bubble_chart Overview

Fetal distress is caused by fetal hypoxia and mostly occurs during labor, but can also happen during pregnancy. It is a common cause of perinatal fetal death and neonatal neurological sequelae, ranking as the leading cause of perinatal mortality.

bubble_chart Etiology

(1) Maternal factors: Pregnant women with heart disease, heart failure, high fever, acute loss of blood, severe anemia, or the use of anesthetics may lead to insufficient blood volume in the mother, resulting in fetal hypoxia.

(2) Uterine factors: Excessive or frequent uterine contractions, or even rigid contractions, can affect uterine blood circulation and cause fetal hypoxia.

(3) Fetal factors: Placental abruption, placenta previa, pregnancy hypertension syndrome, post-term pregnancy, and chronic nephritis can lead to placental circulatory disorders, resulting in fetal hypoxia.

(4) Umbilical cord factors: Umbilical cord knots, prolapse, entanglement around the neck or body, and umbilical bleeding can obstruct blood flow and cause fetal hypoxia.

(5) Fetal factors: Fetal heart and cardiovascular system dysfunction, fetal intracranial hemorrhage, fetal malformations, and maternal-fetal blood type incompatibility.

bubble_chart Clinical Manifestations

(1) Changes in fetal heart rate are the first symptom of fetal distress. The fetal heart sounds initially become faster but remain strong and regular, then slow down, becoming weak and irregular. Therefore, vigilance should be heightened as soon as an increase in fetal heart rate is detected. During uterine contractions, the fetal heart rate slows due to temporary interference with the uterine-placental blood circulation, but it quickly returns to normal after the contractions cease. Thus, the fetal heart rate should be assessed between contractions. A fetal heart rate above 160 beats per minute or below 120 beats per minute is considered abnormal. A rate below 100 indicates severe hypoxia. If conditions permit, fetal heart monitoring should be performed.

(2) Meconium-stained amniotic fluid Under hypoxic conditions, the fetus experiences vagal stimulation, leading to increased intestinal peristalsis and relaxation of the anal sphincter, resulting in meconium discharge. The amniotic fluid then appears grass-green. This is diagnostically significant in cephalic presentations. In breech presentations, meconium may be expelled due to compression of the fetal abdomen, so its presence in the amniotic fluid does not necessarily indicate fetal distress.

(3) Abnormal fetal movements Excessive fetal activity is a sign of struggle due to hypoxia. As hypoxia worsens, fetal movements may decrease or even cease.

(4) Fetal scalp blood pH measurement As fetal distress progresses, the pH of fetal scalp blood decreases (<7.25), indicating fetal acidosis.

bubble_chart Treatment Measures

(1) Oxygen administration increases maternal blood oxygen levels to improve fetal hypoxia.

(2) Intravenous injection of a triple-drug combination, consisting of 50% glucose (60 ml), vitamin C (500 mg), and nikethamide (0.375 g). Glucose protects brain tissue and enhances hypoxia tolerance; vitamin C reduces capillary permeability and fragility; nikethamide is a central nervous system stimulant. In recent years, some believe that nikethamide may increase fetal oxygen consumption, and to avoid worsening fetal hypoxia, its use is not recommended.

(3) Take corresponding measures based on the disease cause.

(4) Terminate childbirth: When the cervix is fully dilated, perform an episiotomy for cephalic presentation, or assist delivery with vacuum extraction or forceps. For breech presentation, breech extraction may be performed. If the cervix is not fully dilated and vaginal delivery cannot be achieved within a short time, consider a cesarean section. If the fetus is deceased, await spontaneous delivery or perform craniotomy.