Fetal distress refers to a condition where the fetus experiences acute or chronic hypoxia in utero, threatening its health and survival. The incidence varies between 2.7% and 38.5%. Acute fetal distress typically occurs during labor, while chronic fetal distress tends to arise in late pregnancy and may persist or worsen during delivery.
Etiology
Fetal distress can result from insufficient maternal oxygen levels, impaired oxygen transport and exchange between the mother and fetus, or fetal abnormalities.
Acute Fetal Hypoxia
Acute hypoxia is commonly caused by disruptions in oxygen transport or blood circulation between the mother and fetus, or by umbilical cord complications. Contributing factors include:
- Placental abnormalities, such as placenta previa or placental abruption
- Umbilical cord complications, such as true umbilical cord knots, cord torsion, cord prolapse, or hematoma
- Severe maternal cardiovascular dysfunction leading to a rapid reduction in placental perfusion, such as in cases of shock
- Medication-related factors, including improper use of oxytocin or excessive administration of anesthetics or sedatives
Chronic Fetal Hypoxia
Contributing factors include:
- Insufficient maternal oxygen levels due to conditions such as congenital heart disease, heart failure, pulmonary infections, chronic lung dysfunction, recurrent asthma, or severe anemia
- Insufficient intervillous blood perfusion due to uteroplacental vascular sclerosis, narrowing, or infarction, caused by conditions such as hypertensive disorders of pregnancy, chronic nephritis, diabetes, or prolonged pregnancy
- Reduced fetal capacity to utilize oxygen due to severe cardiovascular or respiratory conditions, serious structural anomalies, anemia, intrauterine infections, intracranial hemorrhage, or brain injury
Pathophysiology
The uteroplacental unit provides the fetus with oxygen and nutrients while eliminating carbon dioxide and metabolic waste. The fetus has a degree of compensatory capacity for hypoxia. Mild to moderate and transient hypoxia can be alleviated through compensation; however, prolonged severe hypoxia can lead to serious complications. Chronic intrauterine hypoxia during pregnancy reduces uteroplacental perfusion, restricting fetal growth and reducing renal blood flow, which leads to oligohydramnios. Acute intrapartum hypoxia results in decompensation of uteroplacental function, decreasing fetal blood oxygen levels. The redistribution of systemic fetal blood flow directs blood toward critical organs, such as the heart, brain, and adrenal glands. Persistent hypoxia leads to increased anaerobic glycolysis and metabolic acidosis, causing progressive damage to vital fetal organs, particularly the brain and heart. If medical intervention is delayed, severe and permanent outcomes such as hypoxic-ischemic encephalopathy or intrauterine fetal death may occur. Severe hypoxia may also deepen fetal respiratory efforts, leading to aspiration of amniotic fluid and subsequent neonatal aspiration pneumonia.
Clinical Manifestations and Diagnosis
Acute Fetal Distress
Acute fetal distress predominantly occurs during labor and is often associated with umbilical cord abnormalities, placental abruption, hypertonic uterine contractions, prolonged labor, or maternal shock.
Abnormal Intrapartum Fetal Heart Rate (FHR)
Abnormal fetal heart rate patterns during labor are critical signs of acute fetal distress. Regular fetal heart rate monitoring or continuous electronic fetal monitoring (EFM) is essential during labor. The interpretation of EFM results follows the three-tier classification system. Category III tracings, characterized by absent baseline variability along with recurrent late decelerations, recurrent variable decelerations, or bradycardia (baseline FHR <110 bpm), indicate severe fetal hypoxia.
Meconium-Stained Amniotic Fluid
The fetus may expel meconium into the amniotic fluid. Although hypoxia is a possible trigger for meconium passage, gestational age is the primary determinant, with higher probabilities in late-term pregnancies. Certain high-risk conditions, such as intrahepatic cholestasis of pregnancy, also increase the likelihood of meconium passage. Meconium-stained amniotic fluid is observed in 10–20% of deliveries and is classified into three grades based on severity: Grade I (light green), Grade II (yellow-green and cloudy), and Grade III (thick and dark brown). Alone, meconium-stained amniotic fluid is insufficient to diagnose fetal distress; comprehensive evaluation, including fetal monitoring, is required. Continuous electronic FHR monitoring is recommended if meconium staining is noted. Normal FHR patterns indicate no special interventions are needed, while abnormal FHR patterns consistent with intrauterine hypoxia may lead to complications such as meconium aspiration syndrome (MAS), resulting in adverse fetal outcomes.
