Preeclampsia/Eclampsia 1

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WHO-ICD-10 version:2010

Pregnancy, childbirth and the puerperium

Oedema, proteinuria and hypertensive disorders in pregnancy, childbirth and the puerperium

OMIM Number

189800

Mode of Inheritance

Autosomal dominant

Gene Map Locus

1q42.2, 1q24.2, 1p36.22,2p13,3q24 ,6p21.33,7q36.1,Xq23

Description

Preeclampsia is a common condition experienced during pregnancy, characterized by hypertension and proteinuria. About 10% of all pregnancies are associated with preeclampsia. Other symptoms of this condition include severe headaches, nausea, dizziness, increased serum creatinine levels, sudden weight gain, severe upper abdominal pain (which may be confused with heartburn), pulmonary edema, thrombocytopenia, and a failure of the fetus to grow. The condition usually occurs after the 32nd week of gestation and is more commonly seen in women in their first pregnancies, especially those who have a pre-existing condition of hypertension, diabetes, autoimmune diseases, like SLE, thrombophilia, or renal disease. The condition can get complicated if either eclampsia or HELPP Syndrome develops. Eclampsia is a condition where seizures occur during pregnancy, while HELPP Syndrome is characterized by hemolytic anemia, elevated liver enzymes, and low platelet count.

Diagnosis of eclampsia is made on the basis of blood pressure higher than 140/90, and > 300 mg of protein in a 24-hour urine sample. In late stages of pregnancy, the best mode of management of the condition is to induce labor. Magnesium sulfate may be administered during the period of delivery to avoid the occurrence of seizures. In stages of pregnancy where it is too early to consider giving birth, the disease is managed for the duration of pregnancy by taking bed rest, anti-hypertensive medications, and corticosteroids to improve liver and platelet functioning. The condition reverts back to normal within a few weeks after delivery. However, in some cases, preeclampsia may occur 6-8 weeks after delivery.

A definite genetic risk is associated with the development of preeclamspia. Women with affected mother or sisters has three times greater risk of developing the condition. However, it seems that the inheritance pattern is complex and more than one gene may be involved. Genes that have been implicated in providing some kind of susceptibility to preeclampsia include Angiotensin (AGT), Angiotensin Receptors Type 1 and 2 (AGTR1 and AGTR2), Tumor Necrosis Factor Alpha (TNF-Alpha), Nitric Oxide Synthase (NOS3), factor V Leiden variant, and MTHFR genes.

Epidemiology in the Arab World

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Other Reports

Iraq

Al-Jawadi and Fattohe (2004) designed a hospital based study to identify the pregnancy outcomes in mothers with eclampsia or pre-eclampsia in Iraq. A total of 177 pregnant women with PEE were compared to the same number of pregnant women without a history of hypertension, treated as controls. Both cases and control subjects showed high rates of consanguinity (57.6% and 53.1%). The subjects were interviewed, and the neonates were assessed physically. Results showed that Pre-eclampsia (PE) was significantly associated with still birth, low birth weight, as well as low APGAR score. No significant difference was found between cases with PE and those with eclampsia in terms of stillbirths, and low birth weight. However, those with eclampsia were more significantly associated with undergoing a Cesarean section as well as giving birth to babies with low APGAR scores. Most cases of PE fell in the moderate (37.3%) and severe groups (36.7%), while the mild group accorded for only 26% of all PE cases. The severe form was more significantly associated with a low weight or still birth. Interestingly, the cases showed a higher male:female ratio (1.15:1) when compared to control subjects (0.76:1). [Al-Jawadi AA, Fattohe BY. Pre-eclampsia, eclampsia and subsequent pregnancy outcome. J Bahrain Med Soc. 2004; 16(1):24-7.]

Kuwait

Omu et al. (1995) evaluated the levels of interleukin-4 in the sera of 25 preeclamptic women and the cord blood of their newborn infants. Five milliliters of blood were withdrawn from the cubital vein of preeclamptic participants at 24 and 36 wk gestation, at term, and just before onset of labor or in early labor. At delivery, cord blood was withdrawn from each woman's corresponding newborn. The control group was 25 women without any obstetric complication. Interleukin-4 levels were significantly higher in the preeclamptic women than the control women (p < 0.05). Similarly, the interleukin-4 level was significantly higher in the maternal blood of the preeclamptic women than in the cord blood of their newborns (p < 0.01). Omu et al. (1995) suggested that since interleukin-4 increases the expression of class II histocompatibility, it may be important in immunorecognition and immunosuppression. For this, excessive interleukin-4 production may contribute to the pathophysiology of preeclampsia.

