Preeclampsia. Preparation and management of pregnancy after preeclampsia

Preeclampsia

The patient is urgently hospitalized in the intensive care unit of the nearest hospital with a delivery room. The main therapeutic goal is to reduce reflex and central hyperreactivity, prevent seizures, stabilize vital functions, and correct multiple organ disorders. A pregnant woman with preeclampsia is prescribed a strict medical and protective regimen. The treatment regimen includes the following groups of drugs:

• Anticonvulsants
  . The “gold standard” is the administration of magnesium sulfate through an infusion pump. The drug has a sedative, anticonvulsant, antispasmodic, hypotensive effect, and effectively reduces intracranial pressure. Simultaneously with the improvement of cerebral hemodynamics, the myometrium relaxes and increases the intensity of blood flow in the uterus. If necessary, tranquilizers are additionally used.
• Antihypertensive drugs
  . Imidazoline derivatives are preferred, which have a central α2-adrenomimetic effect, stimulate I1-imadazoline receptors in the nucleus of the solitary tract and thereby enhance the parasympathetic effect on the myocardium. Parenteral administration of peripheral vasodilators, hybrid β- and α1-blockers with a rapid antihypertensive effect is possible.
• Infusion formulations
  . To normalize oncotic and osmotic pressure, colloidal, protein, and balanced crystalloid solutions are administered intravenously. Infusion therapy can improve the rheological properties of blood, central and peripheral hemodynamics, tissue perfusion, reduce the severity of multiple organ disorders, and restore water and electrolyte balance.

According to indications, sedatives, direct anticoagulants, antioxidants, membrane stabilizers, and drugs to improve blood flow in tissues and prevent fetal respiratory distress syndrome are used. If intensive care is ineffective within 24 hours of hospitalization, emergency delivery by cesarean section is recommended. For patients with rapidly increasing symptoms of preeclampsia, surgery is performed within 2-4 hours. Natural childbirth with high-quality anesthesia (long-term epidural anesthesia), perineotomy or episiotomy is possible only with a significant improvement in the patient’s well-being, stable stabilization of blood pressure, and laboratory parameters.

National Institute of Health (NICE) guidelines

Aspirin 75 mg is recommended from 12 weeks of pregnancy if there is at least one high risk:

• arterial hypertension in a previous pregnancy;
• chronic renal pathology;
• autoimmune diseases (such as APS);
• diabetes;
• chronic arterial hypertension.

Aspirin 75 mg is recommended from 12 weeks if there are two or more moderate risks:

• first pregnancy;
• age over 40 years;
• the interval between pregnancies is more than 10 years;
• family history of preeclampsia;
• multiple pregnancy;
• BMI>35.

What will happen if left untreated? Risks of Preeclampsia

Preeclampsia is dangerous for both the pregnant woman and the baby. Without treatment, it threatens to develop eclampsia. This is a severe seizure that can result in coma, stroke or myocardial infarction. It is accompanied by increasing renal failure, pulmonary edema, placental abruption, sudden intrauterine fetal death, and loss of vision due to retinal detachment are possible.

Even if preeclampsia goes away, the woman remains at risk for hypertension and other cardiovascular diseases, stroke and heart attack. To control these risks, it is important to maintain a healthy lifestyle and follow-up with doctors after pregnancy.

Important!

For a woman who has experienced preeclampsia, her risk will be higher with each subsequent pregnancy, and if preeclampsia develops again, it will be more severe each time.

During and after preeclampsia, a woman may develop the following conditions and diseases:

• HELLP syndrome. Associated with functional liver failure, accompanied by disruption of other internal organs (kidneys, lungs, brain, etc.), threatening death to both the mother and the fetus.
• DIC syndrome. Disturbances in the blood coagulation system with the formation of blood clots, a subsequent decrease in the blood's ability to clot and the appearance of bleeding.
• Pulmonary edema. Accompanied by shortness of breath, cough, breathing problems.
• Acute renal failure. Manifests itself as a result of kidney damage during preeclampsia.
• Hypertensive encephalopathy. A vascular disease of the brain that develops as a complication of arterial hypertension.

Complications of preeclampsia that are dangerous for the fetus:

• placental abruption;
• acute hypoxia;
• slow fetal growth and low birth weight;
• the need for premature birth;
• intrauterine fetal death.

With preeclampsia, emergency delivery may be necessary to save the mother's life. If this occurs early, the baby may die or be born very preterm, which carries many health risks².

