Diagnosing preeclampsia may be a little difficult as the mild to moderate forms may be asymptomatic and hence, most cases are detected through routine prenatal check-ups. A patient suffering from preeclampsia may present with the following signs and symptoms which are usually endorgan effects: headache, blurred vision, altered mental state, cortical or retinal blindness, edema of the lower limbs or facial edema, dyspnoea, abdominal pain and weakness [5]. There is high blood pressure as a rule.

Complications include seizures, stoke, pulmonary edema, heart failure, blindness and bleeding post-delivery. It is one of the leading causes of premature births, the complications of which include: cerebral palsy, epilepsy and learning disabilities. It also causes stillbirths.

Women, who present with hypertension during pregnancy i.e. new onset hypertension, should have the following tests as mentioned: complete blood counts, serum creatinine, uric acid, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, 24-hour urine collection to check for protein and creatinine [6].

If HELLP syndrome is suspected, the following tests are to be done: peripheral blood smear, indirect bilirubin and serum lactate dehydrogenase (LDH) level. Prothrombin time and platelet count may also be done [5] [6]. A head CT scan may be done to detect intracranial haemorrhage in patients who present with sudden severe headaches and seizures. It is also important to assess the status of the fetus by doing an utrasonogaphy.

In cases of preeclampsia, delivery at the earliest is the only cure. It is usually induced after the 37th week of pregnancy and in severe cases, delivery should be considered after the 34th week of gestation. However, if a patient presents with severe preeclampsia before 34 weeks gestation but appears to be stable and if the condition of the foetus is reassuring, expectant management may be considered if the patient meets the criteria set by Sibai et al. Also, it should only be considered in a tertiary centre. 

Delivery might not be the best option if the fetus is still premature. Before taking any step towards expectant management, a patient must be evaluated for at least 24 hours during which all laboratory values must fall within the normal range. Priority must be given to controlling blood pressure and seizures. It is important to deliver the fetus when there is uncontrollable blood pressure, ruptured membranes, oligohydraminos, non-reassuring fetal heart status, increased levels of serum creatinine and dyspnea. In case of seizures, the airway, breathing and circulation (ABC) should be monitored; magnesium sulphate is the treatment of choice for seizures and is a prophylactic treatment indicated in severe eclampsia [7]. Lorazepam and phenytoin are second-line treatments for seizures.

Various medications such as hydralazine, nifedipine and sodium nitroprusside is used to control blood pressure. To manage fluids patients should be fluid restricted when possible, diuretics should be avoided, and total fluids should be restricted to 80 ml/hour. A check must be kept on liver function tests and the blood pressure levels prior to hospital discharge. Postpartum patients on blood pressure medication should be carefully monitored for up to 4 weeks to rule out recurrent preeclampsia [7] [8].

The prognosis of preeclampsia is not well defined, however most women will have positive outcomes for their pregnancies that have been complicated by preeclampsia. Signs and symptoms generally go away within 6 weeks after pregnancy. Some women will continue to have problems with their blood pressure and will thus need to be monitored closely during the post-partum period.

Most babies do well however, premature babies require a longer stay in the hospital. Seizures during the post-partum period are an uncommon complication. If a woman develops preeclampsia at the end of her pregnancy, she has around 10% chances of developing pre-eclampsia in the subsequent pregnancy. In cases of severe preeclampsia, the woman has a 20% risk of developing it in subsequent pregnancies.

The etiology of preeclampsia is presently unknown although there are around 4 hypotheses which point out to the most probable cause.

The first hypothesis is that of placental ischemia which causes increased trophoblast deploration. Secondly, it could be due to very low-density lipoprotein (VLDL) toxicity wherein to compensate for the increased energy demand during pregnancy, non-esterified fatty acids are mobilized. The third hypothesis suggests an immune maladaptation which causes a shallow invasion of the spiral arteries by the endovascular cytotrophoblast cells [2]. And lastly, genetic imprinting; it is thought that preeclampsia might be the result of a single recessive gene or one dominant gene having incomplete manifestation.

Preeclampsia is commonly seen in women who are nulliparous, above the age of 40 years, is more common amongst the black race and when there is a family history of the disease.

Women with chronic renal disease, diabetes mellitus, high body mass index, anti-phospholipid syndrome and chronic hypertension are also predisposed to developing preeclampsia in their pregnancies. Women with twin pregnancies are also at a risk for the same.

Among all cases, 10% occur in pregnancies of less than 34 weeks gestation. In developing countries, the incidence is 4-18% [3].

Usually, in normal pregnancies the villous cytotrophoblast invades the inner third of the myometrium. The spinal arteries shed the endothelium and majority of their muscle fibres, because of which they become low-resistance vessels making them poorly sensitive, almost insensitive, to vasoconstrictive substances.

The primary cause of preeclampsia is abnormal placentation which is caused by an abnormal invasion of the cytotrophoblast cells into the spiral arteries [3] [4]. The abnormalities may also be associated with the nitric oxide pathway, that is known to contribute to vascular tone and play a role in the inhibition of maternal synthesis of nitric oxide that prevents embryo implantation. An increased resistance from uterine arteries leads to higher sensitivity to vasoconstriction. This effectively causes chronic placental ischemia and increased oxidative stress.

