Diagnosis of gestosis

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

Diagnosis of preeclinical gestosis at the beginning of the second trimester of pregnancy is carried out on the basis of the following changes in laboratory indicators:

• test with inverting (three times the measurement of blood pressure with an interval of 5 minutes in the position of a woman on her side, on her back and again on her side). The test is considered positive when the diastolic pressure changes by more than 20 MMHg;
• violation of uteroplacental blood flow (no decrease in SDS in the uterine arteries and spiral arteries of the myometrium in the period of 14-16 weeks);
• the decrease in the number of platelets progressing as pregnancy progresses (less than 160-10 ⁹ / L);
• hypercoagulation in the cellular and plasma links of hemostasis (increase in platelet aggregation to 76%, reduction in APTT less than 20 seconds, hyperfibrinogenemia up to 4.5 g / l);
• decrease in the level of anticoagulants (endogenous heparin up to 0.07 units ml, antithrombin III up to 63%);
• lymphopenia (18% or less);
• activation of lipid peroxidation;
• decrease in the level of antioxidant activity of blood.

The criterion of gestosis is proteinuria of more than 0.3 g / L, hypertension - at arterial pressure above 135/85 mm Hg. And, with hypotension, an increase in systolic blood pressure of more than 30 mm Hg. Art. From the initial, and diastolic - 15 mm Hg. P. Swelling should be considered only if they do not disappear after a night's sleep.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11]

Special methods of research in gestosis

Compulsory examination methods include measurement of body weight, blood pressure on both hands, pulse, diuresis, clinical blood and urine analysis, 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).

As additional methods of examination apply:

• daily monitoring of arterial pressure, ECG, CTG;
• dopplerometry of maternal and fetal hemodynamics;
• examination of the fundus;
• urine analysis according to Nechiporenko, urine analysis according to Zimnitsky, Reberg's test, bacterial culture of urine;
• Ultrasound of the vital organs of the mother and fetus;
• hemostasiogram [thromboelastography, activated partial thromboplastin time (APTT), number and aggregation of platelets, fibrinogen, products of its degradation, endogenous heparin concentration, antithrombin III];
• definition of lupus anticoagulant;
• the definition of antibodies to the chorionic gonadotropin;
• measurement of central venous pressure (CVP).

Diagnosis of gestosis in the I and II trimesters before the manifestation of clinical signs is carried out on the basis of the following changes:

• progressive decrease in the number of platelets (up to 160 × 10 ⁹ / l or less) as pregnancy progresses ;
• hypercoagulation in the cellular and plasma links of hemostasis:
  • increase platelet aggregation up to 76%;
  • decrease of APTT less than 20 s;
  • hyperfibrinogenemia up to 4.5 g / l;
• decrease in the level of anticoagulants:
  • 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 method of determination);
• decrease in the level of antioxidant activity of blood (below the norm, depending on the method of determination);
• violation of blood flow in the vessels of the utero-placental bed. The presence of 2-3 of the above signs indicates a high probability of gestosis after 20 weeks of pregnancy.

Gestosis may manifest as an increase in blood pressure in the form of monosymptom, and also in combination with proteinuria and / or edema that occur after 20 weeks of gestation.

Persistent edema is an early symptom of gestosis. There are the following types of edema.

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

In 88-90% of cases, edema of pregnant women becomes gestosis.

The organization of gestosis assesses the severity of gestosis similar to the scale.

To assess the severity of gestosis, the Goecke scale is used in the GM modification. Savelieva et al.

In terms of severity, gestosis is divided into easy (up to 7 points), medium (8-11 points) and heavy (12 points or more).

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

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

• systolic blood pressure 160 mm Hg. Art. And above, diastolic 110 mm Hg. Art. And higher;
• proteinuria up to 5 g / day or more;
• oliguria (volume of urine per day <400 ml);
• hypokinetic type of central uterine hemodynamics (CMG) with increased OPSS, pronounced disorders of renal blood flow, bilateral disturbance of blood flow in the uterine arteries, an increase in the pulsation index in the internal carotid artery> 2.0, retrograde blood flow in the suprapubic arteries;
• absence of normalization or worsening of hemodynamic parameters against the background of intensive therapy of gestosis;
• thrombocytopenia (100 × 10 ⁹ / l);
• hypocoagulation;
• increased activity of hepatic enzymes;
• hyperbilirubinemia.