Figure 2. Differential diagnosis of preeclampsia. Source: Russian Society of Obstetricians and Gynecologists (ROAG)

Diagnosis of preeclampsia

The risk of preeclampsia begins to be assessed in the first trimester. This is usually done during routine screening. To do this, the obstetrician-gynecologist measures blood pressure and prescribes a blood test. The doctor also collects medical history data. He needs to be told about existing and past diseases, health status, well-being and complaints. Already in the first trimester, Doppler testing is prescribed. This is an ultrasound examination that evaluates blood flow in both uterine arteries.

In the future, additional ultrasound examination may be prescribed if preeclampsia is suspected. During such a study, fetal fetometry is performed (its size, anatomical structure, position, etc. are analyzed), and the condition of the placenta and amniotic fluid is assessed².

Important!

Already in the first trimester, diagnostics are carried out, which helps to assess the risk of developing preeclampsia. Early identification of this risk allows for the prevention of severe complications, so it is important for pregnant women to register with the antenatal clinic in a timely manner - the sooner the better.

At every doctor's appointment, a pregnant woman's blood pressure is measured. The doctor also regularly orders a urine test. This is necessary to control the risk of preeclampsia. When blood pressure rises to 140/90 mm Hg. Art. (or more) and the appearance of protein in the urine, the woman will be referred for additional examination.

Blood test results for the levels of sFlt-1, PlGF proteins and their ratio can predict preeclampsia 4 weeks before the onset of symptoms.

If preeclampsia is suspected, your doctor may order the following tests:

• blood test to determine the level of total hemoglobin and estimate the hematocrit;
• blood test to determine platelet levels;
• biochemical blood test to assess the level of total protein, blood glucose, creatinine, total bilirubin, urea, uric acid, determination of ALT, AST.

The quality of blood flow in the uterine arteries indicates whether the fetus is adequately supplied with oxygen and nutrients.
Source: olesiabilkei / Depositphotos During diagnosis, blood pressure is measured at least twice, with an interval of 4-6 hours (except in emergency cases). Proteinuria is diagnosed by a 24-hour urine test (loss of 300 mg of protein or more). Diagnosis is also possible by the ratio of protein and creatinine or by the result of a test with an indicator test strip (1+ and above).

Preeclampsia can be diagnosed even in cases where protein is absent in the urine, provided that new-onset hypertension is combined with any of the following conditions:

• thrombocytopenia;
• renal failure or impaired liver function;
• pulmonary edema;
• visual impairment;
• dysfunction of the brain.

Edema can accompany preeclampsia due to impaired renal function, but during diagnosis they are not considered as a symptom, since they can also occur during the normal course of pregnancy.

It is important to distinguish preeclampsia from other conditions that occur during pregnancy due to high blood pressure (Fig. 2):

• Chronic arterial hypertension - observed up to 20 weeks of pregnancy.
• Gestational hypertension occurs in the second half of pregnancy and is not accompanied by proteinuria or other symptoms of preeclampsia.

After the studies are completed, the doctor determines the severity of preeclampsia and prescribes appropriate therapy.

Degrees of preeclampsia

Preeclampsia can be early, with the first symptoms appearing before 34 weeks, and late, developing after 34 weeks of pregnancy. With early preeclampsia, the risk of severe course and consequences for mother and child is higher.

Preeclampsia can range in severity from moderate to severe. The severity of the condition affects the prognosis, as well as the choice of pregnancy management tactics, treatment, and obstetric care².

Preeclampsia is considered moderate if proteinuria is diagnosed and blood pressure is elevated between 140/90 and 159/99 mmHg. Art. In severe conditions, blood pressure is higher than these indicators (confirmed by at least two measurement results with an interval of 4-6 hours). The amount of protein in the urine is 300 mg/day. The condition is also considered severe if, in addition to the symptoms of moderate preeclampsia, there are the following signs:

• shortness of breath, respiratory failure, symptoms of pulmonary edema;
• vomiting, nausea, pain in the right hypochondrium;
• headache, visual disturbances, tinnitus, confusion;
• onset of symptoms before 34 weeks;
• fetal growth restriction;
• formation and excretion of urine in a volume of less than 500 ml.

Preeclampsia (PE) is one of the most important problems in modern obstetrics, given its medical and socio-economic significance. Since the consequences of severe hypertensive disorders during pregnancy reduce the quality of life of women of reproductive age, and the frequency of disturbances in the physical and psychosomatic development of prematurely born children is quite high, this problem is significant both medically and socially [1-3].

