Pregnancy syndrome pre-eclampsia hypertension-Preeclampsia and High Blood Pressure During Pregnancy - ACOG

Preeclampsia is a pregnancy complication characterized by high blood pressure and signs of damage to another organ system, most often the liver and kidneys. Preeclampsia usually begins after 20 weeks of pregnancy in women whose blood pressure had been normal. Left untreated, preeclampsia can lead to serious — even fatal — complications for both you and your baby. If you have preeclampsia, the most effective treatment is delivery of your baby. Even after delivering the baby, it can still take a while for you to get better.

Pregnancy syndrome pre-eclampsia hypertension

Pregnancy syndrome pre-eclampsia hypertension

The decision for hospital or outpatient Sexy seethrough l bodies will depend heavily on the sociocultural conditions of the patient, and when identifying any problems that may compromise the proper surveillance of cases, hospitalization becomes essential. However, it is more frequent in these associations. Antihypertensive drug therapy formild tomoderatehypertensionduring pregnancy. Patients in this category are Pregnancy syndrome pre-eclampsia hypertension well, without any signs of superimposed pre-eclampsia. Pre-eclampsia is a multifactorial and multisystemic disease specific to gestation. Hence, concerning the diagnosis, preeclampsia is considered hypertension after the twentieth week and one of the following criteria:. Endothelial activation basically determines: vasoconstriction and consequent increase in peripheral resistance; changes in capillary permeability, which are responsible for edema; and activation of the coagulation system.

Women ovulation induction clomid. Preeclampsia and High Blood Pressure During Pregnancy

Related Urinalysis. Delivery by cesarean delivery C-section may be necessary if there are clinical or obstetric conditions that require a speedy delivery. In general, none of the signs of synndrome are specific, and even convulsions in pregnancy are more pree-clampsia to Heather hays naked causes other than eclampsia in modern practice. Dan Louis Because pre-eclampsia Pregnancy syndrome pre-eclampsia hypertension to a mismatch between the maternal energy supply and fetal energy demands, pre-eclampsia can lead to IUGR in the developing fetus. Make sure you attend your prenatal visits so that your care provider can monitor your blood pressure. Swelling especially in the hands and face was originally considered an important sign for a diagnosis of pre-eclampsia. This prevents maternal vasoconstriction in the spiral arteries and allows for continued blood and nutrient supply to the growing fetus with low resistance and high blood flow. Obstetrics and gynecology 6th ed. This impairs extravillus trophoblast cells invasion to the maternal spiral arteries, causing high resistance and low blood flow and low nutrient supply to the fetus. Left untreated, postpartum preeclampsia can cause seizures and other serious complications. Those with Pregnancy syndrome pre-eclampsia hypertension term high blood pressure have a risk 7 to 8 times higher than those without. Pre-eclampsia is one of the leading causes of maternal and perinatal morbidity and mortality worldwide.

Pre-eclampsia is a multifactorial and multisystemic disease specific to gestation.

  • Pre-eclampsia PE is a disorder of pregnancy characterized by the onset of high blood pressure and often a significant amount of protein in the urine.
  • Gestational hypertension or pregnancy-induced hypertension PIH is the development of new hypertension in a pregnant woman after 20 weeks' gestation without the presence of protein in the urine or other signs of pre-eclampsia.
  • Preeclampsia is a pregnancy complication characterized by high blood pressure and signs of damage to another organ system, most often the liver and kidneys.
  • Postpartum preeclampsia is a rare condition that occurs when you have high blood pressure and excess protein in your urine soon after childbirth.
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Pre-eclampsia PE is a disorder of pregnancy characterized by the onset of high blood pressure and often a significant amount of protein in the urine. Risk factors for pre-eclampsia include obesity , prior hypertension , older age, and diabetes mellitus. Rarely, pre-eclampsia may begin in the period after delivery. Recommendations for prevention include: aspirin in those at high risk, calcium supplementation in areas with low intake, and treatment of prior hypertension with medications.

Swelling especially in the hands and face was originally considered an important sign for a diagnosis of pre-eclampsia.

However, because swelling is a common occurrence in pregnancy, its utility as a distinguishing factor in pre-eclampsia is not high. Pitting edema unusual swelling, particularly of the hands, feet, or face, notable by leaving an indentation when pressed on can be significant, and should be reported to a health care provider.

