Diagnosis of gestosis

The diagnosis of gestosis can be made based on a combination of clinical and laboratory criteria.

Diagnosis of gestosis at the preclinical stage at the beginning of the second trimester of pregnancy is carried out on the basis of the following changes in laboratory parameters:

• inversion test (measuring blood pressure three times at 5-minute intervals with the woman lying on her side, on her back, and again on her side). The test is considered positive if the diastolic pressure changes by more than 20 MMHg;
• violation of uteroplacental blood flow (absence of a decrease in SDO in the uterine arteries and spiral arteries of the myometrium at 14-16 weeks);
• progressive decrease in platelet count as pregnancy progresses (less than 160-10 ⁹ / l);
• hypercoagulation in the cellular and plasma links of hemostasis (increased platelet aggregation up to 76%, decreased APTT to less than 20 sec, hyperfibrinogenemia up to 4.5 g/l);
• reduction in the level of anticoagulants (endogenous heparin to 0.07 units/ml, antithrombin III to 63%);
• lymphopenia (18% or less);
• activation of lipid peroxidation;
• decrease in the level of antioxidant activity in the blood.

Criteria for gestosis include proteinuria over 0.3 g/l, hypertension - with blood pressure above 135/85 mm Hg, and hypotension - an increase in systolic blood pressure by more than 30 mm Hg from the initial value, and diastolic - 15 mm Hg; edema should be taken into account only if it does not disappear after a night's sleep.

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Special research methods for gestosis

Mandatory examination methods include measuring body weight, blood pressure in both arms, pulse, diuresis, clinical blood and urine tests, daily urine analysis for protein, biochemical blood test (total protein, albumin, urea, glucose, electrolytes, creatinine, residual nitrogen, cholesterol, direct and indirect bilirubin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, triglycerides).

The following additional examination methods are used:

• 24-hour monitoring of blood pressure, ECG, CTG;
• Doppler ultrasound of maternal and fetal hemodynamics;
• fundus examination;
• urine analysis according to Nechiporenko, urine analysis according to Zimnitsky, Reberg test, bacterial urine culture;
• Ultrasound of vital organs of mother and fetus;
• hemostasis [thromboelastography, activated partial thromboplastin time (APTT), platelet count and aggregation, fibrinogen, its degradation products, endogenous heparin concentration, antithrombin III];
• lupus anticoagulant determination;
• determination of antibodies to human chorionic gonadotropin;
• measurement of central venous pressure (CVP).

Diagnosis of gestosis in the first and second trimesters before the appearance of clinical signs is carried out on the basis of the following changes:

• progressive decrease in the platelet count as pregnancy progresses (up to 160×10 ⁹ /l or less);
• hypercoagulation in the cellular and plasma links of hemostasis:
  • increase in platelet aggregation up to 76%;
  • decrease in APTT to less than 20 s;
  • hyperfibrinogenemia up to 4.5 g/l;
• decrease in anticoagulant levels:
  • endogenous heparin up to 0.07 U/ml;
  • antithrombin III up to 63%;
• lymphopenia (18% or less);
• activation of lipid peroxidation (above the norm, depending on the determination method);
• decreased level of antioxidant activity in the blood (below the norm, depending on the method of determination);
• disruption of blood flow in the vessels of the uteroplacental bed. The presence of 2-3 of the above symptoms indicates a high probability of developing gestosis after 20 weeks of pregnancy.

Gestosis can manifest itself as an increase in blood pressure as a monosymptom, as well as in combination with proteinuria and/or edema that occurs after 20 weeks of gestation.

Persistent edema is an early symptom of gestosis. The following types of edema are distinguished.

• Hidden edema (pathological weight gain of 500 g or more in 1 week, positive ring symptom, nocturia, decrease in diuresis below 900–1000 ml with a water load of 1400–1500 ml).
• Obvious (visible) swelling:
  • I degree - swelling of the lower and upper extremities;
  • II degree - swelling of the lower and upper extremities, abdominal wall;
  • Grade III - swelling of the lower and upper extremities, abdominal wall and face;
  • IV degree - anasarca.

In 88–90% of cases, edema in pregnant women develops into gestosis.

The organization of gestosis evaluates the severity of gestosis similarly to the scale.

To assess the severity of gestosis, the Goecke scale is used as modified by G.M. Savelyeva et al.

According to severity, gestosis is divided into mild (up to 7 points), moderate (8–11 points) and severe (12 points or more).

The point scale for assessing the severity of nephropathy is quite convenient. However, it does not take into account the arterial pressure before pregnancy, which is very important for diagnosing hypertensive conditions. Therefore, the allocation of 3 degrees of arterial hypertension severity is based on the level of increase in arterial pressure during pregnancy compared to before pregnancy.