For many years, PE remains one of the serious multisystem pathological complications of pregnancy, the frequency of which does not tend to decrease. Even Hippocrates in the 4th century BC. described a disease in pregnant women, the symptoms of which he compared with epilepsy. It was only in 1827 that R. Bright suggested that eclampsia (translated from Greek as “lightning”, “flash”) is a kidney disease based on the definition of albuminuria. In 1843, J. Lever described edema, albuminuria, pigment spots and headache in eclampsia. A. Delore in 1884 put forward an infectious theory and even isolated the so-called Bacillus eclampsae

. In 1886, E. Leyden introduced the term “nephropathy,” and in 1908, S.D. Mikhnov - “preeclampsia”. In 1905, J. De Lee suggested that eclampsia is the result of the action of toxins, and W. Freund coined the term “toxicosis of pregnancy.” Finally, in 1913, W. Zangemeister described the classic triad: arterial hypertension, edema, proteinuria, which is the basis for diagnosing and assessing the severity of P.E. Today, the diagnosis of PE is based on the occurrence of arterial hypertension, proteinuria and generalized edema, usually after 20 weeks of pregnancy, or on a sudden increase in blood pressure, the appearance or exacerbation of proteinuria in patients with chronic arterial hypertension (CAH) [4, 5].

Despite ongoing prevention and repeated attempts to select therapy, it was not possible to reduce the incidence of P.E. Data on the prevalence of PE in the world in the general population vary - from 2.3 to 23% [4, 6, 7]. According to O.V. Makarova et al. [4], in Russia P.E. occurs in 13-16% of the total number of births. Prevalence of P.E. among pregnant women in the Russian Federation in 2011 accounted for 17.4% of all those who completed pregnancy, and in 2012 - 16.7% [8]. When analyzing the frequency of this pathology during childbirth, an increase in the frequency of PE and eclampsia in parturient and postpartum women was revealed from 27.1% in 2011 to 30.3% in 2012 (by 11.6%) [9]. In some developed countries, in particular the USA, an increase in the incidence of PE has been noted in recent years [10]. Probably the reason for this is the increase in the incidence of conditions such as diabetes mellitus, obesity and CAH in the population [4, 11]. The leading risk factors for the development of PE are extragenital pathology (endocrinopathy, diseases of the cardiovascular system, kidneys), inflammatory processes of the genital organs and a burdened obstetric history [12]. B. Sibai [13] found that the frequency of PE in primiparous women varied from 4 to 11%, while the frequency of PE in women who gave birth was lower, although it also varied widely. At the same time, according to C. Ananth et al. [14], the probability of delivery at term is higher in multiparous women with hypertension than in primiparous women. The main risk factors for the development of PE, identified from anamnesis and clinically, are chronic kidney disease (58.6%), vascular pathology (51.7%), endocrine pathology (38.0%), metabolic syndrome (24.0%), heart disease (22.0%), gastrointestinal tract diseases (20.7%) [15]. According to our data [16], in 68% of cases, PE is of a combined nature and develops against the background of extragenital pathology, in particular against the background of CAH and kidney diseases. In pregnant women with CAH, the addition of PE was noted in 19% of cases. Other risk factors for PE include maternal age over 35 years, obesity, and multiple pregnancies [4].

According to the World Health Organization, PE is the main cause of premature birth, premature abruption of a normally located placenta, the development of placental insufficiency, intrauterine growth retardation, and the birth of low birth weight children. Complications of P.E. are hemorrhage and retinal detachment, acute renal failure, acute fatty hepatosis, HELLP syndrome, pulmonary edema and stroke [4, 5, 11, 17, 18].

In the global structure of maternal mortality, the share of PE is 12-15%, and in developing countries this figure reaches 30% [19]. According to Russian authors [20], this pathology remains one of the main causes of maternal mortality and accounts for about 20% of all cases of maternal deaths in the Russian Federation.

According to the Ministry of Health of the Russian Federation, hypertensive complications of pregnancy occupy 3-4th place in the list of causes of maternal mortality over the last decade and are its direct cause in 6.9-17.4% of cases [4, 8, 9, 18 , 20].

In Moscow, maternal mortality from various forms of PE and their complications ranks first among all causes of maternal mortality, ranging from 17 to 28% per year, i.e. the share of PE in Moscow turned out to be slightly higher than in Russia as a whole [ 9, 20]. PE requires close attention and monitoring of the patient not only during pregnancy and childbirth, but also in the postpartum period, especially in the early period. Up to 44% of cases of eclampsia occur in the postpartum period, especially during full-term pregnancy [21, 22]. Of the total number of women who died from PE, 96.8% died after childbirth [23].