In general, none of the signs of pre-eclampsia are specific, and even convulsions in pregnancy are more likely to have causes other than eclampsia in modern practice.

Further, a symptom such as epigastric pain may be misinterpreted as heartburn. Diagnosis, therefore, depends on finding a coincidence of several pre-eclamptic features, the final proof being their regression after delivery. There is no definitive known cause of pre-eclampsia, though it is likely related to a number of factors.

Some of these factors include: [2] [10]. Those with long term high blood pressure have a risk 7 to 8 times higher than those without. Physiologically, research has linked pre-eclampsia to the following physiologic changes: alterations in the interaction between the maternal immune response and the placenta, placental injury, endothelial cell injury, altered vascular reactivity, oxidative stress, imbalance among vasoactive substances, decreased intravascular volume, and disseminated intravascular coagulation.

While the exact cause of pre-eclampsia remains unclear, there is strong evidence that a major cause predisposing a susceptible woman to pre-eclampsia is an abnormally implanted placenta. Endothelial dysfunction results in hypertension and many of the other symptoms and complications associated with pre-eclampsia. Abnormal chromosome 19 microRNA cluster C19MC impairs extravillus trophoblast cell invasion to the spiral arteries, causing high resistance, low blood flow, and low nutrient supply to the fetus.

Known risk factors for pre-eclampsia include: [6] [20]. Although much research into mechanism of pre-eclampsia has taken place, its exact pathogenesis remains uncertain. Pre-eclampsia is thought to result from an abnormal placenta, the removal of which ends the disease in most cases. The placenta of women with pre-eclampsia is abnormal and characterized by poor trophoblastic invasion.

The clinical manifestations of pre-eclampsia are associated with general endothelial dysfunction, including vasoconstriction and end-organ ischemia. Both sFlt-1 and sEng are upregulated in all pregnant women to some extent, supporting the idea that hypertensive disease in pregnancy is a normal pregnancy adaptation gone awry.

As natural killer cells are intimately involved in placentation and placentation involves a degree of maternal immune tolerance for a foreign placenta, it is not surprising that the maternal immune system might respond more negatively to the arrival of some placentae under certain circumstances, such as a placenta which is more invasive than normal. Initial maternal rejection of the placental cytotrophoblasts may be the cause of the inadequately remodeled spiral arteries in those cases of pre-eclampsia associated with shallow implantation, leading to downstream hypoxia and the appearance of maternal symptoms in response to upregulated sFlt-1 and sEng.

Oxidative stress may also play an important part in the pathogenesis of pre-eclampsia. The main source of reactive oxygen species ROS is the enzyme xanthine oxidase XO and this enzyme mainly occurs in the liver. One hypothesis is that the increased purine catabolism from placental hypoxia results in increased ROS production in the maternal liver and release into the maternal circulation that causes endothelial cell damage.

Abnormalities in the maternal immune system and insufficiency of gestational immune tolerance seem to play major roles in pre-eclampsia. These findings have given rise to the hypothesis that pre-eclampsia is a disease process by which a placental lesion such as hypoxia allows increased fetal material into the maternal circulation, that in turn leads to an immune response and endothelial damage, and that ultimately results in pre-eclampsia and eclampsia.

One hypothesis for vulnerability to pre-eclampsia is the maternal-fetal conflict between the maternal organism and fetus. Another evolutionary hypothesis for vulnerability to pre-eclampsia is the idea of ensuring pair-bonding between the mother and father and paternal investment in the fetus. In normal early embryonic development, the outer epithelial layer contains cytotrophoblast cells, a stem cell type found in the trophoblast that later differentiates into the fetal placenta.

These cells differentiate into many placental cells types, including extravillous trophoblast cells. Extravillous trophoblast cells are an invasive cell type which remodel the maternal spiral arteries by replacing the maternal epithelium and smooth muscle lining the spiral arteries causing artery dilation.