The following signs are considered objective criteria for the severity of gestosis:

• systolic blood pressure 160 mmHg and above, diastolic 110 mmHg and above;
• proteinuria up to 5 g/day or more;
• oliguria (daily urine volume <400 ml);
• hypokinetic type of central uterine hemodynamics (CMH) with increased total peripheral vascular resistance, severe renal blood flow disorders, bilateral blood flow disorders in the uterine arteries, increased pulsatility index in the internal carotid artery >2.0, retrograde blood flow in the suprapubic arteries;
• lack of normalization or deterioration of hemodynamic parameters against the background of intensive therapy for gestosis;
• thrombocytopenia (100×10 ⁹ /l);
• hypocoagulation;
• increased activity of liver enzymes;
• hyperbilirubinemia.

Given the severity of complications that arterial hypertension entails during pregnancy, it is extremely important to use daily blood pressure monitoring for timely and correct diagnosis of arterial hypertension in pregnant women and prediction of gestosis, as well as determination of indications and drugs for hypotensive therapy. 24-hour monitoring with 20-30-minute intervals between measurements reproduces the daily dynamics of blood pressure quite fully. In addition, daily blood pressure monitoring allows identifying cases of overdiagnosis, which is extremely important, since the prescription of hypotensive therapy can cause iatrogenic complications.

When studying maternal hemodynamics, four main pathogenetic variants of systemic circulatory disorders are distinguished.

• Hyperkinetic type of CMG regardless of the values of OPSS and eukinetic type with normal values of OPSS. With this type, moderate disorders of cerebral (in 9%), renal (in 9%), uteroplacental-fetal (in 7.2%) and intraplacental (in 69.4%) blood circulation are recorded. Intrauterine growth retardation of the fetus is noted in 11%. In 91%, mild severity of gestosis is clinically detected. The conducted therapy of gestosis is effective in most cases. The prognosis for the mother and fetus is favorable.
• Eukinetic CMG type with increased OPSS values and hypokinetic CMG type with normal OPSS values. This type is characterized by blood flow disorders mainly of the second degree in the renal artery system, uteroplacental-fetal and intraplacental blood flow. Moderate forms of gestosis prevail. Intrauterine growth retardation of the fetus is detected in 30%, decompensated placental insufficiency - in 4.3%, preeclampsia - in 1.8%. The conducted therapy of gestosis is effective in 36%.
• Hypokinetic type of CMG with increased OPSS. Renal, uteroplacental and intraplacental blood flow disorders, mainly grades II and III, are detected in 100%. Bilateral blood flow disorders in the uterine arteries are determined in 42%. This type is characterized by moderate and severe forms of gestosis, intrauterine growth retardation in 56%, decompensated fetoplacental insufficiency in 7%, and preeclampsia in 9.4%. No improvement in hemodynamic and clinical parameters is observed against the background of the therapy, and deterioration is observed in half of the pregnant women. The prognosis for the mother and fetus is unfavorable, since this type of hemodynamics is characterized by the greatest number of severe forms of gestosis, decompensated placental insufficiency, as well as premature delivery and perinatal losses.
• Severe cerebral hemodynamic disorders (increased pulsation index in the internal carotid artery over 2.0 and/or retrograde blood flow in the suprapubic arteries). This type is characterized by forms of gestosis with a rapid increase in clinical picture (within 2–3 days). Regardless of the central, renal, uteroplacental and intraplacental hemodynamic parameters, preeclampsia develops in 100% of cases with this type. The maximum period from recording pathological blood flow values in the internal carotid arteries to the development of the clinical picture of preeclampsia does not exceed 48 hours.

Differential diagnosis of gestosis

Increased blood pressure during pregnancy may be due to arterial hypertension that preceded pregnancy (usually essential hypertension), diabetes mellitus, kidney disease, hypothyroidism, obesity, arterial hypertension that occurs during pregnancy (arterial hypertension of pregnancy), and preeclampsia. Despite the commonality of manifestations, these are different diseases. Their pathogenesis, treatment, and prognosis for the mother and fetus differ. However, it is important to remember that these diseases can be combined.

Classic complications of gestosis:

• acute renal failure;
• cardiopulmonary failure;
• HELLP syndrome and acute fatty hepatosis of pregnancy (AFGP);
• cerebral edema and hemorrhage;
• cerebral coma.
• retinal detachment;
• premature detachment of a normally located placenta.

Currently, HELLP syndrome and AFGB are becoming increasingly important.

The question of whether HELLP syndrome should be considered as an independent disease or as one of the complications of pregnancy has long remained controversial. HELLP syndrome was first described by J. A. Pritchard in 1954. In 1982, Weinstein proposed the term "HELLP syndrome" to define a special group of pregnant women with preeclampsia who had hemolysis, hyperfermentemia, and decreased platelet levels. Many clinicians consider HELLP syndrome a complication of gestosis.