Makhseed and Musini (1996) examined the maternal and fetal outcome and the risk factors for developing eclampsia in Kuwait by studying 167,080 subjects during 1981 to 1993 (excluding 1990-1991 because of the Iraqi invasion). A total of 101 mothers suffered from eclampsia, hence, comprising an incidence rate of 6/10,000 that continued to be partly stable throughout the study. The significant risk factors for eclampsia consisted of low birth weight of 2500g or less (RR = 13.96), primiparity (relative risk [RR] = 8.93), preeclampsia (RR = 8.69), multiple pregnancy (RR = 4.15), and age of 30 years or younger (RR = 3.86). Stillbirth, early neonatal death, and Cesarean section occurred more significantly in eclamptic women. One woman passed away due to eclampsia with a maternal mortality rate of 0.99%, representing a higher rate than preeclampsia (0.0405%) and hypertension (0.0396%). Makhseed and Musini (1996) concluded that eclamptic mothers were subjected to poorer pregnancy outcomes compared to other mothers and the risk factors for eclampsia included primiparity, young maternal age, multiple pregnancy, and the presence of preeclampsia.

Omu et al. (1998) studied the correlation among maternal HLA class II and intrauterine growth retardation with associated birth weight of the newborn, in 60 indigenous Kuwaiti women at the time of delivery. The cohort was divided into two groups consisting of 30 preeclamptic women and 30 normotensive controls matched for age, parity and gestation. Results demonstrated a more common DQw3 in controls (p < 0.05) while HLA class II DR2, DR4, DRw11, DRw14 and DRw2 were found to be more common in preeclamptic women (p < 0.04, 0.03, 0.05, 0.03, 0.05). The mean birth weight, low birth weight and mean placental weight were found to be 2.71 +/- 0.73kg, 56.7% and 474.8 +/- 100.8gm, respectively, for preeclampsia in contrast with 3.4 +/- 0.4kg, 6% and 692.0 +/- 107.3gm, respectively, in controls. Furthermore, significant association was found among HLA class II haplotypes DR4 and DQw2 with intrauterine growth retardation with correlated low birth weight and placental weight (p < 0.01). Omu et al. (1998) suggested the possibility of the association between HLA and intrauterine growth retardation being a direct susceptibility factor with the requirement of further elucidation.

Khan et al. (1999) studied NHE1 and cycclooxeganse gene expression patterns in preeclampsia, by measuring the placental protein levels in preeclampsic patients. NHE1 and COX1 levels were found to be reduced in preeclamptic placentas, while COX2 levels remained unaltered. Khan et al. (1999) suggested that suppression of placental NHE1 could be involved in impairment in the uptake of water and electrolytes, thereby precipitating preeclampsia.

In 2000, Olusi et al. analyzed 32 primigravidas with preeclampsia but without any clinical evidence of infection and 32 age-matched primigravidas with uncomplicated normal pregnancies. Phlebotomy was performed at 32 weeks of gestation and blood was subject to immunoassays of interleukin-2 (IL2), interleukin-2 receptor (IL-2R), interleukin-6 (IL-6), interleukin-8 (IL-8) and interleukin-10 (IL-10). Maternal plasma IL-6 and IL-8 concentrations were significantly higher (P<0.05) in normal pregnancy (158.0+/-35.4 pg/mL and 5163.6+/-800 pg/mL, respectively) than in pregnancy complicated with preeclampsia (60.0+/-13.7 pg/mL and 2495.8+/-729.4 pg/mL, respectively). On the other hand, maternal plasma concentration of IL-10 was significantly higher (P<0.05) in preeclampsia (93.2+/-24.1 pg/mL) than in normal pregnancy (31.07+/-7.0 pg/mL). Olusi et al. (2000) concluded that the elevated maternal plasma IL-10 concentration in preeclampsia may be a protective response to maternal immunorejection.

