Obstetrics and Gynecology - A.M. Gromova 2000

Fetoplacental insufficiency
Fetal hypoxia and neonatal asphyxia
Fetal hypoxia

Fetal Hypoxia is classified according to its type, intensity, duration, and clinical course.

The MAIN TYPES OF oxygen deprivation include hypoxic (resulting from reduced Blood oxygen saturation), circulatory (caused by adequate blood oxygen saturation but impaired delivery to Tissues), hemic (resulting from impaired oxygen binding by Hemoglobin or decreased blood hemoglobin levels), and tissue (caused by reduced tissue capacity to utilize oxygen). Additionally, tissue hypoxia can occur due to an increased affinity of hemoglobin for oxygen.

According to its intensity, hypoxia is classified into:

1. Functional hypoxia — the mildest form of oxygen insufficiency, accompanied only by hemodynamic disorders (tachycardia, elevated blood pressure).

2. Metabolic hypoxia — a more severe form of oxygen deficiency where reduced oxygen supply to tissues leads to metabolic disturbances (these changes are reversible).

3. Destructive hypoxia — a manifestation of severe oxygen deprivation that causes cellular damage (irreversible hypoxia).

Depending on the clinical course, fetal hypoxia is divided into acute and chronic. Chronic fetal hypoxia develops during complicated pregnancies (gestosis, post-term or preterm Pregnancy, extragenital diseases, immunological incompatibility, fetal infection, etc.). Chronic fetal hypoxia is caused by prolonged inadequate supply of nutrients to the fetus and frequently leads to growth and developmental restriction.

Acute fetal hypoxia occurs during labor (abnormal labor, prolapsed or compressed umbilical cord, true knot of the umbilical cord, nuchal cord, prolonged HEAD compression in the pelvic cavity) and less commonly during pregnancy (Uterine rupture, premature placental abruption, etc.).

During physiological labor, the fetus may utilize anaerobic Glycolysis, resulting in a blood pH lower than that of the mother. Mandatory correction is required only in cases where the pH drops below 7.2. Acidosis leads to impaired membrane permeability, electrolyte imbalance (hyperkalemia and intracellular hypernatremia), and disruption of enzymatic processes. Intensive anaerobic glycolysis depletes Glycogen stores. The fetus develops hemodynamic disorders caused, on the one hand, by bradycardia resulting from hyperkalemia or excessive vagal tone, and on the other hand, by microcirculatory disturbances resulting from peripheral vasospasm, so-called centralization of Blood Circulation, hemoconcentration, and tissue edema. Against this Background, hemorrhages readily develop, including intracranial hemorrhages.

The main symptoms of intrauterine fetal hypoxia are:

1. Changes in fetal Heart rate patterns:

a) tachycardia (in grade I hypoxia);

b) bradycardia (in grade II hypoxia);

c) arrhythmia (in grade III hypoxia);

d) deterioration of heart sound clarity (initially a slight accentuation, followed by progressive weakening).

2. Decreased intensity of fetal movements.

3. Passage of meconium during cephalic presentation.

4. Alterations in acid-base balance parameters in Amniotic Fluid and blood obtained from the fetal presenting part.

The comprehensive Treatment method for fetal hypoxia includes: Oxygen therapy, therapies aimed at improving uteroplacental blood flow and blood rheology, normalization of Metabolic Disorders, and increasing the fetus's resistance to hypoxia. To this end, the following measures are carried out:

1. Inhalation of pure, humidified oxygen via a tightly sealed mask.

2. Intravenous administration of glucose with Insulin, ascorbic acid, and cocarboxylase (40 ml of 40% glucose with 4 IU of insulin or 500 ml of 10% glucose with 10 IU of insulin, 5 ml of 5% ascorbic acid, 50 mg of cocarboxylase).

3. Intravenous administration of 10 ml of 10% calcium gluconate.

4. Intravenous administration of 1 ml of 1% sigetin or 10 ml of 2.4% aminophylline.

5. Curantil 0.025 g 3 times a day or intravenously via drip infusion of 2 ml in a 5% glucose solution.

6. Complamin 150 mg 3 times a day for 10–14 days or 2 ml of a 15% solution 1–2 times a day intramuscularly.

7. Trental, 100 mg 3 times daily for 4–6 weeks, or an intravenous drip of 5 ml of a 2% solution in 500 ml of a 5% glucose solution.

8. Rheopolyglucin, 400 ml intravenously as a drip 2–4 times a week.

9. ATP, 2–4 ml intramuscularly.

10. Hyperbaric Oxygenation: breathing oxygen under a pressure of 3 atm.

11. Enteral oxygen therapy: administration of oxygen foam into The Stomach as a cocktail (chicken egg white with rosehip infusion, glucose, and Vitamins B and C).

12. Cytochrome C, 5–7.5 mg in a glucose solution; sodium succinate intravenously as a 5% solution.

13. Glutamic acid, Methionine.

Treatment for fetal hypoxia, aimed at improving the function of the fetoplacental complex and the fetal Cardiovascular system, as well as correcting metabolic disorders in the fetus, does not always eliminate the cause of oxygen deficiency. In such cases, prompt delivery is necessary. During pregnancy and The First stage of labor, treatment-resistant fetal hypoxia is an indication for a Cesarean Section. During the Second Stage of labor, if acute fetal hypoxia develops, obstetrical forceps or Breech Extraction are used depending on the clinical conditions and obstetric situation. At the end of the second stage of labor, an Episiotomy is performed to expedite delivery.