Fetal intrauterine distress

　　Fetal intrauterine distress is a syndrome of incomplete respiratory and circulatory function caused by fetal oxygen deficiency. It can be divided into acute, chronic, and prenatal or interlaboral fetal intrauterine distress. There are many causes of fetal intrauterine distress.

　　I. Acute distress

　　1. Pathogenesis

　　Through the uteroplacental blood flow exchange, oxygen and nutrients reach the fetus, maintaining fetal growth and development. The fetus can store energy, but cannot store oxygen. During uterine contractions, the pressure in the uterine muscle layer increases beyond that of the amniotic cavity and uterine vessels. At the peak of uterine contractions, it can cause temporary interruption of blood flow in the villous spaces, causing the fetus to receive insufficient oxygen and nutrients. In the presence of sufficient oxygen, through the tricarboxylic acid cycle, glucose decomposition, and the mitochondria of the cell produce enough 38 ATP. However, during oxygen deficiency, through anaerobic glycolysis, each glucose molecule produces only 1/19 of the energy of aerobic metabolism, leading to the accumulation of a large amount of lactic acid, causing metabolic acidosis with a decrease in pH, causing the inactivation of enzymes necessary for the metabolic function of various cells, leading to cell death and leaving permanent brain damage.

　　2. Common causes

　　(1) Fetus at high risk of pregnancy

　　The placenta has low function, and there are no obvious signs of fetal distress before labor, but the stress of uterine contractions during labor can cause the fetus to show acute distress;

　　(2) Oxygen deficiency during labor

　　The fetus does not show signs of oxygen deficiency before labor, which may be due to a prolonged labor, exhaustion of the mother with dehydration and hypotension, leading to insufficient placental perfusion and causing fetal oxygen deficiency; or due to frequent and strong natural uterine contractions, or the use of oxytocin intravenous infusion causing frequent and strong uterine contractions, even rigid contractions, which keep the fetus mostly in a state of insufficient oxygen supply, or even oxygen cessation, leading to fetal distress;

　　(3) Overly expanded uterus

　　Excessive muscle tension increases the external resistance of the uterine muscle wall vessels, such as in cases of multiple pregnancies and excessive amniotic fluid;

　　(4) Umbilical cord factors

　　1) Umbilical cord prolapse is common in cases of臀位胎膜早破、excessive amniotic fluid, and multiple pregnancies, and if the umbilical cord is compressed after prolapse, it can lead to a decrease or even cessation of fetal blood supply;

　　2) Umbilical cord entanglement includes umbilical cord around the neck, body, etc;

　　3) The incidence of umbilical cord knot is 0.4% to 1.1%, generally without harm to the fetus, but during the delivery process, the tightening of the umbilical cord causes the umbilical blood vessels to be blocked, leading to intrauterine fetal death;

　　4) The cause of umbilical cord torsion is not yet clear, the umbilical vessels twist along their longitudinal axis for 9 to 11 weeks, causing vascular occlusion

　　5) Short umbilical cord.

　　(5) Fetal heart dysfunction

　　The normal heart function of the fetus is one of the important keys to ensure the circulation of fetal blood circulation and avoid hypoxia. When the fetus has serious congenital cardiovascular disease, hypotension and heart failure caused by drugs and hemorrhage, or when the fetal skull is compressed for a long time and intracranial hemorrhage occurs concurrently, it can affect the function of the cardiovascular center, and fetal distress will occur in these cases.

　　II. Chronic fetal distress in utero

　　High-risk pregnancy, such as pregnancy-induced hypertension syndrome, chronic hypertension, nephritis, diabetes, heart disease, asthma, severe anemia, post-term pregnancy, gestational diabetes, gestational heart disease, etc., or due to vascular lesions causing a decrease in uterine blood flow, or due to placental degeneration, or due to low blood oxygen concentration, causing the fetus to receive insufficient oxygen supply, leading to growth retardation of the fetus; polycythemia; decreased fetal movement; even severe fetal distress, leading to fetal death. It may also be due to fetal malformation, intrauterine infection, incompatibility of maternal and fetal blood types, and other inherent fetal diseases.

　　Fetal distress in utero can lead to a series of complications such as brain edema, brain cell necrosis, brain hemorrhage, and others due to brain ischemia and hypoxia in utero. The following are some common complications列举如下：

　　1. Fetal perinatal death:Perinatal period refers to the period from 28 weeks of pregnancy to 7 days after delivery. The death of the fetus after entering the perinatal period is called perinatal death.

　　2. Neonatal nervous system sequelae:The sequelae can be generally divided into intellectual disability, language disorder, and motor disorder. Intellectual disability: poor thinking and reaction ability, even the possibility of idiocy, language disorder, speaking not fluently or aphasia, motor disorder, gait unsteady or limb paralysis.