HELLP syndrome: hemolysis H (Hemolysis), elevated liver enzymes EL (elevated liver enzymes), low platelet count LP (low platelet count). In severe gestosis and eclampsia, it develops in 4-12% and is characterized by high maternal (up to 75%) and perinatal mortality. HELLP syndrome develops in the third trimester of pregnancy from 33 to 39 weeks, more often at 35 weeks. HELLP syndrome is detected in the postpartum period in 30% of cases. The clinical picture is characterized by an aggressive course and a rapid increase in symptoms. Initial manifestations are nonspecific and include headache, fatigue, vomiting, abdominal pain, often localized in the right hypochondrium or diffuse. Then vomiting, stained with blood, hemorrhages at injection sites, increasing jaundice and liver failure, convulsions, and severe coma appear. Liver rupture with bleeding into the abdominal cavity is often observed. In the postpartum period, profuse uterine bleeding may occur due to a disorder of the coagulation system. HELLP syndrome may manifest itself as a clinical picture of total premature detachment of a normally located placenta, accompanied by massive coagulopathic bleeding and rapid development of hepatorenal failure.

Laboratory signs of HELLP syndrome are:

• increased levels of transaminases (AST>200 U/l, ALT>70 U/l, LDH>600 U/l);
• thrombocytopenia (<100×10 ⁹ /l); decrease in the level of antithrombin III below 70%;
• intravascular hemolysis and increased bilirubin levels, increased prothrombin time and APTT;
• decreased fibrinogen levels - they become lower than necessary during pregnancy;
• increased levels of nitrogenous waste in the blood;
• lowering blood sugar levels to the point of hypoglycemia.

Not all signs of HELLP syndrome may always be observed. In the absence of hemolytic syndrome, the symptom complex is designated as HELLP syndrome. If thrombocytopenia is absent or slightly expressed, the disease is called HEL syndrome.

Acute fatty hepatosis of pregnancy (AFGP) is a rare, occurring with a frequency of 1 in 13 thousand births, but dangerous complication of pregnancy, more often developing in primigravidas. Maternal mortality in this case is 60-85%, the fetus dies even more often. In the clinical course of the disease, 3 stages are distinguished.

• The first is pre-icteric, usually beginning at 30-34 weeks of pregnancy. Mild signs of gestosis appear. Typical complaints include nausea, vomiting, loss of appetite, abdominal pain, weakness, lethargy, itching, heartburn, which is initially short-term, intermittent, and then becomes painful, untreatable and ends in "coffee ground" vomiting. The pathomorphological basis of this symptom is erosion or ulceration of the esophageal mucosa during the development of disseminated intravascular coagulation syndrome (DIC syndrome).
• The second (1-2 weeks after the onset of the disease) is icteric. Jaundice is usually intense, but can be moderate. By this time, weakness increases, heartburn, nausea and vomiting (usually bloody), tachycardia of 120-140 per minute, burning behind the breastbone, abdominal pain, fever, oliguria, peripheral edema, fluid accumulation in the serous cavities, and symptoms of liver failure increase. Renal failure of varying degrees of severity develops as a result of kidney damage. Clinical signs are combined with a rapid decrease in the liver.
• The third (1–2 weeks after the onset of jaundice) is characterized by severe fulminant liver failure and acute renal failure. Patients remain conscious for a long time, right up to the terminal stage of the disease. Severe DIC syndrome develops with severe bleeding from the uterus, other organs and tissues. AFGB is often complicated by ulceration of the mucous membranes of the esophagus, stomach, and intestines. Massive hemorrhages occur in the brain and pancreas, which accelerates the fatal outcome of the disease. With AFGB, hepatic coma often develops with impaired brain function from minor disturbances of consciousness to its profound loss with suppression of reflexes. In contrast to the usual hepatic coma, this pathology does not develop alkalosis, but metabolic acidosis. The duration of the disease ranges from several days to 7–8 weeks.

A biochemical blood test reveals:

• hyperbilirubinemia due to direct fraction;
• hypoproteinemia (<60 g/l); hypofibrinogenemia (<2 g/l);
• mild thrombocytopenia; slight increase in transaminase levels, sharp decrease in antithrombin III levels;
• increased levels of uric acid in the blood serum, leukocytosis (up to 20,000–30,000), metabolic acidosis.

Ultrasound of the liver reveals increased echogenicity, and computed tomography reveals decreased radiographic density.

Morphological signs of AFGB are very specific and are characterized by the fact that in the centrolobular part of the organ, pronounced fatty degeneration of hepatocytes is found in the absence of necrosis. Liver cells in the central lobes of the organ appear swollen and have a foamy appearance due to the accumulation of tiny droplets of fat in the cytoplasm.

Liver biopsy is usually impossible due to severe blood clotting disorders.

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