Some doctors recommend complete bed-rest for the mother coupled with massive intakes of protein as a therapy to try to counteract the syndrome. Research completed shows these nutritional supplements do work. Diet supplementation was associated with lower overall incidence of TTTS (20/52 versus 8/51, P = 0.02) and with lower prevalence of TTTS at delivery (18/52 versus 6/51, P = 0.012) when compared with no supplementation. Nutritional intervention also significantly prolonged the time between the diagnosis of TTTS and delivery (9.4 ± 3.7 weeks versus 4.6 ± 6.5 weeks; P = 0.014). The earlier nutritional regimen was introduced, the lesser chance of detecting TTTS ( P = 0.001). Although not statistically significant, dietary intervention was also associated with lower Quintero stage, fewer invasive treatments, and lower twin birth weight discordance. Diet supplementation appears to counter maternal metabolic abnormalities in monochorionic twin pregnancies and improve perinatal outcomes in TTTS when combined with the standard therapeutic options. Nutritional therapy appears to be most effective in mitigating cases that are caught in Quintero Stage I, little effect has been observed in those that are beyond Stage I.

This procedure involves the tearing of the dividing membrane between fetuses such that the amniotic fluid of both twins mixes under the assumption that pressure is different in either amniotic sac and that its equilibration will ameliorate progression of the disease. It has not been proven that pressures are different in either amniotic sac. Use of this procedure can preclude use of other procedures as well as make difficult the monitoring of disease progression. In addition, tearing the dividing membrane has contributed to cord entanglement and demise of fetuses through physical complications.

The treatment depends on the cause.

Severely anemic fetuses, including those with Rh disease and alpha thalassemia major, can be treated with blood transfusions while still in the womb. This treatment increases the chance that the fetus will survive until birth.

If ongoing and rapid haemorrhage is occurring then immediate delivery of the foetus may be indicated if the fetus is sufficiently developed. If the haemorrhage has already occurred and now stopped, an inutero transfusion of red cells to the foetus may be recommended.

The non-immune form of hydrops fetalis has many causes including:

- Iron deficiency anemia

- Paroxysmal supraventricular tachycardia resulting in heart failure

- Deficiency of the enzyme beta-glucuronidase. This enzyme deficiency is the cause of the lysosomal storage disease called mucopolysaccharidosis type VII.

- Congenital disorders of glycosylation

- Parvovirus B19 (fifth disease) infection of the pregnant woman

- Cytomegalovirus in mother

- Congenital pulmonary airway malformation

- Maternal syphilis and maternal diabetes mellitus

- Alpha-thalassemia can also cause hydrops fetalis when all four of the genetic loci for α globin are deleted or affected by mutation. This is termed Hb Barts (consists of y-4 tetramers).

- Uncommonly, Niemann-Pick disease Type C (NPC) and Gaucher disease type 2 can present with hydrops fetalis.

- Turner Syndrome

- Tumors, the most common type of fetal tumor being teratoma, particularly a sacrococcygeal teratoma.

- Twin-twin transfusion syndrome in pregnancies in which twins share a single placenta (hydrops affects the recipient twin)

- Maternal hyperthyroidism

- Fetal cardiac defects and skeletal defects

- Noonan syndrome

- Mirror syndrome, in which fetal and placental hydrops develops in association with maternal preeclampsia, edema and hypertension

Mirror syndrome or triple oedema or Ballantyne syndrome is a rare disorder affecting pregnant women. It describes the unusual association of fetal

and placental hydrops with maternal preeclampsia.

The name "mirror syndrome" refers to the similarity between maternal oedema and fetal hydrops. It was first described in 1892 by John William Ballantyne.

The etiology may be any of the variety of obstetric problems that range from immunological disorders, including Rh-isoimmunization, to fetal infections, metabolic disorders, and fetal malformations. Ballantyne syndrome can result from the maternal reaction to a fetus that has hemoglobin Bart's disease due to inherited double thalassemia trait from both parents.

Causes of increased foetal-maternal haemorrhage are seen as a result of trauma, placental abruption or may be spontaneous with no cause found.