　　3. Neonatal brain ischemia and hypoxia syndrome.

　　4. Brain edema:Brain edema is a pathological phenomenon caused by an increase in intracerebral water content, leading to an increase in brain volume, which is the brain tissue's response to various pathogenic factors. It can cause intracranial hypertension, damage brain tissue, and is commonly seen in clinical practice. The main manifestations of brain edema are signs of intracranial hypertension.

　　5. Brain cell necrosis:The necrosis of brain cells generally leads to a decrease in memory, motor disorders, and neurological disorders.

　　6. Intracerebral hemorrhage:The degree of headache, nausea and vomiting, unclear speech, urinary incontinence, limb movement disorder, and consciousness disturbance is related to the location, amount, speed of bleeding, size of hematoma, and general condition of the patient. Small bleeding in non-functional areas may only manifest as headache and mild neurological dysfunction, while large bleeding, deep brain hemorrhage, thalamic hemorrhage, or brainstem hemorrhage can lead to rapid coma and even death within a few hours or days.

　　Fetal distress in utero usually occurs during labor, but it can also occur in the later stages of pregnancy. Fetal distress that occurs during labor can generally be treated promptly by medical personnel. The common symptoms are as follows:

　　(One) Fetal heart rate change: It is the first symptom of fetal distress. The fetal heart rate first becomes faster, but it is strong and regular, then it becomes slower, weak, and irregular. Therefore, we should be vigilant when we find the fetal heart rate to be faster. When uterine contractions occur, due to the temporary interference with the uteroplacental blood circulation, the fetal heart rate becomes slower, but it quickly returns to normal after the uterine contractions stop. Therefore, the fetal heart rate between two uterine contractions should be used as a standard. The normal fetal heart rate is between 110 to 160 beats per minute. When fetal hypoxemia occurs, it can stimulate the fetal adrenal glands to produce catecholamines, which are manifested as an increased heart rate, fetal heart rate >160 beats per minute, and persistently above 180 beats per minute, indicating that the fetus is experiencing intrauterine distress. If acidosis continues to worsen, myocardial contractility decreases, and the fetal heart rate slows down, it can be below 110 beats per minute.

　　(Two) Amniotic fluid meconium contamination: The characteristics and composition of amniotic fluid change continuously with the increase of gestational weeks. At term pregnancy, amniotic fluid is a slightly turbid, opaque liquid containing substances such as fetal fat, epithelial cells, and lanugo. In the case of hypoxia, the vagus nerve is excited, causing increased peristalsis and relaxation of the anal sphincter muscle, resulting in the excretion of meconium. Once meconium contamination occurs, the amniotic fluid turns yellow-green, and it is divided into three degrees according to the degree of contamination: Ⅰ degree: light green; Ⅱ degree: yellow-green, turbid; Ⅲ degree: brown-yellow, thick.

　　(Three) Abnormal fetal movement: Fetal movement is an indirect method to monitor the integrity and functional state of the fetal central nervous system, but it is related to the pregnant woman's own cognitive ability. Normally, the fetal movement count per hour in the late pregnancy should be 3 to 5 times. Abnormally active fetal movement is a struggle phenomenon when the fetus is hypoxic, and with the worsening of hypoxia, fetal movement may decrease, even stop. In addition, due to the lack of a unified standard for the number of fetal movements, there is no clear boundary for frequent fetal movements, and pregnant women have certain difficulties in accurate counting. Single abnormal fetal movement cannot be used as a diagnostic criterion for fetal distress, but it should be taken seriously.

　　(Four) Fetal scalp blood pH value decline: The normal fetal scalp blood pH value is above 7.25. If the pH value is below 7.2, it indicates acidosis. However, this examination is invasive, the cervix must be dilated, the amniotic membrane must be ruptured, and it cannot be repeated repeatedly, and there is also a risk of infection, so its clinical application is limited.

　　Fetal distress in utero usually occurs during labor, but it can also occur in the later stages of pregnancy. Fetal distress that occurs during labor can generally be treated promptly by medical personnel. Fetal distress during pregnancy, if modern scientific technology can monitor the safety of the fetus, but it is impossible for pregnant women to be monitored at all times, so some abnormal conditions cannot be corrected, leading to tragedies. Early signs of fetal hypoxia may include some abnormalities. If we learn these self-monitoring methods, we can detect abnormalities in a timely manner and receive timely correction or treatment.

