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A case is presented of a primigravida with severe preeclampsia who, 24 hours after delivery, became hemiparetic and deeply comatose due to acute ischaemia of the left cerebral hemisphere. She was treated with high-dose pentobarbitone therapy when conventional treatment to control raised ICP had failed. A loading dose of pentobarbitone 400 mg (5 mg/kg) was followed by a continuous infusion of 1.0 to 2.5 mg/kg/hour. Withdrawal of the barbiturate after four days of therapy resulted in a rise in ICP above 20 mmHg which necessitated resumption of the drug. After an additional eight days of pentobarbitone therapy with normal ICP values the infusion was discontinued without any change in ICP. The patient made an excellent recovery with no neurologic deficit. The specific pathophysiologic features of pre-eclampsia which were encountered in the patient are detailed. The potential problems which may arise in the pre-eclamptic patient who requires intensive care in the puerperium are emphasised.
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PMID:Postpartum stroke successfully treated with high-dose pentobarbitone therapy: a case report. 682 90

To investigate the association of serum levels of progesterone (P), estradiol (E2), and estriol (E3) with the initiation of regular contractions, venous blood samples were taken prior to and 3 hours after the successful induction of labor in 83 parturients by means of low amniotomy and intravenous oxytocin infusion. The serum P level and P/E2 ratio decreased and serum E2 level increased after induction in healthy primigravidas and in parturients with an initial P dominance (serum P/E2 ratio more than 5). There was also a decrease in the serum P level and P/E2 ratio in postterm patients and parturients with a ripe cervical state. Cholestasis of pregnancy was associated with a rise in the serum level of E2 and a decrease in the P/E2 ratio. In an unfavorable cervical state there was a rise in the serum E2 level; patients with an initial E2 dominance (serum P/E2 ratio 5 or less) showed a rise in the serum P level and P/E2 ratio. Healthy multigravidas and patients with pre-eclampsia did not show any hormonal changes. The onset of induced labor seems to be associated with a rise in serum E2 concentration and/or with a drop in P concentration. The increase in serum E2 level is thought to be due to the activation of the anterior pituitary--adrenal axis. The lower P level is supposedly a result of diminished uteroplacental circulation.
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PMID:Serum progesterone, estradiol, and estriol before and during induced labor. 738 31

Abnormal liver tests occur in 3%-5% of pregnancies, with many potential causes, including coincidental liver disease (most commonly viral hepatitis or gallstones) and underlying chronic liver disease. However, most liver dysfunction in pregnancy is pregnancy-related and caused by 1 of the 5 liver diseases unique to the pregnant state: these fall into 2 main categories depending on their association with or without preeclampsia. The preeclampsia-associated liver diseases are preeclampsia itself, the hemolysis (H), elevated liver tests (EL), and low platelet count (LP) (HELLP) syndrome, and acute fatty liver of pregnancy. Hyperemesis gravidarum and intrahepatic cholestasis of pregnancy have no relationship to preeclampsia. Although still enigmatic, there have been recent interesting advances in understanding of these unique pregnancy-related liver diseases. Hyperemesis gravidarum is intractable, dehydrating vomiting in the first trimester of pregnancy; 50% of patients with this condition have liver dysfunction. Intrahepatic cholestasis of pregnancy is pruritus and elevated bile acids in the second half of pregnancy, accompanied by high levels of aminotransferases and mild jaundice. Maternal management is symptomatic with ursodeoxycholic acid; for the fetus, however, this is a high-risk pregnancy requiring close fetal monitoring and early delivery. Severe preeclampsia itself is the commonest cause of hepatic tenderness and liver dysfunction in pregnancy, and 2%-12% of cases are further complicated by hemolysis (H), elevated liver tests (EL), and low platelet count (LP)-the HELLP syndrome. Immediate delivery is the only definitive therapy, but many maternal complications can occur, including abruptio placentae, renal failure, subcapsular hematomas, and hepatic rupture. Acute fatty liver of pregnancy is a sudden catastrophic illness occurring almost exclusively in the third trimester; microvesicular fatty infiltration of hepatocytes causes acute liver failure with coagulopathy and encephalopathy. Early diagnosis and immediate delivery are essential for maternal and fetal survival.
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PMID:Liver disease in pregnancy. 1826 10

