicity of MgSO4 can be linked to its concentration in plasma. A concentration of 1.8 to 3.0 mmol/L has been suggested for treatment of eclamptic convulsions. The actual magnesium dose and concentration needed for prophylaxis has never been estimated. Maternal toxicity is rare when MgSO4 is carefully administered and monitored. The first warning of impending toxicity in the mother is loss of the patellar reflex at plasma concentrations between 3.5 and 5 mmol/L. Respiratory paralysis occurs at 5 to 6.5 mmol/L. Cardiac conduction is altered at greater than 7.5 mmol/L, and cardiac arrest can be expected when concentrations of magnesium exceed 12.5 mmol/L. Careful attention to the monitoring guidelines can prevent toxicity. Deep tendon reflexes, respiratory rate, urine output and serum concentrations are the most commonly followed variables. In this review, we will outline the currently available knowledge of the pharmacokinetics of MgSO4 and its clinical usage for women with pre-eclampsia and eclampsia.

Animals↗
PubMed1986

Eclampsia. V. The incidence of nonpreventable eclampsia.

The development of eclamptic convulsions is an obstetric complication that is generally considered to be avoidable. The purpose of this study was to investigate the perinatal events associated with 179 consecutive cases of eclampsia, in order to identify specific preventable factors. Based on a careful analysis of medical care received before the onset of eclampsia, the following factors were judged to be at least partially responsible for the failure to prevent eclamptic convulsions: physician error (n = 65), magnesium sulfate failure (n = 23), late-onset eclampsia (n = 22), early onset (less than 21 weeks) preeclampsia/eclampsia (n = 5), abrupt onset eclampsia (n = 32), and failure of patient to start prenatal care before the onset of eclampsia (n = 34). Fifty-six (31.3%) of the patients received obstetric care that met or exceeded all current standards for delivery of obstetric services. These cases were classified as "unavoidable."

Adolescent↗
PubMed2004

Methodological and technical issues related to the diagnosis, screening, prevention, and treatment of pre-eclampsia and eclampsia.

In contrast with advances made in treating or eliminating many other serious disorders, severe morbidity and mortality associated with pre-eclampsia/eclampsia remain among the leading problems that threaten safe motherhood, particularly in developing countries. This article reviews technical issues related to diagnosis, screening, prevention, and treatment of pre-eclampsia and identifies corresponding needs. The authors stress the lack of standardized definitions of pre-eclampsia and eclampsia and discuss problems in blood-pressure measurements and assessment of urinary protein. They summarize the evidence for prevention strategies and screening tests for early detection. For treatment, magnesium sulfate has been proven effective, but not widely used. The authors outline priorities for narrowing the identified gaps and emphasize the need for coordinated efforts to reduce the morbidity and mortality due to pre-eclampsia/eclampsia. They conclude that the mystery of this disease must be resolved to achieve primary prevention of it.

Developing Countries↗
PubMed2005

The arterial system in pre-eclampsia and chronic hypertension with superimposed pre-eclampsia.

OBJECTIVES: To determine if the normal gestational changes in mechanical properties of the arterial system are altered in pre-eclampsia. DESIGN: Prospective controlled observational study. SETTING: University urban tertiary medical centre. POPULATION: Eleven pre-eclamptics and 10 chronic hypertensives with superimposed pre-eclampsia were compared with 14 normotensive gravidas experiencing preterm labour, all receiving MgSO(4). Two additional control groups were studied as well: (A) nine normal pregnant women receiving neither magnesium nor epidural, for baseline comparisons; and (B) eight normotensive gravidas receiving epidural anaesthesia. METHODS: Two-dimensional targeted M-mode echocardiograms and continuous wave Doppler velocity were used to obtain instantaneous pressure and flow data. Total vascular resistance (TVR) quantified the steady component of systemic arterial load; pulsatile arterial load was characterised by global arterial compliance (AC), aortic input impedance spectrum (Z(1)) and characteristic impedance (Z(0)). MAIN OUTCOME MEASURES: TVR, AC, Z(1), Z(0). RESULTS: Controls, pre-eclamptics and chronic hypertensives with superimposed pre-eclampsia, respectively: TVR index 1328 [299], 1973 [609]*, 2428 [562]*(,#) dyn second cm(-5) m(2); AC area index 1.69 [0.46], 1.19 [0.46]*, 0.93 [0.38]* mL mmHg(-1) m(-2); Z(0) index 253.2 [61.3], 327.0 [135.1], 307.5 [130.9] dyn second cm(-5) m(2); and Z(1) index 184.2 [56.5], 283.6 [81.6]*, 357.1 [119.5]* dyn second cm(-5) m(2) (*P < 0.05 vs control;(#)P < 0.05 vs pre-eclampsia). Normal gravidas (in secondary controls group A) had decreased mean systolic and diastolic blood pressures, and increased AC and cardiac indices, compared with women receiving magnesium tocolysis, verifying the need for these primary controls. No differences were noted between normotensive gravidas receiving epidural anaesthesia (secondary controls group B) and the non-anesthetised controls (group A), eliminating epidural as a confounder. CONCLUSIONS: The normal gestational changes in systemic arterial mechanical properties are significantly altered in pre-eclampsia and these alterations are more marked with superimposed hypertensive disease.

Adult↗
PubMed1995

Which anticonvulsant for women with eclampsia? Evidence from the Collaborative Eclampsia Trial.