　　(1)胎动监测

　　(1) Fetal movement monitoring

　　Fetal movement is a good sign of fetal survival and also the most sensitive indicator of intrauterine hypoxia. Fetal movement counting is a simple method to monitor fetal intrauterine conditions during pregnancy and can be used for a long time. Generally, pregnant women can feel fetal movement around 20 weeks. After 28 weeks, pregnant women should learn to count fetal movements: if the fetus moves continuously, count it as one fetal movement, and count it again if it moves after an interval, and so on. Pregnant women should take a left lateral lying position for one hour in the morning, afternoon, and evening, and record the number of fetal movements during these three hours according to their subjective feelings. Multiply the total number of fetal movements in the morning, afternoon, and evening by 4 to get the 12-hour fetal movement count. A 12-hour fetal movement count of ≥30 is normal. If the 12-hour

　　(2) Fetal heart monitoring

　　Husbands can learn to directly listen to the fetal heart rate using a stethoscope under the guidance of a doctor. The normal fetal heart rate should be 120-160 beats per minute. The fetal heart rate should increase by more than 10 beats per minute during fetal movement, or the fetal heart rate should be irregular. If the fetal heart rate slows down or exceeds this number, it indicates fetal hypoxia and it is necessary to go to the hospital for treatment promptly.

　　(3) Regular prenatal examinations

　　What laboratory tests should be done for fetal intrauterine distress

　　Because there are differences in detection methods and the judgment of results, and the level of hospitals and doctors has a certain impact on the results of the detection, the diagnosis of fetal distress lacks a unified standard. The judgment results have the problems of false negatives and false positives. Moreover, over-diagnosis can lead to overly aggressive treatment and unnecessary intervention, and late diagnosis can delay treatment and lead to neonatal complications.

　　Diagnostic criteria

　　(1) Abnormal fetal heart rate

　　(2) Abnormal fetal heart rate monitoring

　　During labor, electronic fetal heart rate monitoring can detect fetal intrauterine hypoxia in a timely manner. When fetal hypoxia occurs, fetal heart rate monitoring can show: abnormal fetal heart rate baseline, such as tachycardia baseline exceeding beats per minute or bradycardia baseline below beats per minute (China's standard is below beats per minute); reduced variability of the fetal heart rate baseline.

　　(3) Decreased pH value

　　(4) Amniotic fluid meconium contamination

     Dietary taboos for patients with intrauterine fetal distress

　　The following are the Western medical treatment measures for fetal intrauterine distress:

　　1. General Treatment

　　(1) If intrauterine distress is found, the lateral position can be changed. During pregnancy, the enlarged uterus rotates to the right, compressing the abdominal aorta, inferior vena cava, and pelvic vessels, causing supine hypotensive syndrome, affecting uterine blood perfusion, and leading to fetal hypoxia. Lateral or semi-lateral position is a simple way to improve fetal blood supply.

　　(2) Oxygen should be inhaled immediately for the pregnant woman, and high-flow pure oxygen can quickly improve the hypoxia condition of the mother and fetus. Generally, oxygen therapy is required with a mask, with a flow rate of 10L per minute, but long-term oxygen therapy may cause vasoconstriction of the maternal and fetal vessels, reduce placental blood flow, and reduce fetal blood supply, thereby aggravating fetal hypoxia. Therefore, intermittent oxygen therapy is advocated, with oxygen therapy for 30 minutes and stopping for 10 minutes, and repeated for several times. Oxygen therapy can be continued during the second stage of labor due to the strong intermittent uterine contractions.

　　2. Drug Treatment

　　(1) Intravenous injection of 50% glucose and vitamin C to enhance the fetus's tolerance to hypoxia, prevent increased capillary permeability and fragility, and reduce the possibility of intracranial hemorrhage. Before delivery, amniocentesis can be performed on the fetal scalp to take blood for pH measurement. If pH≤7.25, it indicates fetal distress. According to fetal heart rate and labor progress, take positive measures based on different causes and labor progress.

　　(2) Correct acidosis, due to labor pain, tension, or prolonged physical exertion, maternal and fetal acidosis may occur. At this time, 5% sodium bicarbonate can effectively correct maternal acidosis, and amniotic fluid infusion can also be performed.

　　(3) Adjust the intensity of uterine contractions, reduce the speed of the entry of uterotonics into the mother's body. For tetanic uterine contractions, uterine contraction inhibitors such as magnesium sulfate can be used, and anesthetics can be used if necessary. For strong uterine contractions, intravenous infusion of β-receptor stimulant drugs such as Oxytrol can be used. If abnormal fetal heart rate occurs during the infusion of oxytocin, the infusion rate should be slowed down or stopped.

　　3. Surgical Treatment

　　It may be necessary to terminate the pregnancy if necessary, such as if the above treatment is not effective, the pregnancy should be terminated quickly. A comprehensive estimate should be made in a short period of time whether it can be delivered vaginally based on the opening of the cervix, the condition of the cervix, the size of the fetus, and the descent of the presenting part, or whether labor assistance is needed, and cesarean section should be performed if necessary.