This prevents maternal vasoconstriction in the spiral arteries and allows for continued blood and nutrient supply to the growing fetus with low resistance and high blood flow. In pre-eclampsia, abnormal expression of chromosome 19 microRNA cluster C19MC in placental cell lines reduces extravillus trophoblast migration. This impairs extravillus trophoblast cells invasion to the maternal spiral arteries, causing high resistance and low blood flow and low nutrient supply to the fetus.

Immune factors may also play a role. Testing for pre-eclampsia is recommended throughout pregnancy via measuring a woman's blood pressure. Pre-eclampsia is diagnosed when a pregnant woman develops: [32].

Suspicion for pre-eclampsia should be maintained in any pregnancy complicated by elevated blood pressure, even in the absence of proteinuria. Pre-eclampsia is a progressive disorder and these signs of organ dysfunction are indicative of severe pre-eclampsia. There have been many assessments of tests aimed at predicting pre-eclampsia, though no single biomarker is likely to be sufficiently predictive of the disorder.

Examples of notable tests include:. Pre-eclampsia can mimic and be confused with many other diseases, including chronic hypertension, chronic renal disease, primary seizure disorders, gallbladder and pancreatic disease , immune or thrombotic thrombocytopenic purpura , antiphospholipid syndrome and hemolytic-uremic syndrome. It must be considered a possibility in any pregnant woman beyond 20 weeks of gestation.

It is particularly difficult to diagnose when pre-existing conditions such as hypertension are present. Other disorders that can cause high blood pressure include thyrotoxicosis , pheochromocytoma , and drug misuse.

Preventive measures against pre-eclampsia have been heavily studied. Because the pathogenesis of pre-eclampsia is not completely understood, prevention remains a complex issue. Below are some of the currently accepted recommendations. Supplementation with a balanced protein and energy diet does not appear to reduce the risk of pre-eclampsia. Supplementation with antioxidants such as vitamin C, D and E has no effect on pre-eclampsia incidence; [39] [40] therefore, supplementation with vitamins C, E, and D is not recommended for reducing the risk of pre-eclampsia.

Calcium supplementation of at least 1 gram per day is recommended during pregnancy as it prevents pre-eclampsia where dietary calcium intake is low, especially for those at high risk. There is insufficient evidence to recommend either exercise [46] or strict bedrest [47] as preventive measures of pre-eclampsia. In low-risk pregnancies, the association between cigarette smoking and a reduced risk of pre-eclampsia has been consistent and reproducible across epidemiologic studies.

High-risk pregnancies those with pregestational diabetes, chronic hypertension, history of pre-eclampsia in a previous pregnancy, or multifetal gestation showed no significant protective effect.

The reason for this discrepancy is not definitively known; research supports speculation that the underlying pathology increases the risk of pre-eclampsia to such a degree that any measurable reduction of risk due to smoking is masked.

Some studies have suggested the importance of a woman's gestational immunological tolerance to her baby's father, as the baby and father share genetics.

There is tentative evidence that ongoing exposure either by vaginal or oral sex to the same semen that resulted in the pregnancy decreases the risk of pre-eclampsia.

Several other studies have since investigated the decreased incidence of pre-eclampsia in women who had received blood transfusions from their partner, those with long preceding histories of sex without barrier contraceptives, and in women who had been regularly performing oral sex.

Having already noted the importance of a woman's immunological tolerance to her baby's paternal genes, several Dutch reproductive biologists decided to take their research a step further. Consistent with the fact that human immune systems tolerate things better when they enter the body via the mouth, the Dutch researchers conducted a series of studies that confirmed a surprisingly strong correlation between a diminished incidence of pre-eclampsia and a woman's practice of oral sex, and noted that the protective effects were strongest if she swallowed her partner's semen.

The team has found that certain men, dubbed "dangerous males", are several times more likely to father pregnancies that would end in either pre-eclampsia or miscarriage. As the theory of immune intolerance as a cause of pre-eclampsia has become accepted, women who with repeated pre-eclampsia, miscarriages, or in vitro fertilization failures could potentially be administered key immune factors such as TGF-beta along with the father's foreign proteins, possibly either orally, as a sublingual spray, or as a vaginal gel to be applied onto the vaginal wall before intercourse.