Up to 30 mL of foetal-maternal transfusion may take place with no significant signs or symptoms seen in either mother or foetus. Loss in excess of this may result in significant morbidity and mortality to the fetus. Foetal-maternal haemorrhage is one cause of intrauterine death (IUD).

Fetal disease refers to disorders originating in utero.

Examples include hydrops fetalis and chorioamnionitis

Turning the baby, technically known as external cephalic version (ECV), is when the baby is turned by gently pressing the mother’s abdomen to push the baby from a bottom first position, to a head first position. ECV does not always work, but it does improve the mother’s chances of giving birth to her baby vaginally and avoiding a cesarean section. The World Health Organisation recommends that women should have a planned cesarean section only if an ECV has been tried and did not work.

Women who have an ECV when they are 36–40 weeks pregnant are more likely to have a vaginal delivery and less likely to have a cesarean section than those who do not have an ECV. Turning the baby before this time makes a head first birth more likely but ECV before the due date can increase the risk of early or premature birth which can cause problems to the baby.

There are treatments that can be used which might affect the success of an ECV. Drugs called beta-stimulant tocolytics help the woman’s muscles to relax so that the pressure during the ECV does not have to be so great. Giving the woman these drugs before the ECV improves the chances of her having a vaginal delivery because the baby is more likely to turn and stay head down. Other treatments such as using sound, pain relief drugs such as epidural, increasing the fluid around the baby and increasing the amount of fluids to the woman before the ECV could all effect its success but there is not enough research to make this clear.

Turning techniques mothers can do at home are referred to Spontaneous Cephalic Version (SCV), this is when the baby can turn without any medical assistance. Some of these techniques include; a knee to chest position, the breech tilt and moxibustion, these can be performed after the mother is 34 weeks pregnant. Although there is not a lot of evidence to support how well these techniques work, it has worked for some mothers.

In twin pregnancies, it is very common for one or both babies to be in the breech position. Most often twin babies do not have the chance to turn around because they are born prematurely. If both babies are in the breech position and the mother has gone into labour early, a cesarean section may be the best option. About 30-40% of twin pregnancies result in only one baby being in the breech position. If this is the case, the babies can be born vaginally. After the first baby who is not in the breech position is delivered, the baby who is presented in the breech position may turn itself around, if this does not happen another procedure may performed called the breech extraction. The breech extraction is the procedure that involves the obstetrician grabbing the second twin's feet and pulling him/her into the birth canal. This will help with delivering the second twin vaginally. However, if the second twin is larger than the first, complications with delivering the second twin vaginally may arise and a cesarean section should be performed. At times, the first twin (the twin closest to the birth canal) can be in the breech position with the second twin being in the cephalic position (vertical). When this occurs, risks of complications are higher than normal. In particular, a serious complication known as Locked twins. This is when both babies interlock their chins during labour. When this happens a cesarean section should be performed immediately.

In 2003, the incidence of Rh(D) sensitization in the United States was 6.8 per 1000 live births; 0.27% of women with an Rh incompatible fetus experience alloimmunization.

Neonatal hypoglycemia is a transient or temporary condition of decreased blood sugar or hypoglycemia in a neonate.

Those infants that have an increased risk of developing hypoglycemia shortly after birth are:

- preterm

- asphyxia

- cold stress

- congestive heart failure

- sepsis

- Rh disease

- discordant twin

- erythroblastosis fetalis

- polycythemia

- microphallus or midline defect

- respiratory disease

- maternal glucose IV

- maternal epidural

- postmaturity

- hyperinssulinnemia

- endocrine disorders

- inborn errors of metabolism

- diabetic mother

- maternal toxemia

- intrapartum fever

After birth, treatment depends on the severity of the condition, but could include temperature stabilization and monitoring, phototherapy, transfusion with compatible packed red blood, exchange transfusion with a blood type compatible with both the infant and the mother, sodium bicarbonate for correction of acidosis and/or assisted ventilation.

- Phototherapy - Phototherapy is used for cord bilirubin of 3 or higher. Some doctors use it at lower levels while awaiting lab results.

