I. Can a fetus develop fluid retention too? What is it?
Fetal hydrothorax (FHT) is an excessive accumulation of fluid in the pleural cavity (the potential space between the dirty layer and the wall pleura).
Causes: The pathogenesis of fetal hydrothorax differs from that of adults, and the degree of damage to the fetus varies depending on the cause, the early and late gestational weeks at which the fluid accumulation occurs, the volume of fluid accumulation, and the rate of progression. Although detailed ultrasonography and karyotype analysis may clarify some of the causes of secondary fetal pleural effusion, most of the etiology remains unclear, even at autopsy.
Simply put, fetuses can also develop pleural effusion, but what causes it is indeed more complicated!
Second, how to distinguish fetal pleural effusion ah?
Fetal pleural effusion can occur unilaterally or bilaterally in the chest cavity, and is divided into primary pleural effusion due to celiac disease and secondary pleural effusion due to systemic fluid retention (often associated with immune or non-immune edema), while the secondary factors of fetal pleural effusion are much higher than the proportion of neonates.
Primary pleural effusion The incidence of primary fetal pleural effusion in live births is about 1/10,000. the most common cause is congenital celiac disease, with an incidence of l/10,000 to 1/15,000; it is mostly unilateral and rare bilaterally. It is caused by impaired lymphatic vessel formation or its integrity, but its exact cause is not fully understood. Anatomical causes have been confirmed only in a few fetuses: mainly thoracic duct developmental abnormalities such as atresia, fistula, and agenesis; others such as congenital lymphatic duct dilatation or dysplasia, congenital lymphatic duct fistula, etc.
2.Secondary pleural effusion The incidence of secondary fetal pleural effusion in live births is about 1/1500. mostly one of the symptoms of fetal edema caused by immune or some non-immune diseases.
(1) Immune disorders are mainly Rh, ABO maternal and child blood group discordance, thalassemia, etc. Antibodies in the mother’s serum react with fetal red blood cells in an antigen-antibody immune reaction, resulting in fetal hemolysis, anemia, cardiac failure, and then fetal edema syndrome, which manifests as fetal pleural effusion.
(2) Non-immune diseases occur for a wide range of etiologies, including.
(1) congenital cystic adenomatoid malformation of the lung and pulmonary isolation disease can cause fetal pleural effusion, but clinically such pleural effusion is not serious;
(2) Fetal chromosomal abnormalities in combination with other malformations: trisomy 21, Turner’s syndrome, Noonan syndrome, Down syndrome, trisomy 10, trisomy 18 and trisomy 13, etc;
(3) Thyroid factors: In fetal congenital hypothyroidism, due to the lack of thyroxine, the stimulation of adrenergic receptors in the lymphatic system is reduced, and the lymphatic fluid flow is slow and sludges and leaks in the thoracic cavity and interstitial space, forming pleural effusion;
④ Heart malformation: fetus with congenital heart disease or cardiac arrhythmia resulting in heart failure, body circulation stasis or even fetal generalized edema, may show pleural effusion;
⑤ Intrauterine infection: rubella virus, cytomegalovirus, herpes simplex virus, human microvirus B19, Toxoplasma gondii, Chlamydia intrauterine infection can cause fetal pleural effusion. Among them, human microvirus B19 can specifically bind to red blood cells and inhibit fetal erythropoiesis, resulting in severe fetal anemia, pleural effusion, ascites and other symptoms;
(6) Other diseases such as blood disorders, gastrointestinal disorders, metabolic disorders, twin-birth transfusion syndrome, abnormalities of the placenta and umbilical cord can also be the cause of non-immune fetal pleural effusion;
(7) Abnormal fetal cardiac function, such as supraventricular tachycardia, complete conduction block, etc.
How to diagnose the fetal pleural effusion in the mother’s tummy?
1. Prenatal ultrasound: Prenatal diagnosis of FHT mainly relies on ultrasound examination, which shows an echogenic zone between the heart and lungs in the fetal chest cavity. Unilateral massive pleural effusion may have an occupying effect, with the heart and mediastinum displaced and the lungs often compressed and small. Pleural effusion secondary to fetal edema is mostly bilateral, and bilateral pleural effusion may appear as a “bat wing” sonogram.
Prenatal MR: MR can clearly show the volume of the lung, the degree of pulmonary dysplasia and the ratio of the lung to the chest cavity in the case of pleural effusion, which is helpful for the clinician to evaluate the prognosis of the fetus. For FHT in the T1 phase of MR examination, it shows a low signal, while in the T2 phase it shows a high signal, which can be diagnosed and analyzed according to the correlation between the location and the surrounding adjacent organs.
IV. Besides this pleural effusion, are there any other possible problems with the fetus?
Comorbidities
1. congenital structural abnormalities of the thoracic cavity. 20-25% of fetal pleural effusions are combined with other structural malformations, and the percentage of secondary pleural effusions can be as high as 40%. For example, congenital diaphragmatic hernia has a 20% probability of complicating fetal pleural effusion, so it needs to be differentiated from it. Other diseases of the thoracic cavity, such as cystic adenoma and pulmonary isolation, may present with fetal edema in the form of FHT or ascites when compression symptoms occur, but the percentage is small.
2. Congenital heart disease. About 5% of prenatally diagnosed fetal pleural effusions have congenital heart disease. It needs to be identified. However, fetal pleural effusion causes mediastinal shift and heart compression due to fluid accumulation, which makes fetal heart ultrasound examination seem difficult, so it needs to be treated with caution.