The definitive treatment for pre-eclampsia is the delivery of the baby and placenta. The timing of delivery should balance the desire for optimal outcomes for the baby while reducing risks for the mother. Treatment can range from expectant management to expedited delivery by induction of labor or Caesarean section , in addition to medications. Important in management is the assessment of the mothers organ systems, management of severe hypertension, and prevention and treatment of eclamptic seizures.

Bed rest has not been found to be useful and is thus not routinely recommended. The World Health Organization recommends that women with severe hypertension during pregnancy should receive treatment with anti-hypertensive agents. The goal of treatment of severe hypertension in pregnancy is to prevent cardiovascular, kidney, and cerebrovascular complications.

The intrapartum and postpartum administration of magnesium sulfate is recommended in severe pre-eclampsia for the prevention of eclampsia. Pre-eclampsia is one of the leading causes of maternal and perinatal morbidity and mortality worldwide. Pre-eclampsia is much more common in women who are pregnant for the first time. Eclampsia is a major complication of pre-eclampsia.

Eclampsia affects 0. Complications of pre-eclampsia can affect both the mother and the fetus. Acutely, pre-eclampsia can be complicated by eclampsia , the development of HELLP syndrome , hemorrhagic or ischemic stroke , liver damage and dysfunction, acute kidney injury , and acute respiratory distress syndrome ARDS. Pre-eclampsia is also associated with increased frequency of Caesarean section , preterm delivery , and placental abruption. Furthermore, an elevation in blood pressure can occur in some individuals in the first week postpartum attributable to volume expansion and fluid mobilization.

Long-term, an individual with pre-eclampsia is at increased risk for recurrence of pre-eclampsia in subsequent pregnancies.

Eclampsia is the development of new convulsions in a pre-eclamptic patient that may not be attributed to other cause. It is a sign that the underlying pre-eclamptic condition is severe and is associated with high rates of perinatal and maternal morbidity and mortality. HELLP syndrome is defined as hemolysis microangiopathic , elevated liver enzymes liver dysfunction , and low platelets thrombocytopenia.

There is also an increased risk for cardiovascular complications, including hypertension and ischemic heart disease, and kidney disease. Lowered blood supply to the fetus in pre-eclampsia causes lowered nutrient supply, which could result in intrauterine growth restriction IUGR and low birth weight.

Because pre-eclampsia leads to a mismatch between the maternal energy supply and fetal energy demands, pre-eclampsia can lead to IUGR in the developing fetus. Associated adult diseases of the fetus due to IUGR include, but are not limited to, coronary artery disease CAD , type 2 diabetes mellitus T2DM , cancer, osteoporosis, and various psychiatric illnesses.

The risk of pre-eclampsia and development of placental dysfunction has also been shown to be recurrent cross-generationally on the maternal side and most likely on the paternal side.

The word "eclampsia" is from the Greek term for lightning. An outdated medical term for pre-eclampsia is toxemia of pregnancy, a term that originated in the mistaken belief that the condition was caused by toxins.

From Wikipedia, the free encyclopedia. Pre-eclampsia Other names Preeclampsia, toxaemia PET A micrograph showing hypertrophic decidual vasculopathy , a finding seen in gestational hypertension and pre-eclampsia. Shorthand for laboratory values commonly used in pre-eclampsia. Journal of Pregnancy.

Journal of Clinical Medicine Research. Archived PDF from the original on

Wei SQ. Maternal morbidity associated with early-onset and late-onset preeclampsia. A hemochorial placenta optimizes the amount of oxygen and nutrients that can be absorbed into the fetal blood supply, while at the same time ensuring rapid diffusion of wastes away from the fetus. Heart J. American Journal of Emergency Medicine. An outdated medical term for pre-eclampsia is toxemia of pregnancy, a term that originated in the mistaken belief that the condition was caused by toxins. Archived PDF from the original on

Pregnancy syndrome pre-eclampsia hypertension

Pregnancy syndrome pre-eclampsia hypertension

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Accessed March 12, Committee Opinion No. Giwa A, et al. Late onset postpartum preeclampsia 3 months after delivery. American Journal of Emergency Medicine.

Skurnik G, et al. Labor therapeutics and BMI as risk factors for postpartum preeclampsia: A case-control study. Walls RM, et al. Acute complications of pregnancy. Philadelphia, Pa. Accessed March 5, Bigelow CA, et al. Risk factors for new-onset late postpartum preeclampsia in women without a history of preeclampsia. American Journal of Obstetrics and Gynecology. Gabbe SG, et al. Preeclampsia and hypertensive disorders.