Omu et al. (2004) compared 76 Kuwaiti preclampsic women with age, parity and gestation-matched normotensive controls to study their HLA Class II profiles, and evaluate the expression of T-helper cytokines in preeclampsia. HLA Class II phenotyping revealed a highly significant relative risk ratio of developing preeclampsia with DR4, DRw18, and DQw2. The normotensive controls showed DR1, DRw9, and DQw3 more commonly. Omu et al. (2004) further studied the morphological pattern of the intervillous space in 14 preeclampsic patients with the DR4-DRw18-DQw2 haplotype and compared it to normotensive controls with the DR1-DRw9-DQw3 haplotype. The former group showed excessive syncitial knots, intervillous thrombi, leukocyte and macrophage infiltration, and lack of villous vascularity. In addition, the former group had significantly higher levels of T helper I cytokines IL-8, TNF-alpha, and IFN-gamma in the placental tissue compared to the maternal serum. These same cytokines were also found to be significantly higher in preeclampsics with intrauterine growth retardation than in preeclampsics with neonates of appropriate weight. Omu et al. (2004) proposed a poor development of the immunoregulatory mechanisms associated with a normal pregnancy in preeclampsia. They concluded that women with a DR4-DRw18-DQw2 haplotype may be prone to developing preeclampsia, leading to an increased expression of T helper 1 cytokines and a poor pregnancy outcome as IUGR.

Oman

Bhattacharya and Varghese (2000) reported the development of HELLP syndrome in a 35-year old Omani pregnant lady who was referred because of high blood pressure. At 24 weeks, she suddenly gained four kg and by 28 weeks she had protinuria (1+) without infection. A growth lag with the fetus being 24 weeks was detected by ultrasound which showed normal liquor but a calcified placenta. At 33 weeks, she complained of headache for two days, and examination revealed edema all over. However, there was no protinuria, the optic disc was normal, and her blood pressure was 160/100 mm Hg. Investigations revealed low hemoglobin of 9.2 g/dl, and elevated values of liver and renal function tests. Ultrasound revealed a 31-32 weeks active fetus, grade 2 placenta, and normal liquor. As termination of pregnancy was decided, she received dexamethasone (to improve fetal lung maturity) and the blood pressure was controlled by aldomet 1.5 grams/day, but as she developed features of immenent eclampsia (severe epigastric pain, protinuria 4+, high blood pressure of 190/100 mmHg, and fluid in the perihepatic area on ultrasound), she was operated on with emergency LSCS and a preterm baby (1.57 kg) was born with good Apgar scores. Intraoperatively, no abdominal abnormality was detected except for some perihepatic omental adhesions. She was transfused with whole blood for anemia and low platelets. After eight hours, she developed breathing difficulty, high blood pressure (200/120 mmHg), elevated liver enzymes and low platelets of 50,000/ml with normal morphology and normal coagulation profile (prothrombin time and APTT), and was managed in the intensive care unit with parenteral Hydralazine (for blood pressure), and platelet rich plasma. On the next day, she developed hemoglobinuria and ascites (CT scan ruled out intrahepatic hematoma). Over two days, she received a total of five units of platelet rich plasma as the platelets were still low, which improved by the fourth postoperative day. By the sixth day, her condition improved with improvement of the hematological, hepatic and renal parameters with normalization of her blood pressure. The baby was discharged from the SCBU after a month.

[Bhattacharya P, Varghese P. Platelet dysfunction in pregnancy. Oman Med J. 2000; 17(2):21-5.]

Qatar

Saad et al. (2000) performed a review of cases of Intra-Uterine Fetal Death (IUFD) in Qatar. Of the 10,188 births that took place in the year 1997, a total of 83 were stillborn. Three of these stillbirths were attributed to pregnancy induced hypertension, giving the condition an incidence of 0.3 per 1000 births and 3.6 per 100 stillbirths.

Shahara and Othman (2002) retrospectively studied the incidence, maternal and perinatal complications of eclampsia in Qatar. All cases of eclampsia managed in the Women's Hospital in Qatar between the years 1991 and 2000 were included in the study. Of the total of 94,138 deliveries, there were 39 cases of eclampsia, giving the condition an incidence of 4.1 in 10,000 deliveries. Upon studying the individual annual incidences, no steady trend was noted, with ups and downs since 1991. Pre-term eclampsia (74%) was more common than eclampsia (26%), and was associated with more maternal and perinatal complications. About 24% of the women were noted to have at least one major complication, although there were no maternal fatalities. No antenatal care was provided in the case 36% of these patients. Perinatal mortality was observed to be higher in these patients (25%) when compared to those who received antenatal care (10%). In addition, maternal complications were higher in patients with sub-standard antenatal care (21%), as opposed to those with proper care (8%).

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