- IVIG - IVIG has been used to successfully treat many cases of HDN. It has been used not only on anti-D, but on anti-E as well. IVIG can be used to reduce the need for exchange transfusion and to shorten the length of phototherapy. The AAP recommends "In isoimmune hemolytic disease, administration of intravenousγ-globulin (0.5-1 g/kg over 2 hours) is recommended if the TSB is rising despite intensive phototherapy or the TSB level is within 2 to 3 mg/dL (34-51 μmol/L) of the exchange level . If necessary, this dose can be repeated in 12 hours (evidence quality B: benefits exceed harms). Intravenous γ-globulin has been shown to reduce the need for exchange transfusions in Rh and ABO hemolytic disease."

- Exchange transfusion - Exchange transfusion is used when bilirubin reaches either the high or medium risk lines on the nonogram provided by the American Academy of Pediatrics (Figure 4). Cord bilirubin >4 is also indicative of the need for exchange transfusion.

Rh disease (also known as rhesus isoimmunisation, Rh (D) disease, rhesus incompatibility, rhesus disease, RhD hemolytic disease of the newborn, rhesus D hemolytic disease of the newborn or RhD HDN) is a type of hemolytic disease of the newborn (HDN). The disease ranges from mild to severe, and typically occurs only in some second or subsequent pregnancies of Rh negative women where the fetus's father is Rh positive, leading to a Rh+ pregnancy. During birth, the mother may be exposed to the infant's blood, and this causes the development of antibodies, which may affect the health of subsequent Rh+ pregnancies. In mild cases, the fetus may have mild anaemia with reticulocytosis. In moderate or severe cases the fetus may have a more marked anaemia and erythroblastosis fetalis (hemolytic disease of the newborn). When the disease is very severe it may cause hydrops fetalis or stillbirth.

Rh disease is generally preventable by treating the mother during pregnancy or soon after delivery with an intramuscular injection of anti-RhD immunoglobulin (Rho(D) immune globulin). The RhD protein is coded by the RHD gene.

Suggestions have been made that women of child bearing age or young girls should not be given a transfusion with Kell positive blood. Donated blood is not currently screened (in the U.S.A.) for the Kell blood group antigens as it is not considered cost effective at this time.

It has been hypothesized that IgG anti-Kell antibody injections would prevent sensitization to RBC surface Kell antigens in a similar way that IgG anti-D antibodies (Rho(D) Immune Globulin) are used to prevent Rh disease, but the methods for IgG anti-Kell antibodies have not been developed at the present time.

Hemolytic disease of the newborn (anti-Kell) is the second most common cause of severe hemolytic disease of the newborn (HDN) after Rh disease. Anti-Kell is becoming relatively more important as prevention of Rh disease is also becoming more effective.

Hemolytic disease of the newborn (anti-Kell) is caused by a mismatch between the Kell antigens of the mother and fetus. About 91% of the population are Kell negative and about 9% are Kell positive. A fraction of a percentage are homozygous for Kell. Therefore, about 4.5% of babies born to a Kell negative mother are Kell positive.

The disease results when maternal antibodies to Kell are transferred to the fetus across the placental barrier, breaching immune privilege. These antibodies can cause severe anemia by interfering with the early proliferation of red blood cells as well as causing alloimmune hemolysis. Very severe disease can occur as early as 20 weeks gestation. Hydrops fetalis can also occur early. The finding of anti-Kell antibodies in an antenatal screening blood test (indirect Coombs test) is an indication for early referral to a specialist service for assessment, management and treatment.

Most Rh disease can be prevented by treating the mother during pregnancy or promptly (within 72 hours) after childbirth. The mother has an intramuscular injection of anti-Rh antibodies (Rho(D) immune globulin). This is done so that the fetal rhesus D positive erythrocytes are destroyed before the immune system of the mother can discover them and become sensitized. This is passive immunity and the effect of the immunity will wear off after about 4 to 6 weeks (or longer depending on injected dose) as the anti-Rh antibodies gradually decline to zero in the maternal blood.

It is part of modern antenatal care to give all rhesus D negative pregnant women an anti-RhD IgG immunoglobulin injection at about 28 weeks gestation (with or without a booster at 34 weeks gestation). This reduces the effect of the vast majority of sensitizing events which mostly occur after 28 weeks gestation. Giving Anti-D to all Rhesus negative pregnant women can mean giving it to mothers who do not need it (because her baby is Rhesus negative or their blood did not mix). Many countries routinely give Anti-D to Rhesus D negative women in pregnancy. In other countries, stocks of Anti-D can run short or even run out. Before Anti-D is made routine in these countries, stocks should be readily available so that it is available for women who need Anti-D in an emergency situation.