3. Excessive amniotic fluid. About 60% of fetal pleural effusion will be combined with excessive amniotic fluid. This is related to the mediastinal shift that affects fetal swallowing during pleural effusion and the abnormal amniotic fluid secretion due to fetal lung compression.
Chromosomal abnormalities: 6-17% of fetuses with pleural effusion have chromosomal abnormalities such as trisomy 21 and Turner’s syndrome, which require karyotype analysis of fetal chromosomes.
V. Is there any risk for this fetus to have this effusion?
There are definitely risks, including
1. Persistent fetal pleural effusion may cause compression of the developing lung and decrease the fluid in the lung, resulting in a decrease in the number of alveolar cells and small bronchioles, which may lead to lung dysplasia in severe cases.
2. A large amount of pleural effusion can displace the mediastinum, compress the inferior vena cava and heart, and cause fetal heart failure. Many problems require effective prenatal intervention. Pleural effusion combined with excessive amniotic fluid may be due to the large amount of pleural effusion compressing the esophagus and affecting the fetus to swallow amniotic fluid. Therefore, interventions should be performed for massive fetal pleural effusion to relieve fetal symptoms and promote fetal lung development through non-invasive or invasive treatment.
3. Various risks associated with comorbidities.
Six, it sounds like it is quite scary, so how can we help the child when it is in the mother’s tummy?
In fact, when fetal pleural effusion is found, it is more important to find out its cause in time to deal with it symptomatically.
For simple pleural effusion, because there is a possibility of natural regression, a period of observation and follow-up is routinely performed. For unilateral pleural effusion with small amount of fluid and no signs of tense pleural effusion, only observation and follow-up are needed.
In contrast, termination of pregnancy may be an option for fetuses with early pleural effusion under 24 weeks and those with life-threatening complications, chromosomal abnormalities and other risks.
For fetal pleural effusion at gestational age greater than 32 weeks, thoracentesis given after birth with established venous access to ensure blood volume in the body circulation and close observation may be the best option.
If the diagnosis of fetal congenital celiac disease is clear, a mother’s formula diet with an oral diet containing low-fat and long-chain triglyceride-free foods to stop the production and reflux of celiac disease may limit the continued development of fetal pleural effusion. After birth, the same formula should be given to the newborn.
For pleural effusion due to fetal supraventricular tachycardia, the mother’s oral administration of digoxin and flecainide may relieve fetal symptoms. In contrast, for complete fetal conduction block, the mother’s oral dexamethasone or prednisone can be used for therapeutic purposes.
For moderate to severe fetal anemia and fetal pleural effusion due to cytomegalovirus B19 infection, maternal and child blood group incompatibility, intrauterine intra-umbilical blood transfusion can achieve treatment. Cytomegalovirus-negative O-concentrated red blood cells are selected, and the amount of blood input depends on the fetal HCT and fetal weight, and can be transfused several times to relieve symptoms depending on the condition.
In addition, prenatal surgical treatment of the fetus is considered.
In fetuses with FHT less than 32 weeks, there are 3 options offered: thoracentesis, thoracic-amniotic shunt, and thoracic-maternal subcutaneous drainage. However, it should be noted that all of these operations carry the risk of infection, bleeding, premature rupture of membranes, preterm delivery, and injury to the fetus.
7. Is it necessary to perform a cesarean section?
Fetal pleural effusion is not an indication for cesarean section, and stable fetuses can wait until full term for vaginal delivery. If the fetus has received intrauterine treatment before 36 weeks of gestation and is in remission, termination can be considered between 37 and 38 weeks of gestation, but it must be performed in a medical institution where neonatal asphyxia resuscitation can be performed quickly, such as receiving prenatal
If the fetus is delivered with a thoracic-amniotic shunt, the drainage tube must be clamped or removed to avoid neonatal pneumothorax. If the fetal pleural effusion is still progressively increasing after intrauterine treatment, termination of pregnancy at 35-36 weeks of gestation may be considered and neonatal thoracentesis may be performed after delivery to improve the survival rate of the newborn.
What will happen to the baby born with fetal pleural effusion?
Overall, the prognosis of fetal pleural effusion is worse than that of infant pleural effusion.
Self-healing is possible: comprehensive literature reports that 5-22% of fetal pleural effusions can be self-absorbed.
The survival rate of primary fetal pleural effusion without hypertonic manifestations such as mediastinal shift/diaphragmatic exstrophy is greater than 90%. In contrast, the literature reports 52% for bilateral pleural effusions.
The prognosis is poor and the perinatal mortality rate is increased if the following factors are present: (i) simple pleural effusion progressing to an edematous fetus with a mortality rate of more than 50%; (ii) pulmonary dysplasia; (iii) prematurity; (iv) presence of structural cardiac malformations; (v) failure to expand the fetal lung on ultrasound after thoracentesis or expansion less than the normal range for the corresponding gestational week, indicating irreversible damage to the fetal lung or the presence of pulmonary dysplasia.
A large amount of effusion (effusion covering more than 1/2 of the thoracic area), bilateral effusion, recurrent effusion, occurrence early in pregnancy, and fetal edema are the main factors of poor prognosis. The earlier the age of onset and the larger the volume of effusion, the more likely it is to develop into tension pleural effusion, edema, and neonatal death secondary to pulmonary insufficiency.
However, with the development of prenatal diagnostic techniques, timely neonatal articulation management-neonatal resuscitation techniques, and pediatric thoracic surgery techniques, the survival rate is incessantly improving.