For a long time, the prevailing idea was that this complication of pregnancy does not have a noticeable effect on the woman’s health in the long term after childbirth. However, today it is known that PE affects not only the course of pregnancy and childbirth, but also significantly affects the health of the mother and child and long-term prognosis.

The long-term prognosis of women who have undergone PE is characterized by an increased incidence of CAH, coronary heart disease, diabetes mellitus and strokes [24]. The results of recent studies indicate the presence of a high cardiovascular risk in this group of women in later life. According to G.T. Sukhikh [18], in the long term of the life cycle in women who have previously undergone PE (especially during the first birth), the risk of developing cardiovascular complications, including fatal ones, increases. Also, with the simultaneous combination of three cardiovascular risk factors in the obstetric history (preeclampsia, premature birth and low body weight for gestational age of the infant), a sevenfold increase in subsequent fatal outcomes is observed.

There is a tendency to earlier development of ischemic brain lesions in young women after undergoing P.E. The likelihood of developing an ischemic cerebral stroke in women who have suffered PE during childbirth is 60% higher than the likelihood of developing a stroke in those who have not suffered it [25]. PE is also a risk factor for the early development of atherosclerosis, as evidenced by the discovery of a greater thickness of the intima-media complex of the coronary vessels of the heart and femoral artery in women who underwent PE during childbirth than in women after a normal pregnancy [25]. G. Smith et al. [26] reported that 20% of women with PE exhibit residual microalbuminuria 1 year after birth, as well as increased blood pressure, total cholesterol, low-density lipoproteins, triglycerides, body mass index, fasting insulin, and creatinine.

In the UK, L. Bellamy et al. [27] conducted a meta-analysis of clinical studies to evaluate the relationship between PE and subsequent development of cardiovascular diseases. At the end of the meta-analysis, mortality from all causes was assessed among women who experienced PE during pregnancy. PE is characterized by an increased risk of developing various cardiovascular diseases and all-cause mortality in later life. There is no established relationship between PE and the development of malignant neoplasms, including breast cancer, which is the main cause of morbidity and mortality in older age.

Since women who have undergone PE often give birth early and by cesarean section, the frequency of disturbances in the physical and psychosomatic development of prematurely born children is quite high, and they subsequently suffer from various metabolic, hormonal, and cardiovascular diseases.

Children born to mothers with PE have higher blood pressure and body mass index, which must be taken into account in the primary prevention of cardiovascular diseases in such people [28].

Until now, the etiology and pathogenesis of PE are not fully known, scientists around the world are making attempts to connect all the links together, to determine the sequence and subordination of all changes that occur in the body of a pregnant woman, but so far all assumptions remain only assumptions and each previous one, often, is refuted by what follows. Currently, the highest priority is the placental theory of development, which explains the occurrence of PE as a result of pathological placentation, which in turn leads to placental ischemia with the further development of generalized vasospasm, endotheliosis and multiple organ failure. Even in the recent past, the issue of unified terminology and classification of various forms of arterial hypertension in pregnant women in the Russian Federation was extremely relevant.

In 2013, the Russian Society of Obstetricians and Gynecologists developed Federal clinical guidelines “Hypertensive disorders during pregnancy, childbirth and the postpartum period. Preeclampsia. Eclampsia”, where a clinical classification of hypertensive disorders during pregnancy was proposed [29, 30]:

- preeclampsia and eclampsia;

— preeclampsia and eclampsia against the background of chronic arterial hypertension;

- gestational (pregnancy-induced) arterial hypertension;

- chronic arterial hypertension (existing before pregnancy).

The use of a unified terminology and classification will allow for a correct assessment of statistical data on the prevalence of PE, will reduce the overdiagnosis of this condition, will facilitate the correct diagnosis, determination of the severity of the disease and the development of adequate management tactics both at the outpatient and inpatient stages and will ensure continuity between different medical institutions.

Among the many problems associated with PE and eclampsia, the problem of diagnosis, prognosis and assessment of severity occupies one of the most important places and is of great importance both for obstetricians and gynecologists and for doctors of related specialties. Reducing perinatal and maternal morbidity and mortality remains the main goal of obstetricians and gynecologists.