Given the severity of the complications that lead to hypertension in pregnancy, it is extremely important to use 24-hour monitoring of blood pressure for timely and correct diagnosis of hypertension in pregnant women and predict gestosis, as well as determining indications and preparations for hypotensive therapy. The 24-hour monitoring with 24-30 minute intervals between the measurements sufficiently reproduces the daily dynamics of arterial pressure. In addition, daily monitoring of blood pressure makes it possible to identify cases of overdiagnosis, which is extremely important, since the appointment of antihypertensive therapy can cause iatrogenic complications.

In the study of maternal hemodynamics, four major pathogenetic variants of circulatory system disorders are identified.

• Hyperkinetic type of CMG, regardless of the values of OPSS and eukinetic type with normal values of OPSS. With this type, moderate violations of cerebral (9%), renal (9%), utero-placental-fetal (7.2%) and intraluminal (in 69.4%) circulation are recorded. In 11%, the intrauterine retardation of fetal development is noted. In 91% of the patients, mild gestosis is clinically detected. Conducted therapy of gestosis is effective in most cases. The prognosis for the mother and fetus is favorable.
• Eukinetic type of CMG with elevated OPSS values and hypokinetic type of CMG with normal OPSS values. In this type, blood flow disorders of predominantly grade II are recorded in the renal artery system, utero-placental-fetal and intraplacental blood flow. Prevalent moderate forms of gestosis. Intrauterine fetal development delay is revealed in 30%, decompensated placental insufficiency - in 4,3%, pre-eclampsia - in 1,8%. Conducted therapy of gestosis is effective in 36%.
• Hypokinetic type of CMG with an increase in OPSS. Abnormalities of renal, utero-placental and intraplacental blood flow predominantly of II and III degree are revealed in 100%. In 42%, a bilateral disturbance of blood flow in the uterine arteries is determined. For this type, moderate and severe forms of gestosis are characteristic, intrauterine retardation of fetal development in 56%, decompensated fetoplacental insufficiency of 7%, preeclampsia at 9.4%. Improvements in hemodynamic and clinical indices against the background of ongoing therapy are not noted, and half of pregnant women are seeing deterioration. The prognosis for the mother and fetus is unfavorable, since with the given type of hemodynamics the greatest number of severe forms of gestosis, decompensated placental insufficiency, as well as early delivery and perinatal losses are noted.
• Expressed disorders of cerebral hemodynamics (increase in pulsational index in the internal carotid artery more than 2.0 and / or retrograde blood flow in the suprapubic arteries). With this type, the forms of gestosis are revealed with a rapid increase in the clinical picture (within 2-3 days). Regardless of the indices of central, renal, utero-placental and intraplacental hemodynamics, a type of 100% develops preeclampsia. The maximum period from registration of pathological values of blood flow 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 can be due to hypertension, pre-pregnancy (usually hypertension), diabetes, kidney disease, hypothyroidism, obesity, hypertension occurring during pregnancy (hypertension of pregnant women), and preeclampsia. Despite the common manifestations, these are different diseases. Their pathogenesis, treatment and prognosis for the mother and fetus vary. However, it is important to remember that these diseases can be combined.

Classic complications of gestosis:

• acute renal insufficiency;
• cardiopulmonary insufficiency;
• HELLP-syndrome and acute fatty hepatosis of pregnant women (OZHGB);
• edema of the brain and hemorrhage in it;
• cerebral coma.
• retinal disinsertion;
• premature detachment of the normally located placenta.

At present, HELLP-syndrome and OZHGB acquire increasing importance.

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. The first HELLP syndrome was described by JA Pritchard in 1954. In 1982, Weinstein proposed the term "HELLP-syndrome" for the determination of a special group of pregnant women with pre-eclampsia who noted hemolysis, hyperfermentemia and a decrease in platelet count. Many clinicians consider HELLP-syndrome as a complication of gestosis.