Abnormal Fetal Movements
Fetal movements become weaker and fewer, potentially disappearing altogether.
Umbilical Arterial Blood Gas Analysis
Post-delivery umbilical cord blood gas analysis may reveal acidemia if pH is <7.00, base excess is <-12.00 mmol/L, or lactate levels are ≥6.00 mmol/L.
Chronic Fetal Distress
Chronic fetal distress primarily occurs in late pregnancy and often persists or worsens during labor. Common causes include hypertensive disorders of pregnancy, chronic nephritis, and diabetes.
Reduced or Absent Fetal Movements
A significant reduction in fetal movements is an important sign of fetal hypoxia. Fetal heart activity often ceases within 24 hours of the cessation of movements. Normal fetal movement counts (≥10 times in 2 hours) suggest no significant concerns, while counts of <6 times in 2 hours raise suspicion for hypoxia.
Abnormal Antenatal Electronic FHR Monitoring
Abnormal non-stress test (NST) results may indicate potential fetal hypoxia.
Low Biophysical Profile (BPP) Scores
BPP scores of ≤4 suggest fetal hypoxia, while scores of 5–6 are suspicious for hypoxia.
Abnormal Doppler Blood Flow Studies
In small-for-gestational-age fetuses, elevated umbilical artery pulsatility indices suggest placental dysfunction. Absent or reversed end-diastolic flow in the umbilical artery, along with reversed a-wave flow in the ductus venosus, indicates a high risk of intrauterine fetal demise.
Management
Acute Fetal Distress
It is necessary to adopt decisive measures to alleviate fetal hypoxia and address the underlying cause.
General Management
Interventions may include correcting maternal hypotension, improving maternal oxygenation, modifying maternal positioning, halting the use of oxytocin, and suppressing uterine contractions. The underlying cause, such as umbilical cord prolapse, severe placental abruption, or uterine rupture, must be identified and managed accordingly. If these measures fail, emergency delivery may be required. For suspected fetal distress, comprehensive evaluation with continuous fetal heart rate monitoring and other diagnostic methods can help determine the presence of fetal hypoxia. Intrauterine resuscitation may be considered to improve the fetal condition.
Etiological Treatment
If excessive uterine contractions result from incoordinate uterine activity or inappropriate use of oxytocin, tocolytics such as terbutaline or other beta-agonists can be used to reduce uterine activity.
If signs of umbilical cord compression are detected in cases of oligohydramnios, amnioinfusion via abdominal access may be performed, provided conditions permit.
Expedited Delivery
Decisions regarding the mode of delivery should be based on the stage of labor, ensuring that preparations for neonatal resuscitation are in place.
If Category III fetal heart rate tracings are observed and the cervix is not fully dilated or vaginal delivery is not anticipated in the short term, cesarean delivery is recommended immediately.
If the cervix is fully dilated, the pelvic dimensions are normal, and the fetal head's biparietal diameter has descended below the ischial spines, vaginal operative delivery should be performed as soon as possible once fetal distress is confirmed.
Regardless of whether delivery occurs vaginally or via cesarean section, preparations for neonatal resuscitation are crucial. In cases of thick meconium-stained amniotic fluid, the upper airway should be cleared immediately after the fetal head is delivered. If the newborn exhibits signs of reduced vitality, endotracheal intubation followed by airway suctioning is performed prior to initiating positive pressure ventilation. Following delivery, an umbilical arterial blood sample should be collected for blood gas analysis to assess fetal oxygenation and acid-base balance.
Chronic Fetal Distress
Management decisions for chronic fetal distress depend on the characteristics and severity of the pregnancy-related complications, as well as the gestational age, fetal maturity, and degree of hypoxia.
General Management
For cases where decreased fetal movement is reported, thorough evaluation of maternal and fetal conditions is warranted, including non-stress testing (NST) and/or fetal biophysical profile (BPP) scoring. Lateral positioning may improve placental perfusion. Treatment of maternal complications or comorbidities should be undertaken actively, and fetal monitoring should be intensified with close attention to changes in fetal movements.
Conservative Management
For pregnancies where the gestational age is early and the likelihood of fetal survival after delivery is low, conservative treatment may be adopted to prolong gestation while promoting fetal lung maturity. The potential risk of intrauterine fetal demise during conservative management should be clearly explained to the patient.
Delivery
For pregnancies near term or with a mature fetus, where decreased fetal movements, abnormal electronic fetal monitoring, or a fetal biophysical profile score of ≤4 are observed, cesarean delivery is recommended to terminate the pregnancy.