It is important to remember that even if PE is suspected, a pregnant woman must be hospitalized urgently for additional examination and clarification of the diagnosis. When the diagnosis is confirmed, the condition of the pregnant woman and the functional state of the fetus are assessed, and further management tactics depend on the gestational age and the severity of the disease.

The diagnosis of PE is established by a combination of arterial hypertension (systolic blood pressure - SBP ≥140 mm Hg and/or diastolic blood pressure - DBP ≥90 mm Hg [31]), proteinuria (the presence of protein in the urine ≥0.3 g/l in a daily sample (24 hours) or in two samples taken with an interval of 6 hours; when using a test strip (protein in urine) - indicator (≥"1+" [32]) and generalized edema [4]. Peripheral edema is observed in 70-80% of cases during physiological pregnancy, and therefore cannot be considered as a diagnostic criterion for PE [4, 33].However, edema of the face and hands often precedes the development of PE, and generalized, rapidly increasing edema, anasarca, fluid accumulation in cavities are considered one of the unfavorable prognostic criteria for severe PE [34].At the same time, PE occurring without generalized edema is recognized as more dangerous for the mother and fetus than PE with edema.

There is evidence that 10% of women with PE have no or minimal proteinuria in the urine [33], and 20% of women who develop eclampsia do not have proteinuria [33, 35]. In some women, atypical PE is reported, which is accompanied by multiple organ failure, generalized endotheliosis, but without arterial hypertension, without proteinuria, or without both of these symptoms [33].

The management of patients with PE depends on the gestational age and the severity of the disease.

In 2011, B. Sibai [36] described the following criteria for moderate PE: arterial hypertension: SBP ≥140 mmHg. or DBP ≥ 90 mmHg occurring at >20 weeks' gestation in a woman with a history of normal blood pressure, and proteinuria ≥0.3 g/L protein in a 24-hour urine sample.

Criteria for severe PE (presence of symptoms of moderate PE and ≥1 of the following criteria):

1) arterial hypertension: SBP ≥160 mm Hg. or DBP ≥110 mm Hg. with double measurements with an interval of 6 hours at rest;

2) proteinuria ≥5.0 g/l in a daily urine sample or >3 g/l in two portions of urine taken with an interval of 6 hours, or a value of 3+ on the test strip;

3) oliguria <500 ml in 24 hours;

4) cerebral or visual symptoms (headache, floaters, etc.);

5) pulmonary edema;

6) cyanosis;

7) pain in the epigastrium or right upper quadrant;

liver dysfunction (increased activity of alanine and aspartate aminotransferases);

9) thrombocytopenia (<100·106/l);

10) intrauterine growth retardation.

The criteria for severe PE also include critical forms of PE (severe retinopathy, acute fatty hepatosis, HELLP syndrome, acute renal failure, pulmonary edema) and placental abruption [35].

In addition to the above criteria, severe PE is characterized by a progressive decrease in the blood content of total protein, albumin, platelets, and an increase in proteinuria and hematocrit. Currently, only a progressive deterioration of clinical and laboratory tests over time indicates the worsening of PE and its transition to a more severe form and requires early delivery, while the absolute values ​​of clinical and laboratory indicators are not always reliable in identifying the true severity of the process [4]. For early diagnosis and verification of the severity of the process, it is possible to use 24-hour blood pressure monitoring (ABPM), determination of central hemodynamic parameters and microalbuminuria [4].

Despite the variety of proposed scales and methods, there is still no way to determine with a sufficient degree of reliability the degree of severity of PE and predict its further course: the severity of edema, proteinuria and arterial hypertension does not always determine the true severity of pathological processes in PE, due to which creates the need to search for new biochemical markers [4, 16, 37, 38]. Today, the role of angiogenic growth factors in the pathogenesis of PE and the possibility of using the determination of the imbalance of pro- and antiangiogenic growth factors in the prognosis, diagnosis and differential diagnosis of PE and identifying its severity are widely discussed [16, 37, 38]. The use of additional tests is extremely important nowadays due to the increasing frequency of PE and the registration of its atypical forms. For P.E. characterized by an increase in the level of antiangiogenic (soluble FMS-like tyrosine kinase-1-sFlt-1 and endoglin - sEng) and a decrease in the level of proangiogenic (PlGF - placental growth factor) factors compared to patients with physiological pregnancy [38, 39]. Since angiogenic processes in the body are regulated by a balance of pro- and antiangiogenic growth factors, an angiogenic coefficient (K) has been proposed, which is the ratio of sFlt-1/PlGF protein content. Such a coefficient is intended to quantitatively reflect the balance of angiogenic proteins and, consequently, the direction and/or intensity of angiogenic processes in the body. The higher the value of the K coefficient, the more pronounced is the imbalance between vascular growth factors towards the predominance of the antiangiogenic protein Flt-1 or a decrease in the level of the proangiogenic factor PlGF. The value of the angiogenic coefficient K in PE is 70 times higher than in healthy pregnant women [37, 38] and significantly increases with increasing severity of PE. A highly sensitive (62%) and highly specific (75%) criterion for severe PE is a decrease in proangiogenic placental growth factor (PlGF) to 14.5–42.8 pg/ml, which indicates progression of the pathological process in this category of patients [39].