HELLP-syndrome: hemolysis H (Hemolysis), increased activity of liver enzymes EL (elevated liver enzimes), low platelet count LP (low platelet count). With 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 33rd to 39th weeks, more often at a period of 35 weeks. HELLP-syndrome in 30% of cases are detected in the postpartum period. The clinical picture is characterized by an aggressive course and a rapid increase in symptoms. The initial manifestations are nonspecific and include headache, fatigue, vomiting, abdominal pain, more often localized in the right hypochondrium or diffuse. Then there are vomiting, colored blood, hemorrhages at the injection site, increasing jaundice and liver failure, convulsions, pronounced coma. Often observe a rupture of the liver with a bleeding into the abdominal cavity. In the postpartum period, due to a breach of the coagulation system, profuse uterine bleeding can occur. HELLP-syndrome can be manifested by the clinic of total premature detachment of the normally located placenta, accompanied by massive coagulopathic bleeding and rapid formation of hepatic-renal failure.

The laboratory features of the HELLP syndrome are:

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

Not all signs of HELLP-syndrome can be observed. In the absence of hemolytic syndrome, the symptom complex is referred to as the NELLP syndrome. If there is no or little expressed thrombocytopenia, the disease is called HEL-syndrome.

Acute fatty hepatosis of pregnant women (OZHGB) is rare, occurring with a frequency of 1 to 13 thousand births, but a dangerous complication of pregnancy, often develops in primordial. Maternal mortality with it is 60-85%, the fetus dies even more often. In the clinical course of the disease, there are 3 stages.

• The first - dystonia, begins, as a rule, on the 30-34th week of pregnancy. There are indistinct signs of gestosis. Typical complaints are nausea, vomiting, lack of appetite, abdominal pain, weakness, lethargy, pruritus, heartburn, which at first is brief, intermittent, and then becomes painful, uncontrollable and vomiting "coffee grounds". The pathomorphological basis of this symptom is the erosion or ulceration of the mucosa of the esophagus in the development of the syndrome of disseminated intravascular coagulation (DVS-syndrome).
• The second (after 1-2 weeks from the onset of the disease) is icteric. Jaundice is usually intense, but can be mild. By this time, there is growing weakness, heartburn, nausea and vomiting (more often bloody), tachycardia 120-140 per minute, burning behind the sternum, abdominal pain, fever, oligoanuria, peripheral edema, accumulation of fluid in the serous cavities, and symptoms of hepatic insufficiency. Renal insufficiency develops in one degree or another 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 hepatic insufficiency and acute renal failure. Consciousness of patients persists for a long time, up to the terminal stage of the disease. A severe DVS-syndrome develops with the strongest bleeding from the uterus, other organs and tissues. OZHGB is often complicated by ulceration of the mucous membranes of the esophagus, stomach, and intestines. There are massive hemorrhages in the brain, pancreas, which accelerates the lethal outcome of the disease. With OZGBB often develops a hepatic coma with impaired function of the brain from minor disorders of consciousness to its deep loss with inhibition of reflexes. In contrast to the usual hepatic coma in this pathology, not alkalosis develops, but metabolic acidosis. The duration of the disease is from several days to 7-8 weeks.

When biochemical blood test revealed:

• Hyperbilirubinemia due to direct fraction;
• hypoproteinemia (<60 g / l); hypofibrinogenemia (<2 g / l);
• unexpressed thrombocytopenia; a slight increase in the level of transaminases, a sharp decrease in the level of antithrombin III;
• increased serum uric acid levels, leukocytosis (up to 20 000-30 000), metabolic acidosis.

With ultrasound of the liver, an increased echogenicity is revealed, and with computed tomography, a decrease in the radiographic density.

Morphological signs of OZHGB are very specific and characterized by the fact that in the centrolobular part of the organ they show a pronounced fatty dystrophy of hepatocytes in the absence of necrosis. Hepatic cells in the central lobes of the organ look swollen and have a foamy appearance due to the accumulation in the cytoplasm of the smallest droplets of fat.

A liver biopsy is usually impossible because of severe bleeding disorders.

[12], [13], [14], [15], [16], [17], [18]