bubble_chart Overview

Fetal distress refers to signs of hypoxia in the fetus that endanger its health and life. It is a syndrome and one of the primary indications for cesarean section. Fetal distress mainly occurs during labor but can also occur in the late stage of pregnancy (third trimester). When it occurs during labor, it may be a continuation or worsening of the condition from the late stage of pregnancy.

bubble_chart Etiology

Fetal distress has multifaceted disease causes, which can be categorized into three major types.

1. Maternal Factors Insufficient maternal blood oxygen levels are a significant cause. During grade I hypoxia, the mother may show no obvious symptoms, but the fetus can still be affected. Maternal factors leading to fetal hypoxia include:

(1) Inadequate microcirculation blood supply: such as hypertension, chronic nephritis, and pregnancy-induced hypertension.

(2) Insufficient oxygen-carrying capacity of red blood cells: such as grade III anemia, heart failure due to heart disease, and cor pulmonale.

(3) Acute blood loss: such as prenatal hemorrhagic disorders and trauma.

(4) Impaired uterine-placental blood flow: rapid labor or uncoordinated uterine contractions; improper use of oxytocin, causing excessively strong contractions; prolonged labor, especially in the second stage; uterine overdistension, such as polyhydramnios and multiple pregnancies; premature rupture of membranes, which may compress the umbilical cord, etc.

2. Fetal Factors

(1) Dysfunction of the fetal cardiovascular system, such as severe congenital cardiovascular diseases or intracranial hemorrhage.

(2) Fetal malformations.

3. Umbilical Cord and Placental Factors The umbilical cord and placenta serve as the channels for oxygen and nutrient exchange between the mother and fetus. Their dysfunction inevitably affects the fetus's ability to obtain the necessary oxygen and nutrients.

(1) Impaired umbilical cord blood flow.

(2) Placental insufficiency: such as post-term pregnancy, placental developmental disorders (too small or too large), abnormal placental shape (membranous placenta, circumvallate placenta, etc.), and placental infections.

bubble_chart Clinical Manifestations

1. Chronic fetal distress mostly occurs in the late stage of pregnancy, often extending into labor and worsening. The causes are mostly due to systemic diseases of the pregnant woman or pregnancy-related conditions leading to placental insufficiency or fetal factors. Clinically, besides identifying maternal diseases that cause insufficient placental blood supply, prolonged chronic fetal hypoxia may result in intrauterine growth restriction.

2. Acute fetal distress primarily occurs during childbirth, mostly caused by umbilical cord factors (such as prolapse, entanglement around the neck, knots, etc.), placental abruption, excessively strong and prolonged uterine contractions, or maternal hypotension and shock. Clinical manifestations include changes in fetal heart rate, meconium-stained amniotic fluid, excessive fetal movements, cessation of fetal movements, and acidosis.

bubble_chart Diagnosis

1. Diagnosis of chronic fetal distress

(1) Placental function examination: Measure the 24-hour urinary E₃ value and observe it dynamically and continuously. If it decreases sharply by 30–40%, or if multiple consecutive measurements of the 24-hour urinary E₃ value at the end of pregnancy are below 10mg, it indicates a decline in fetal-placental function.

(2) Fetal heart monitoring: Continuously record the fetal heart rate for 20–40 minutes. The normal baseline fetal heart rate is 120–160 beats per minute. If the acceleration of the fetal heart rate during fetal movement is not significant, the baseline variability <3次/分，提示存在胎兒窘迫。

(3) Fetal movement count: Near full-term pregnancy, fetal movement should be >20 times/24 hours. The calculation method involves instructing the pregnant woman to self-monitor fetal movements for one hour each in the morning, noon, and evening. The sum of the three counts multiplied by 4 approximates the 12-hour fetal movement count. Reduced fetal movement is an important indicator of fetal distress. Daily monitoring of fetal movements can predict fetal well-being. After fetal movements cease, the fetal heart rate will also disappear within 24 hours, so this should be noted to avoid delaying rescue efforts. Frequent fetal movements are often a precursor to the cessation of movements and should also be taken seriously.