A recent review found research into giving Anti-D to all Rhesus D negative pregnant women is of low quality. However the research did suggest that the risk of the mother producing antibodies to attack Rhesus D positive fetal cells was lower in mothers who had the Anti-D in pregnancy. There were also fewer mothers with a positive kleihauer test (which shows if the mother’s and unborn baby’s blood has mixed).

Anti-RhD immunoglobulin is also given to non-sensitized rhesus negative women immediately (within 72 hours—the sooner the better) after potentially sensitizing events that occur earlier in pregnancy.

The discovery of cell-free DNA in the maternal plasma has allowed for the non-invasive determination of the fetal RHD genotype. In May 2017, the Society for Obstetrics and Gynecology of Canada is now recommending that the optimal management of the D-negative pregnant woman is based on the prediction of the fetal D-blood group by cell-free DNA in maternal plasma with targeted antenatal anti-D prophylaxis. This provides the optimal care for D-negative pregnant women and has been adopted as the standard approach in a growing number of countries around the world. It is no longer considered appropriate to treat all D-negative pregnant women with human plasma derivatives when there are no benefits to her or to the fetus in a substantial percentage of cases.

A potential complication that may occur in children that suffer acute anemia with a hemoglobin count below 5.5 g/dl is silent stroke A silent stroke is a type of stroke that does not have any outward symptoms (asymptomatic), and the patient is typically unaware they have suffered a stroke. Despite not causing identifiable symptoms a silent stroke still causes damage to the brain, and places the patient at increased risk for both transient ischemic attack and major stroke in the future.

Individuals heterozygous for the Hb Lepore request no particular treatment. There is no anemia or, if there is, it is very mild.

Hemoglobin Barts, abbreviated Hb Barts, is an abnormal type of hemoglobin that consists of four gamma globins. It is moderately insoluble, and therefore accumulates in the red blood cells. It has an extremely high affinity for oxygen, resulting in almost no oxygen delivery to the tissues. As an embryo develops, it begins to produce alpha-globins at weeks 5-6 of development. When both HBA1 and HBA2, the two genes that code for alpha globins, are non-functional, only gamma globins are produced. These gamma globins bind to form hemoglobin Barts. It is produced in the disease alpha-thalassemia and in the most severe of cases, it is the only form of haemoglobin in circulation. In this situation, a fetus will develop hydrops fetalis and normally die before or shortly after birth, unless intrauterine blood transfusion is performed.

Since hemoglobin Barts is elevated in alpha thalassaemia, it can be measured, providing a useful screening test for this disease in some populations.

The ability to measure hemoglobin Barts makes it useful in newborn screening tests. If hemoglobin Barts is detected on a newborn screen, the patient is usually referred for further evaluation since detection of hemoglobin Barts can indicate either one alpha globin gene deletion, making the baby a silent alpha thalassemia carrier, two alpha globin gene deletions (alpha thalassemia), or hemoglobin H disease (three alpha globin gene deletions). Deletion of four alpha globin genes is not compatible with life.

This variant of hemoglobin is so called as it was discovered at St. Bartholomew's Hospital in London, also called St. Barts.

Treatments for ATR-16 syndrome depend on the symptoms experienced by any individual. Alpha thalassemia is usually self-limiting, but in some cases may require a blood transfusion or chelating treatment.

This can be caused by taking medications that contain sulfonamides under certain conditions (i.e., overdosing of sumatriptan).

Sulfhemoglobinemia is usually drug induced. Drugs associated with sulfhemoglobinemia include sulphonamides and sulfasalazine. Another possible cause is occupational exposure to sulfur compounds.

It can be caused by phenazopyridine.

HPFH may alleviate the severity of certain hemoglobinopathies and thalassemias, and is selected for in populations with a high prevalence of these conditions (which in turn are often selected for in areas where malaria is endemic). Thus, it has been found to affect Americans of African and Greek descent.