In: Obstetrics: Normal and Problem Pregnancies. Lisonkova S, et al. Maternal morbidity associated with early-onset and late-onset preeclampsia. Obstetrics and Gynecology. Elfarra J, et al. Obstetrics and Gynecology Clinics of North America. Roberts JM, et al. August P. Management of hypertension in pregnant and postpartum women.

Related Urinalysis. Associated Procedures Urinalysis. Gestational hypertension or pregnancy-induced hypertension PIH is the development of new hypertension in a pregnant woman after 20 weeks' gestation without the presence of protein in the urine or other signs of pre-eclampsia. No single diagnostic test currently exists to predict the likelihood of developing gestational hypertension. High blood pressure is the major sign in diagnosing gestational hypertension.

Some women with gestational hypertension may present asymptomatic, but a number of symptoms are associated with the condition. There exist several hypertensive states of pregnancy :. Pre-eclampsia and eclampsia are sometimes treated as components of a common syndrome. There is no specific treatment, but is monitored closely to rapidly identify pre-eclampsia and its life-threatening complications HELLP syndrome and eclampsia.

Drug treatment options are limited, as many antihypertensives may negatively affect the fetus. Methyldopa , hydralazine , and labetalol are most commonly used for severe pregnancy hypertension.

The fetus is at increased risk for a variety of life-threatening conditions, including pulmonary hypoplasia immature lungs. If the dangerous complications appear after the fetus has reached a point of viability, even though still immature, then an early delivery may be warranted to save the lives of both mother and baby. An appropriate plan for labor and delivery includes selection of a hospital with provisions for advanced life support of newborn babies.

Gestational hypertension is one of the most common disorders seen in human pregnancies. For years, it has been the belief of the scientific community that gestational hypertension and pre-eclampsia were relatively unique to humans, although there has been some recent evidence that other primates can also suffer from similar conditions, albeit due to different underlying mechanisms.

Humans have evolved to have a very invasive placenta to facilitate better oxygen transfer from the mother to the fetus, to support the growth of its large brain. The origins of gestational hypertension may lie with the development of humans' hemochorial placenta.

A hemochorial placenta optimizes the amount of oxygen and nutrients that can be absorbed into the fetal blood supply, while at the same time ensuring rapid diffusion of wastes away from the fetus.

This hemochorial placenta differs from lower primates' epitheliochorial placentae in the way that it allows the fetal tissues to interact directly with the mother's blood.

The hemochorial placenta thereby promotes more rapid diffusion to and from the fetal blood supply. In animals with epitheliochorial placentae such as horses and pigs, the greatest resistance to maternal blood flow in the vascular system was found within the placenta.

However, in animals with hemochorial placental structures such as rodents and primates, the vascular resistance in the placenta was low, leading scientists to the conclusion that the greatest resistance to maternal blood flow is found elsewhere in the maternal vascular system.

The fetal cells that implant into the uterine wall are known as the trophoblast. The hemochorial placenta bathes the fetal trophoblast in maternal blood by forming lacunae, or lakes, of the mother's blood that surround fetal tissue.

The lacunae are filled by the spiral arteries, which means that the mother's blood pressure is the driving force behind the introduction of new blood, which contains both oxygen and food for the fetus, to the system. It is thought that "failings" in normal hemochorial placental structure lead to pre-eclampsia and gestational hypertension.

Miscarriage and pre-eclampsia are both very rare in other species, but are two of the most common pregnancy-related diseases in humans. One of the potential causes of gestational hypertension and pre-eclampsia is when the trophoblast does not invade far enough into the uterine lining. The highly invasive placenta that is found in humans is thought to be linked to humans' high circulating levels of the hormones CG and hCG.

It has been shown that the higher the levels of these hormones, the deeper the trophoblast's invasion into the uterine wall. Instances of gestational hypertension and pre-eclampsia have been shown to occur when the invasion of the uterine wall is not deep enough, because of lower CG and hCG levels in the mother. Despite these risks for gestational hypertension, the hemochorial placenta has been favored because of its advantages in the way that it aids in diffusion from mother to fetus later in pregnancy.

