Fetal hypoxia is distinguished by type, intensity, duration and course.
The main types of oxygen starvation are hypoxic (with reduced oxygen saturation of the blood), circulatory (with sufficient oxygen saturation, but impairment of its delivery to the tissues), hemic (due to a violation of oxygen binding by hemoglobin or a decrease in the amount of hemoglobin in the blood), tissue tissues to assimilate oxygen). Isolate hypoxia of the tissues, arising in consequence of increased similarity of hemoglobin to oxygen.
The intensity is
1. Functional hypoxia - an easy form of oxygen deficiency, accompanied by only hemodynamic disorders (tachycardia, increased blood pressure).
2. Metabolic hypoxia - a stronger oxygen deficiency, in which oxygen supply to tissues is reduced leads to a metabolic disorder (these changes are reversible).
3. Destructive hypoxia, which is a manifestation of severe oxygen deficiency and causes changes in cells (irreversible hypoxia).
With the flow, acute and chronic fetal hypoxia is distinguished. Chronic hypoxia of the fetus develops during complicated pregnancy (toxicosis of pregnant women, overweight or miscarriage, extragenital diseases, immunological incompatibility, infection of the fetus, etc.). Chronic hypoxia of the fetus is caused by a prolonged insufficient supply of nutrients to its body and often leads to a delay in development and growth.
Acute hypoxia of the fetus occurs in the genus (anomalies of labor, umbilical cord prolapse or clamping, presence of an actual cord, umbilical cord around the neck of the fetus, prolonged compression of the head in the pelvic cavity), and less often during pregnancy (uterine rupture, premature placental abruption, etc.).
At physiological births it is possible to use fetal anaerobic glycolysis, as a result of which the pH of its blood is lower than the pH of the mother's blood. Compulsory correction is required only in those cases where the pH drops below 7.2. Acidosis leads to a violation of the permeability of membranes, electrolyte imbalance (hyperkalemia and intracellular hypernatremia), distortion of enzymatic processes. Intensive anaerobic glycolysis leads to depletion of glycogen stores. The fetus has a hemodynamic disorder due, on the one hand, to the development of bradycardia due to hyperkalemia or excessive vagus tone, on the other hand, to a violation of microcirculation as a result of spasm of peripheral vessels and, so-called centralization of blood circulation, thickening of blood and edema of tissues. Against this background, hemorrhages easily develop, including the brain.
The main symptoms of intrauterine fetal hypoxia are:
1. Change in the character of the fetal heartbeat:
a) tachycardia (with hypoxia and degree);
b) bradycardia (with hypoxia of the second degree);
c) arrhythmia (with grade III hypoxia);
d) worsening of sonority of cardiac tones (first a slight gain, then a growing weakening).
2. Decreased intensity of fetal movements.
3. Departure of meconium in the head presentation of the fetus.
4. Change in acid-base balance of amniotic fluid and. Blood obtained from the fetal part.
The complex method of treatment of fetal hypoxia includes: oxygen therapy, therapy aimed at improving uteroplacental blood circulation and rheological properties of blood, normalization of metabolic disorders, enhancing the fetal organism's resistance to hypoxia. For this purpose:
1. Inhalation of clean, moistened oxygen through a hermetically sealed mask.
2. Intravenous injection of glucose with insulin, ascorbic acid and cocarboxylase (40% glucose 40ml with 4 units of insulin or 500ml of 10% with 10 units of insulin, 5 ml of 5% ascorbic acid, 50 mg of cocarboxylase).
3. Introduction 10ml 10% calcium gluconate.
4. Introduction 1 ml of 1% Sigetin or 10 ml of 24% of euphyllin.
5. Kurantil 0025 g 3 times a day or intravenously drop by 2 ml on a 5% solution of glucose.
6. Compline on 150 mg 3 times a day for 10-14 days or 2 ml of 15% solution 1-2 times a day intramuscularly.
7. Trental 100mg 3 times a day 4-6 weeks or intravenously drip 5ml 2% solution for 500 ml of 5% glucose solution.
8. Reopoliglyukin 400ml drip 2-4 times a week.
9. ATP for 2-4 ml intramuscularly.
10. Hyperbaric oxygenation - breathing oxygen at a pressure of 3 atm.
11. Enteral oxygen therapy - by injecting into the stomach oxygen foam in the form of a cocktail (egg white hen with dogrose infusion, glucose, vitamins of groups B and C).
12. Cytochrome C in 5-7.5 mg in a solution of glucose, sodium succinate intravenously in the form of a 5% solution.
13. Glutamic acid, methionine.
Treatment of fetal hypoxia, aimed at improving the function of the feto-placental complex and the cardiovascular system of the fetus, to correct the changes in metabolic processes in its body, does not always eliminate the cause of oxygen deficiency. In these cases it is necessary to resort to rapid delivery. During pregnancy and in the first stage of labor, fetal hypoxia, which does not respond to treatment, is an indication for cesarean delivery. In the second stage of labor, fetal hypoxia, which began depending on the conditions and obstetric situation, is used by obstetric forceps or extraction of the fetus behind the pelvic end. At the end of the second stage of labor, the perineal incision is performed to rapidly complete labor.