The only treatment for PE today is delivery, removal of the fetus and placenta from the mother’s body. At a gestational age of more than 34 weeks, the tactics of managing patients with PE is reduced to preparing for delivery after stabilization of the pregnant woman’s condition. The method of delivery depends on the biological maturity of the birth canal, the obstetric situation, and the general condition of the pregnant woman and the fetus [4]. Caesarean section for PE is not the only method of choice for delivery. Spontaneous birth, when properly managed, is hemodynamically less stressful for the mother and reduces the incidence of respiratory complications in premature newborns. Caesarean section is the method of choice for the delivery of patients with PE at less than 32 weeks of gestation.

Currently, the main indication for delivery of pregnant women with PE at preterm gestation is deterioration in clinical and laboratory data and/or deterioration in the functional state of the fetus. In gestation periods of less than 34 weeks, management tactics are determined by the severity of P.E. With P.E. severe cases, the only correct treatment is delivery after stabilization of the patient’s condition, regardless of gestational age. The most controversial is the management tactics of pregnant women with moderate PE during premature pregnancy. When we talk about “prolonging” pregnancy during PE in order to stabilize the patient’s condition and prevent fetal RDS syndrome, in essence, we are delaying the transition from moderate to severe PE, which requires emergency delivery, and often resuscitation measures. In patients with moderately severe PE (moderate severity) up to 34 weeks of pregnancy, drug therapy can be used, which is carried out in a hospital setting, accompanied by careful monitoring of the condition of the mother and fetus and ends with preparation for labor and delivery. The use of such tactics in case of a favorable course of the disease in some cases helps to prolong pregnancy by 2 weeks [40]. At a gestational age of less than 34 weeks in pregnant women with moderate PE, according to some authors, the possibility of continuing pregnancy will depend on the effectiveness of therapy. In this situation, careful dynamic monitoring of the patient’s clinical and laboratory parameters is carried out for 24-48 hours [4]. The period of pregnancy prolongation in patients with PE averaged 8.12±1.27 days (from 0 to 19 days) [16], while the period of pregnancy prolongation in patients with moderate PE averaged 11.85±1. 61 days, which is significantly longer than in pregnant women with severe PE – 4.1±0.69 days ( p

<0,05) [16, 37, 39].

The criterion for starting antihypertensive therapy for PE is SBP ≥140 mmHg. or DBP ≥90 mm Hg. Antihypertensive therapy for PE must be carried out under Doppler monitoring, since a decrease in uteroplacental and fetal placental blood flow is possible [4, 40]. The main drugs currently used in the world for the treatment of arterial hypertension during pregnancy are methyldopa (first-line drug), the α-β-blocker labetalol, calcium antagonists (nifedipine) and β-blockers (the drug of choice is metoprolol), also possibly the use of hydrochlorothiazide, furosemide, verapamil, clonidine, prazosin. ACE inhibitors, angiotensin II receptor antagonists, spirolactone, calcium antagonists diltiazem and felodipine are contraindicated during pregnancy. It should be noted that some drugs that have proven themselves in practice and are widely used abroad (labetalol, diazoxide, hydralazine for parenteral administration) are not registered in our country [40].

It is necessary to ensure prolonged administration of a solution of magnesium sulfate before and during childbirth and in the postpartum period in order to prevent seizures [4, 40]. Magnesium sulfate is the drug of choice for the prevention and treatment of seizures, which is superior to benzodiazepines, phenytoin and nimodipine in the prevention of eclampsia and does not increase the incidence of cesarean section, bleeding, infectious diseases and neonatal depression [41]. Administration of magnesium sulfate should be administered before and during delivery, and should continue for at least 24 hours after delivery or 24 hours after the last episode of seizures [42, 43]. Magnesium sulfate is administered only intravenously, always using a device for continuous administration. The loading dose is 4-6 g of dry matter for 10-15 minutes, and the maintenance dose is 1-2 g of dry matter per 1 hour.