The bipedal posture that has allowed humans to walk upright has also led to a reduced cardiac output, and it has been suggested that this is what necessitated humans' aggressive early placental structures.

Similarly, the advantages of having a large brain size have outweighed the deleterious effects of having a placenta that does not always convert the spiral arteries effectively, leaving humans vulnerable to contracting gestational hypertension.

Pre-eclampsia - NHS

Hypertension developing during pregnancy may be caused by a variety of different pathophysiological mechanisms. The occurrence of proteinuric hypertension during the second half of pregnancy identifies a group of women whose hypertensive disorder is most likely to be caused by the pregnancy itself and for whom the risk of complications, including maternal mortality, is highest.

Physicians identifying patients with hypertension in pregnancy need to discriminate between pre-eclampsia and other forms of hypertensive disease. Pre-eclamptic disease requires obstetric intervention before it will resolve and it must be managed in a multidisciplinary environment.

The principles of diagnosis and management of these different entities are outlined in this review. Two hospital-based studies in sub-Saharan Africa have put the prevalence of this disorder at Hypertension during pregnancy is not only common but also associated with a risk of morbidity and mortality.

Pre-eclampsia is uniquely manifest during pregnancy and is associated with a pathophysiological phenotype that encompasses placental disease, growth restriction of the foetus and the development of severe but reversible hypertension during pregnancy. In this review we discuss the different types of hypertension during pregnancy, and the physician evaluation, including physical examination and laboratory investigations of the hypertensive pregnant patient.

Pre-eclampsia affects one in 30 primigravid women and one in 60 women in their second or subsequent pregnancies. Obstetric risk factors include an increasing risk of developing pre-eclampsia related to multiple and even higher-order multiple pregnancies. A large placenta, such as those seen in women with trophoblastic disease or various kinds of foetal aneuploidy, are also associated with an increased risk of developing pre-eclampsia. Other risk factors that have been identified as leading to an increased probability of pre-eclampsia developing during pregnancy include antiphospholipid antibody syndrome, chronic hypertension, chronic renal disease, a maternal age over 40 years, nulliparity, incidence of pre-eclampsia in a previous pregnancy and pre-gestational diabetes.

The highest incidence of pre-eclampsia is among women having their first baby, whereas the greater prevalence of the disease is in multiparous pregnant women. The disease is described as a condition of primigravidity but it is also, to some extent, associated with primipaternity.

Pre-eclampsia is a syndrome characterised by the development of hypertension and proteinuria in the latter part of pregnancy, which then remits after delivery. Hypertension is defined in different ways but the most widely accepted definition is the sustained elevation of diastolic blood pressure above 90 mmHg over a period of four hours. The hour urinary excretion of protein greater than mg is regarded as being pathological.

Pre-eclampsia may present in an asymptomatic form. It may also develop acutely or progress to a phase of illness in which multi-organ disease becomes evident. Many of these complications of pre-eclampsia may be lifethreatening to the foetus and the pregnant woman.

Characteristically, the delivery of the baby signals the onset of disease resolution, although the mother may continue to exhibit worsening disease for up to 24 hours after delivery. The hypertension associated with pre-eclampsia may take up to six weeks to resolve completely, even if the risk of fulminant disease abates within 24 hours of parturition. Pre-eclampsia is a disease of defective placentation. The placenta itself is usually small and infarcted to a greater extent than is usually seen in normal pregnancy.

The evolution of the clinical phenotype follows these pathophysiological events in the placental bed. The precise mechanisms are not fully elucidated but some combination of systemic immune activation in response to an increasing maternal circulatory burden of trophoblastic tissue released from the ischaemic placenta combines with components of oxidative stress and an imbalance in the production of angiogenic and anti-angiogenic factors to give rise to changes in systemic vascular endothelial function.

The volume-overloaded circulation of normal pregnancy is offset by endothelial-dependent vasodilatation to such an extent that normal pregnancy is characterised by falling blood pressure, despite the volume overload. The pattern of hypertension may evolve through stages where the increased systemic pressure may be partly based upon increased cardiac output, compensatory for the diminished perfusion of the placenta through narrow vessels in the placental bed.