(4) Amnioscopy: Observing turbid amniotic fluid stained yellow to dark brown aids in the diagnosis of fetal distress.

2. Diagnosis of acute fetal distress

(1) Changes in fetal heart rate: The fetal heart rate is an important indicator of fetal well-being: ① A fetal heart rate >160 beats per minute, especially >180 beats per minute, is a manifestation of the initial stage of fetal hypoxia (when the maternal heart rate is not elevated); ② A fetal heart rate <120次/分，尤其是>100 beats per minute is a sign of fetal danger; ③ The appearance of late decelerations, variable decelerations, or (and) a lack of baseline variability all indicate fetal distress. When the fetal heart rate is abnormal, a detailed examination of the cause is required. Changes in the fetal heart rate should not be determined based on a single auscultation but should be checked multiple times, with the mother changing to a lateral position followed by continuous monitoring for several minutes.

(2) Meconium staining of amniotic fluid: Fetal hypoxia stimulates the vagus nerve, increases intestinal motility, and relaxes the anal sphincter, causing meconium to be discharged into the amniotic fluid. The amniotic fluid appears green, yellow-green, and then turbid brown-yellow, corresponding to grade I, II, and III meconium staining. After membrane rupture, the amniotic fluid can be directly observed. If the membranes are intact, amnioscopy can be used to assess the amniotic fluid through the membranes. If the fetal presenting part is fixed, the condition of the forewaters may differ from that of the hindwaters above the presenting part. If the forewaters are clear but the fetal heart rate is abnormal, and if membrane rupture is feasible under the circumstances, the presenting part can be slightly pushed upward after disinfection and draping, allowing the hindwaters above to flow out for assessment.

In cases of grade I or even grade II meconium staining with consistently good fetal heart rate, close monitoring of the fetal heart rate should continue, as it may not necessarily indicate fetal distress. For grade III meconium staining, childbirth should be expedited, even if the newborn's Apgar score may be ≥7, as the risk of neonatal asphyxia is high. If grade I meconium staining is accompanied by abnormal findings in fetal heart rate monitoring over about 10 minutes, fetal distress should still be diagnosed.

(3) Fetal movement: In the initial stage of acute fetal distress, frequent fetal movements are first observed, followed by weakening and a reduction in frequency, and eventually cessation.

(4) Acidosis: After membrane rupture, fetal scalp blood can be analyzed for blood gas. Indicators for diagnosing fetal distress include blood pH<7.20，PO₂<1.3kPa（10mmHg），PCO₂>8.0kPa (60mmHg).

bubble_chart Treatment Measures

1. Chronic fetal distress should be managed based on the disease cause, considering gestational age, fetal maturity, and the severity of distress.

(1) For those who can undergo regular prenatal check-ups and whose fetal condition is estimated to be acceptable, the pregnant woman should rest more in a lateral position to improve placental blood supply and prolong the gestational period.

(2) If the condition is difficult to improve and the pregnancy is near term, with a high likelihood of fetal survival after delivery, a cesarean section may be considered.

(3) The farther from term the pregnancy is, the lower the chances of fetal survival after delivery. In such cases, the situation should be explained to the family, and conservative treatment should be pursued to extend the gestational period as much as possible. If the fetal-placental function is indeed poor, fetal development will inevitably be affected, resulting in a poorer prognosis.

2. Acute fetal distress

(1) If the cervix is fully dilated and the fetal presenting part has reached 3 cm below the ischial spine, assisted vaginal delivery should be performed as quickly as possible.

(2) If the cervix is not fully dilated and the fetal distress is not severe, oxygen therapy (via mask) can be administered to improve fetal oxygen supply by increasing maternal blood oxygen levels. The mother should also be advised to lie on her left side and observed for 10 minutes. If the fetal heart rate returns to normal, monitoring can continue. If the abnormal slowing of the fetal heart rate is caused by excessive uterine contractions due to oxytocin use, the infusion should be stopped immediately, and observation should continue to see if the heart rate normalizes. If the condition is urgent or does not improve with the above measures, an immediate cesarean section should be performed to end the childbirth.