It is important to note that regional analgesia or anesthesia is the preferred method of pain management for patients with PE, both during vaginal delivery and during cesarean section (with a platelet level >75 109/L and in the absence of coagulopathy). Spinal and epidural, as well as combined spinal-epidural anesthesia are effective and equally safe.

Currently, the tactics of managing patients with PE in the Russian Federation are regulated by two documents: Order of the Ministry of Health of the Russian Federation No. 572n dated November 1, 2012 “On approval of the Procedure for the provision of medical care in the field of obstetrics and gynecology (except for the use of assisted reproductive technologies)” (as amended and additions) and Federal clinical guidelines “Hypertensive disorders during pregnancy, childbirth and the postpartum period. Preeclampsia. Eclampsia”, developed by the Russian Society of Obstetricians and Gynecologists in 2013.

From all of the above, it follows that the frequency of PE is not decreasing, a huge number of pregnant women are at risk for the development of this pathology, the consequences of PE are dangerous to the life and health of both the woman and the fetus, which leads to an increase in mortality and disability. Despite a large number of studies and publications, the root causes of PE and markers of the rate of progression of pathological changes in vital organs and systems remain unknown, which limits the possibilities of treating and preventing the development of PE. Thus, to reduce maternal mortality from PE and eclampsia, it is necessary to monitor risk factors for the development of this condition, ensure proper monitoring of pregnant women at high risk for PE, comply with the diagnostic criteria for PE when making a diagnosis, and develop adequate tactics for managing patients depending on the gestational age and the severity of the condition, ensure quick and gentle delivery, according to standards, ensure monitoring of patients after delivery in an intensive care unit. Research should be conducted to identify predictors of PE both in the high-risk group and in the general population to determine criteria for early and timely diagnosis and markers of process progression in order to optimize obstetric tactics and timing of delivery.

Where does gestosis come from and what is it? Causes of preeclampsia

Preeclampsia or late gestosis is a dangerous complication of pregnancy, in which blood pressure rises, edema forms, and protein appears in the urine. All this can lead to disruptions in the functioning of the expectant mother’s organs and harm the fetus, slowing down its development.

It is not known exactly why preeclampsia occurs. The prerequisites for its appearance are laid in early pregnancy, when the fertilized egg attaches to the uterus. If it is not attached deeply enough, superficially, the placenta develops incorrectly, the development of vascular channels is disrupted, and this affects the flow of blood to the fetus. Because of this, as pregnancy progresses, the placenta becomes less and less able to provide itself and the fetus with the necessary nutrients. After 20 weeks, this leads to the appearance of symptoms of preeclampsia and a whole range of disorders that damage the blood vessels of various organs of the mother (including kidneys, brain, liver) and threaten her life. Preeclampsia is also dangerous for the baby. It can affect fetal development by causing hypoxia, as well as developmental delays and convulsions¹.

Vitamin D deficiency and the risk of preeclampsia: is there a connection?

Vitamin D affects many physiological processes: on the one hand, on how the fetus attaches to the epithelium of the uterus, on the other, on the regulation of renin biosynthesis (an enzyme associated with increased blood pressure).
Back in the early 1990s, a hypothesis was put forward about the influence of vitamin D levels on the risk of preeclampsia. Later research showed that this was indeed the case³. Low vitamin D levels before 22 weeks of pregnancy are considered an independent risk factor for the development of preeclampsia. If there is a vitamin D deficiency confirmed by tests, taking it from early pregnancy reduces the likelihood of preeclampsia, as well as the development of its severe complications.

Several factors are known to increase the risk of preeclampsia:

• This is the first pregnancy or more than 10 years have passed since the previous pregnancy.
• The age of the pregnant woman is over 35-40 years.
• During a previous pregnancy, there was already preeclampsia (with each new case, the severity of the condition may increase).
• Blood relatives had preeclampsia.
• Pregnancy is multiple.
• The woman has diabetes, obesity or other metabolic diseases, high blood pressure, or kidney disease.
• The pregnancy resulted from IVF.
• The woman has autoimmune diseases (systemic lupus erythematosus and others).

How common is preeclampsia?

Between 5 and 10% of pregnant women have high blood pressure. Hypertension has a high risk of preeclampsia. It occurs in 2-8% of pregnant women and accounts for 10-15% of maternal deaths. Every year, at least 70 thousand pregnant women die due to preeclampsia.