Specific organs show patterns of ischaemic change, and haemorrhage with or without oedema. These include the brain, kidneys, placenta and liver. The liver shows periportal ischaemia and haemorrhage in women with the HELLP syndrome, whereas the kidneys show evidence of endotheliosis, associated in some cases with acute tubular and cortical ischaemic damage. The cardiovascular and pulmonary changes seen are those of pulmonary oedema in severe cases, usually without other overt signs of heart failure.

There are two major causes of death among women with pre-eclampsia, cerebrovascular haemorrhage and pulmonary oedema, and each account for roughly half the number of deaths. Cerebrovascular haemorrhage is related to severe hypertension.

This is commonly considered to be mmHg. It is unusual for women to develop such severe hypertension without associated seizure activity. The development of eclampsia leads to severe hypertension during seizure activity and it is the reason why the case fatality rate for eclampsia is cited as one in 50, whereas the overall case fatality rate of pre-eclampsia is set at one in 1 Pulmonary oedema may develop for different reasons.

The iatrogenic administration of excessive amounts of intravenous fluids may lead to an absolute increase in preload, resulting directly in interstitial pulmonary oedema. The loss of protein in the urine may lower the colloid osmotic pressure and contribute to development of the generalised oedema so characteristic of pre-eclampsia, with similar effects on the lungs.

Changes in capillary permeability and the lymphatic drainage of the lungs all modulate the risk of pulmonary oedema in women with variable changes in vascular resistance and ventricular function. Consequently, the precise mechanism of pulmonary oedema cannot be simply attributed to heart failure in this condition. Pre-eclampsia is not a condition that can be managed adequately outside a hospital environment.

Because the foetus is at risk of impaired growth and likely to deliver prematurely, management needs to take place in an obstetric unit with access to the best available level of paediatric care. Any improvement in neonatal outcome can only be secured by minimising the risks of prematurity. The development of symptoms, an uncontrollable spike in blood pressure or the evolution of defined organ dysfunction signal the onset of life-threatening disease, requiring that the focus of treatment shift from the neonatal outcome to protecting the interests of the mother.

Delivery at this point is inevitable and the neonate will need to be cared for in the best available circumstances. The second means of improving perinatal outcome revolve around the use of corticosteroids, given to the mother. These accelerate the maturation of the foetal lungs and lessen the likelihood of neonatal intraventricular haemorrhage in the newborn. The prevention of eclampsia is ensured by the use of magnesium sulphate, given as a continuous infusion or as intermittent intramuscular doses.

The mechanism of action is poorly understood and the use of magnesium sulphate needs to be weighed against potential risks. These include the development of toxicity, which is more common in women with renal failure. Toxicity leads to respiratory arrest, which can be reversed with intravenous calcium gluconate.

Women who are fitting should have their seizures aborted with intravenous benzodiazepines. Proper management of severe hypertension is always a priority. Drugs used to lower the blood pressure are a variety of agents, including direct-acting vasodilators hydrallazine, dihydrallazine , calcium channel blockers nifedipine , alpha-and beta-blockers labetalol , and combined arterial and venous vasodilators nitroglycerine.

Potent vasodilators such as sodium nitroprusside or diazoxide should not be used because they are associated with a risk of precipitous decline in blood pressure.

Eclampsia requires attention to seizure control as outlined above. Recurrent seizures may only be controllable by continuous infusion of propofol or diazepam; this usually requires intubation and ventilation for up to 24 hours after delivery has been effected.

The co-morbidity associated with seizures needs individual management see below ; specific screening and treatment of aspiration pneumonia is important. Any focal neurological signs merit neuro-radiological investigation to exclude haemorrhage and infarction.

The differential diagnosis of seizure activity also merits consideration and may extend to other possible diagnoses, including metabolic causes for seizure activity, thrombotic thrombocytopaenic purpura, systemic lupus erythematosis, cerebral venous thrombosis, malaria and amniotic fluid embolus.

Renal failure may be manifest on the basis of diminished preload together with peripheral, including renal, vasospasm. Acute renal injury may also cause oliguria and azotaemia. This is the consequence of ischaemia due to pre-eclampsia or pre-eclampsia complicated by hypovolaemia caused by abruptio placentae and haemoglobinuria. The principles of management are those of cautious intravascular volume expansion no more than ml of colloidal solution given as a bolus dose and vasodilatation.