Abnormal liver function tests occur in 3 - 5% of pregnancies for different reasons. Apart from pre-existing liver diseases liver diseases occurring during pregnancy, such as gall stones or viral hepatitis, most liver dysfunctions in pregnancy are caused by one of the five pregnancy-related liver diseases. The five known pregnancy-related liver diseases can be classified in two main categories depending on their association with or without preeclampsia. The preeclampsia-associated liver diseases are the preeclampsia itself, the HELLP-syndrome ("Hemolysis" (H), "Elevated Liver Tests" (EL), "Low Platelet Count" (LP)) and the acute fatty liver of pregnancy. Hyperemesis gravidarum and intrahepatic cholestasis of pregnancy are not associated with preeclampsia. Hyperemesis gravidarum is characterised by intractable vomiting in the first trimester of pregnancy. 50% of patients with this condition have liver dysfunction. Intrahepatic cholestasis of pregnancy presents with pruritus and elevated bile acids in the second half of pregnancy. Patients have often mild jaundice and highly elevated liver enzymes. Treatment of choice is ursodeoxycholic acid to relieve the mother's symptoms. With this condition mainly the fetus is at risk. Severe preeclampsia is the most common cause of liver dysfunction in pregnancy, and is in some cases further complicated by HELLP syndrome. The prompt delivery of the baby is the only definitive therapy. However, many life-threatening maternal complications like liver hematoma or rupture and abruptio placentae can occur. Acute fatty liver of pregnancy is also a severe illness occuring mostly in the third trimester; microvesicular fat deposition in the liver can cause liver failure with coagulopathy and encephalopathy. Only the immediate delivery of the fetus can save mother and child.
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PMID:[Liver diseases in pregnancy]. 1894 56

Liver disorders occurring during pregnancy may be specifically pregnancy-related, or may be due to an intercurrent or chronic liver disease, which may present in anyone, pregnant or not. This review focuses on the liver diseases unique to pregnancy. Hyperemesis gravidarum, which occurs during early pregnancy, may be associated with liver dysfunction. Intrahepatic cholestasis of pregnancy typically occurs during the second or third trimester. Pruritus and the associated biological signs of cholestasis improve rapidly after delivery. Mutations in gene encoding biliary transporters, especially ABCB4 encoding the multidrug resistance 3 protein, have been found to be associated with this complex disease. Ursodeoxycholic acid is currently the most effective medical treatment in improving pruritus and liver tests. Pre-eclampsia, which presents in late pregnancy frequently involves the liver, and HELLP syndrome (Hemolysis-Elevated Liver enzymes-Low Platelets) is a life-threatening complication. Prognosis of acute fatty liver of pregnancy has been radically transformed by early delivery, and clinicians must have a high index of suspicion for this condition when a woman presents nausea or vomiting, epigastric pain, jaundice, or polyuria-polydipsia during the third trimester. Acute fatty liver of pregnancy has been found to be associated with a defect of long-chain 3-hydroxyacyl coenzyme A dehydrogenase in the fetus, and mothers and their offspring should undergo DNA testing at least for the main associated genetic mutation (c.1528G>C).
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PMID:Liver diseases unique to pregnancy: a 2010 update. 2131 Jun 83

Trace elements can play an important role in maternal health and fetal development, and deficiencies in some essential minerals including zinc and copper have been correlated in some individuals to the development of birth defects and adverse health outcomes later in life. The exact etiology of conditions like preeclampsia and the effects of fetal exposure to toxic metals has not been determined, making the assessment of trace element levels crucial to the elucidation of the causes of conditions like preeclampsia. Previous studies analyzing serum and placenta tissue have produced conflicting findings, suggesting the need for a robust, validated sample preparation and analysis method for the determination of trace elements in placenta. In this report, an acid digestion method and analysis by ICP-MS for a broad metallomics/mineralomics panel of trace elements is developed and validated over three experimental days for inter- and intraday precision and accuracy, linear range, matrix impact, and dilution verification. Spike recovery experiments were performed for the essential elements chromium (Cr), iron (Fe), cobalt (Co), nickel (Ni), copper (Cu), and zinc (Zn), and the toxic elements arsenic (As), cadmium (Cd), and lead (Pb) at levels equal to and in excess of native concentrations in control placenta tissue. The validated method will be essential for the development of scientific studies of maternal health and toxic metal exposure effects in childhood.
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PMID:Validation of a Metallomics Analysis of Placenta Tissue by Inductively-Coupled Plasma Mass Spectrometry. 2615 65