Eclampsia, the occurrence of a seizure in association with pre-eclampsia, remains an important cause of maternal mortality. Although it is standard practice to use an anticonvulsant for management of eclampsia, the choice of agent is controversial and there has been little properly controlled evidence to support any of the options. 1687 women with eclampsia were recruited into an international multicentre randomised trial comparing standard anticonvulsant regimens. Primary measures of outcome were recurrence of convulsions and maternal death. Data are available for 1680 (99.6%) women: 453 allocated magnesium sulphate versus 452 allocated diazepam, and 388 allocated magnesium sulphate versus 387 allocated phenytoin. Most women (99%) received the anticonvulsant that they had been allocated. Women allocated magnesium sulphate had a 52% lower risk of recurrent convulsions (95% CI 64% to 37% reduction) than those allocated diazepam (60 [13.2%] vs 126 [27.9%]; ie, 14.7 [SD 2.6] fewer women with recurrent convulsions per 100 women; 2p < 0.00001). Maternal mortality was non-significantly lower among women allocated magnesium sulphate. There were no significant differences in other measures of serious maternal morbidity, or in perinatal morbidity or mortality. Women allocated magnesium sulphate had a 67% lower risk of recurrent convulsions (95% CI 79% to 47% reduction) than those allocated phenytoin (22 [5.7%] vs 66 [17.1%] ie, 11.4 [SD 2.2] fewer women with recurrent convulsions per 100 women; 2p < 0.00001). Maternal mortality was nonsignificantly lower among women allocated magnesium sulphate. Women allocated magnesium sulphate were also less likely to be ventilated, to develop pneumonia, and to be admitted to intensive care facilities than those allocated phenytoin. The babies of women who had been allocated magnesium sulphate before delivery were significantly less likely to be intubated at the place of delivery, and to be admitted to a special care nursery, than the babies of mothers who had been allocated phenytoin. There is now compelling evidence in favour of magnesium sulphate, rather than diazepam or phenytoin, for the treatment of eclampsia.

Adult↗
PubMed2001

Systemic inflammatory indices in pre-eclampsia and eclampsia.

The objective of this study was to test the hypothesis that TNF-alpha, TNFp55 receptor and sICAM-1 are markers of immune activation, protective response to concentrations of TNF-alpha and endothelial cell activation, respectively, in pre-eclampsia. In addition, MPO and sL-selectin were selected as blood discriminators of neutrophil activation. This was a cross-sectional study comparing 21 non-pregnant controls, 29 normal pregnant controls, 21 pre-eclamptic and six eclamptic women. Blood concentrations of TNF-alpha, sTNFp55 receptor, sICAM-1, sL-selectin, myeloperoxidase, leucocyte count, neutrophil count, C-reactive protein and gamma-glutamyl transferase were estimated. The neutrophil count was significantly decreased in pre-eclampsia compared with normal pregnancy (9.12+/-0.95 vs. 12.52+/-0.80 x 10(9)/l, P<0.01). Serum concentrations of sL-selectin were significantly higher in non-pregnant controls compared with pregnant controls (P<0.0001), pre-eclampsia (P<0.0001) and eclampsia (P<0.0001). Serum concentrations of TNF-alpha, sTNFp55 receptor, sICAM-1, sL-selectin and MPO were not significantly different in women with pre-eclampsia compared with normal pregnancy. Serum concentrations of TNF-alpha, sTNFp55, sICAM-1, sL-selectin and MPO did not discriminate between normal and pre-eclamptic pregnancies. The high neutrophil count in normal and eclamptic pregnancies and the lack of shedded L-selectin suggests that neutrophil exudation to inflammatory sites was increased in women with an accompanying inflammatory response.

Journal Article↗
PubMed1978

Studies on plasma fibrinogen level in pre-eclampsia and eclampsia.

The plasma fibrinogen level of maternal blood has been estimated in 30 cases of pre-eclampsia, 60 cases of eclampsia and 35 cases of normal pregnancy of 3rd trimester. The plasma fibrinogen value increased by about 70% and 145% in pre-eclampsia and eclampsia, respectively. In essential hypertension, the fibrinogen level remains more or less the same as in normal pregnancy.

Eclampsia↗
PubMed1977

The management of severe pre-eclampsia and eclampsia.

With improving standards of antenatal care, severe pre-eclampsia dn eclampsia are becoming less common and experience in the management of these conditions is lessening. Co-ordinated plans for the care of patients should be established by obstetricians and anaesthetists working as a team. A suitable regime for drug therapy in severe pre-eclampsia or eclampsia is the following: Initial management Diazepam 10 mg slowly i.v. Pethidine 100-150 mg i.m. or i.v. in incremental dosage, or extradural blocks, if analgesia is also required. Hydrallazine 20 mg i.v. initially, followed by 5 mg at intervals of 20 min until the diastolic pressure is less than 110 mm Hg. Then, preferably by syringe pump in a concentration of 2 mg/ml, at a rate of 2-20 mg/h. If vomiting occurs this can be controlled by administration of atropine. Subsequent management Sedation and anticonvulsant therapy. Continue diazepam and, in severe cases, institute chlormethiazole infusion. Continue analgesia with pethidine or extradural block. Control of hypertension by adjusting the dose of hydrallazine. If tachycardia exceeds 120 beat/min give propanolol 2-4 mg i.v. Plasma protein depletion with groww oedema is treated by administration of salt-free albumin or plasma protein fraction. Diuretic therapy is indicated if there is gross oedema or signs suggestive of acute renal failure. Oliguria associated with increased blood urea may be a result of renal failure or dehydration. The latter should be evident from the patient's condition and central venous pressure, but i.v. fluids and frusemide 20-40 mg can be used as a therapeutic test. Mannitol reduces cerebral oedema and may be given if diuresis has been first produced with frusemide. Potassium chloride is given if the plasma potassium decreases to less than 3 mmol/litre. Heparin therapy is considered if there is clinical evidence of disseminated intravascular coagulation.

Chlormethiazole↗