In Russia, moderate preeclampsia is diagnosed in 2.74% of the total number of pregnant women, severe - in 0.84%.

The number of deaths and severe complications associated with preeclampsia is gradually decreasing. An important role in this is played by proper management of pregnancy, constant monitoring in antenatal clinics and timely diagnosis².

How to cope with postpartum preeclampsia

The time after childbirth can be challenging even without health problems. Recovering from childbirth and caring for a newborn can be stressful. While recovering from pregnancy, it is important to pay attention to your own health by monitoring symptoms and consulting with your doctor.

If you are diagnosed with postpartum preeclampsia while in hospital, you may need a longer hospital stay. Reach out to loved ones or talk to your healthcare provider to learn about options for additional support when you return home.

Causes

The causes of preeclampsia and eclampsia have not yet been precisely established. There are 30 or more theories that explain the causes and mechanisms of development of preeclampsia and eclampsia. But the general opinion of all doctors is that there is a pathology of the placenta, the formation of which is disrupted in the early stages of pregnancy.

If the placental attachment is disrupted (superficially implanted placenta) or there is a deficiency of receptors for placental proteins, the placenta begins to synthesize substances that cause vasoconstriction (vasoconstrictors), which leads to a generalized spasm of all blood vessels in the body to increase pressure in them and increase the supply of oxygen and nutrients substances to the fetus. This leads to arterial hypertension and multiple organ damage (primarily the brain, liver, and kidneys are affected).

Heredity and chronic diseases play an important role in the development of preeclampsia and eclampsia.

Symptoms and signs of preeclampsia

Preeclampsia manifests itself in three characteristic signs:

• high blood pressure;
• swelling;
• proteinuria – the presence of protein in the urine (Fig. 1).

Figure 1. Main signs of preeclampsia.
Source: VectorMine / Depositphotos Systolic blood pressure above 140 mmHg is considered elevated. Art. and/or diastolic blood pressure above 90 mm Hg. Art. Measurements are taken at least twice every 4-6 hours. If blood pressure is elevated two or more times, hypertension is diagnosed. If it is necessary to clarify the diagnosis, daily monitoring of blood pressure is carried out.

Edema is not a mandatory sign of preeclampsia, but its severity allows us to assess the severity of the condition. If the swelling is generalized (appears in several areas or throughout the body), appears from time to time, this can be a dangerous symptom indicating the development of preeclampsia due to other diseases.

Proteinuria is a high level of protein in the urine. It is diagnosed by assessing the amount of protein in a portion of urine (normally up to 30 mg). After 22 weeks of pregnancy, during each appointment at the antenatal clinic, the protein content in the urine is assessed using indicator strips or by submitting morning or daily urine for analysis. If the content turns out to be high, the doctor looks for the cause.

Often, signs of preeclampsia begin to develop unnoticed, and the woman’s health remains normal for a long time. Even when symptoms appear, they can easily be confused with normal pregnancy ailments. In order to identify complications in a timely manner, it is important to tell the obstetrician-gynecologist in charge of the pregnancy in detail at each appointment about your health. Symptoms that occur with preeclampsia may include:

• swelling;
• rapid weight gain;
• decreased visual acuity;
• the appearance of “floaters” before the eyes or an aura around objects;
• sensitivity to light;
• noise in ears;
• heartburn, nausea and vomiting;
• pain in the shoulder girdle or in the right upper abdomen;
• shortness of breath, feeling of lack of air;
• coughing or dry cough;
• difficulty breathing through the nose;
• rare urge to urinate (daily urine volume up to 500 ml per day).

If the condition worsens, confusion and signs of neuromuscular irritability may appear. You may also experience pregnancy seizures (eclampsia), a deadly complication of pregnancy characterized by generalized seizures that occur as one long seizure or a series of seizures. In this case, it is possible to develop apnea (stop breathing), dilated pupils, and foam at the mouth. This condition is very dangerous, and after convulsions a woman can fall into a coma⁴. Severe gestosis also threatens the child: the development of convulsions, hypoxia, damage to the cardiovascular, central nervous, immune, respiratory and other systems is possible.

During 24-hour blood pressure monitoring, a woman is fitted with a monitor and a cuff, and her blood pressure is measured every 15-30 minutes. During the measurement, you should be at rest, the arm with the cuff should be relaxed. Source: BTL Medical Solutions / YouTube