This condition needs to be distinguished from other causes of micro-angiopathic haemolytic anaemia as well as other causes of liver failure. The differential diagnosis therefore includes thrombotic thrombocytopenic purpura, acute fatty liver of pregnancy, auto-immune disease, malaria and sepsis.

The hallmark of the HELLP syndrome is that it reverses after delivery, with the nadir of thrombocytopaenia occurring on the third day postpartum. Patients who do not exhibit the characteristic resolution of the thrombocytopaenia merit investigation for other causes of micro-angiopathic haemolytic anaemia.

The only lethal complication of the HELLP syndrome is the development of a large subcapsular liver haematoma, which ruptures, causing massive intraperitoneal haemorrhage. These features, if present, indicate an alternative diagnosis. Pulmonary oedema is the most difficult complication of severe pre-eclampsia in which to make a specific diagnosis. Pulmonary oedema itself may be the consequence of pre-eclampsia, or pre-eclampsia complicating underlying illness.

These illnesses may include valvular heart disease and ventricular dysfunction due to cardiomyopathy. Regardless of the cause, emergency management is usually the same, involving supportive management of oxygenation and various combinations of diuretic and vasodilator therapy with a view to reducing both afterload and preload. This is commonly accomplished by using direct-acting vasodilators, such as dihydrallazine, together with intravenous furosemide.

The development of pulmonary oedema is a signal for investigation by means of radiology, ECG and echocardiography to try to ascertain as closely as possible what the underlying cause may be.

In some circumstances, the acute management of critically ill women may be facilitated by the use of pulmonary artery catheters to directly measure haemodynamic variables. Delivery of the pre-eclamptic pregnant woman will trigger reversal of the underlying disease. Generalised oedema begins to dissipate as the capillary leak reverses and the pregnancy preload is excreted.

Commonly, 48 to 72 hours after delivery, the left ventricular preload may start to increase as the oedema resolves. The hypertension itself may persist for up to six weeks after delivery, requiring management for this duration with diuretics and second-line agents. Whereas angiotensin converting enzyme ACE inhibitors are commonly used in non-pregnant hypertensives, often calcium channel blockers are more rapidly effective in these circumstances and are a good choice of treatment for the limited period for which they will be required.

One of the most important aspects of managing the postpartum pre-eclamptic is that of counselling. Pre-eclampsia has been shown to be a marker of long-term risk.

Specifically, there is an association between hyperinsulinaemia, dyslipidaemia and the risk of pre-eclampsia. These underlying metabolic disorders are also risk factors for early onset vascular disease both coronary artery and cerebrovascular disease.

Attention therefore needs to be paid to primary prevention of these conditions through regular screening, and treatment for metabolic disorders.

The second long-term consequence of pre-eclampsia is that of an increased risk of renal failure. Chronic hypertension during pregnancy may be divided into two groups: uncomplicated chronic hypertension and chronic hypertension with superimposed pre-eclampsia.

The latter group requires management according to the principles outlined above, whereas the former requires out-patient care, often with an altered approach to therapeutic intervention. The development of pre-eclampsia cannot be averted by controlling blood pressure and there is no therapy that has any major impact on the risk of developing superimposed pre-eclampsia. Despite the modest effect on the incidence of the disease, it remains recommended therapy in women who are at risk.

The second strategy used to reduce the occurrence of pre-eclampsia is based on the prophylactic administration of large doses of oral calcium. Meta-analysis of the studies conducted to date indicate that calcium administered in doses of up to one gram three times a day may significantly reduce the occurrence of pre-eclampsia and may also reduce the development of severe hypertension. Despite these reservations, calcium supplementation is widely accepted practice during pregnancy where there is a suspected risk of pre-eclampsia.

Interventions that are not of benefit in preventing pre-eclampsia include bedrest, the use of anti-oxidant vitamins and antihypertensive therapy itself.

Pregnancy syndrome pre-eclampsia hypertension

Pregnancy syndrome pre-eclampsia hypertension

Pregnancy syndrome pre-eclampsia hypertension