All these factors lead to fetal complications such as intrauterine growth retardation and intrauterine death. Also, oxidative stress causes release of oxidized lipids, cytokines, free radicals, and serum soluble vascular endothelial growth factor 1 (VEGF 1) into the maternal circulation. All these factors thus, contribute to endothelial dysfunction with vascular hyper permeability, thrombophilia and hypertension to make up for the reduced blood supply through the uterine arteries due to peripheral vasoconstriction [4].

The impairment of the hepatic endothelium contributes to the onset of HELLP (Hemolysis, Elevated Liver Enzymes and Low Platelet count) syndrome. THre is also depletion of vascular endothelial growth factors in the podocytes that blocks the slit diaphragms situated in the basement membranes, further adding to reduction in glomerular filtration ultimately producing proteinuria. Vascular hyperpermeability usually associated with low serum albumin causes oedema [4].

There is no particular way to prevent preeclampsia as it is usually diagnosed during antenatal check-ups [9]. Also, preeclampsia is an important disease to screen as it increases maternal and perinatal morbidity and mortality.

No appropriate test is present so far so the only possible way to prevent it would be early detection of modifiable risk factors. For example, nulliparous women above the age of 35 are at higher risk and therefore, interventional care must be provided at the appropriate time.

To prevent the complications of preeclampsia, it is very important to monitor the blood pressure levels frequently, it may help if the placental growth factors and vascular endothelial growth factor levels are monitored [9] [10]. Increased vascular endothelial growth factor combined with decreased placental growth factor is associated with an increased risk of preeclampsia [10]. All these steps for early detection of preeclampsia can enable a practitioner to take the appropriate measures at the right time.

Preeclampsia is a disorder of the vascular endothelium that generally occurs after the 20th week of pregnancy. It is characterized by hypertension and proteinuria with or without the presence of pathological edema.

Mild preeclampsia is usually diagnosed when the blood pressure of a pregnant woman is found to be ≥ 140/90 mm Hg [1]. The condition is termed as severe preeclampsia when one of the following signs or symptoms is present: systolic blood pressure ≥ 160 mm Hg or when the diastolic blood pressure is 110 mm Hg or more, along with proteinuria, oliguria, pulmonary edema and frequent headaches.

There may be signs of impaired foetal growth as well. The HELLP (haemolysis, elevated liver enzyme, low platelets) syndrome may complicate severe preeclampsia as well.

Preeclampsia is a pregnancy related disease whose course cannot be predicted. It can have severe consequences on the life of the mother and the foetus. It is characterized by an elevated blood pressure measuring ≥ 140/90 mm Hg. The patient may experience severe headaches; pain in the stomach, dizziness and shortness of breath.

This disease is usually seen in a woman who is expecting a child when she is above the age of 35 years. There is no known way of preventing preeclampsia however; early diagnosis can reduce the risk of the complications such as the development of seizures, heart failure and liver affections in the mother and also the possibility of a premature baby.

The only way of treating preeclampsia is delivery of the baby. If the pregnancy is not up to term then, then there is a risk if the baby is born premature. It can lead to cerebral palsy, epilepsy and learning disabilities in the baby. Complications of preeclampsia can be controlled if the blood pressure of the mother is monitored regularly.

1. American College of Obstetricians and Gynecologists. Hypertension in pregnancy. ACOG Technical Bulletin No. 219. Washington DC: 1996.
2. Zhou Y, Damsky CH, Fisher SJ. Preeclampsia is associated with failure of human cytotrophoblasts to mimic a vascular adhesion phenotype. One cause of defective endovascular invasion in this syndrome. J Clin Invest. 1997 May 1;99(9):2152-64.
3. Villar J, Betran AP, Gulmezoglu M. Epidemiological basis for the planning of maternal health services.WHO/RHR. 2001.
4. Zhou Y, Damsky CH, Chiu K, et al. Preeclampsia is associated with abnormal expression of adhesion molecules by invasive cytotrophoblasts. J Clin Invest. 1993 Mar;91(3):950-60.
5. Sibai BM. Diagnosis, prevention, and management of eclampsia. Obstet Gynecol. 2005 Feb;105(2):402-10.
6. Baweja S, Kent A, Masterson R, Roberts S, McMahon L. Prediction of pre-eclampsia in early pregnancy by estimating the spot urinary albumin: creatinine ratio using high-performance liquid chromatography. B J OG. 2011 Aug;118(9):1126-32.
7. Sibai BM. Magnesium sulfate prophylaxis in preeclampsia: Lessons learned from recent trials. Am J Obstet Gynecol. 2004 Jun;190(6):1520-6.
8. Sibai BM, Barton JR. Expectant management of severe preeclampsia remote from term: patient selection, treatment, and delivery indications. Am J Obstet Gynecol. 2007 Jun;196(6):514.e1-9.
9. Sibai BM. Prevention of preeclampsia: a big disappointment. Am J Obstet Gynecol. 1998 Nov;179(5):1275-8.
10. Wagner LK. Diagnosis and management of preeclampsia. Am Fam Physician. 2004 Dec 15;70(12):2317-24.