Locations can include:

- subcutaneous tissue/scalp

- pleura (pleural effusion)

- pericardium (pericardial effusion)

- abdomen (ascites)

The edema is usually seen in the fetal subcutaneous tissue, sometimes leading to spontaneous abortion. It is a prenatal form of heart failure, in which the heart is unable to satisfy its demand for a high amount of blood flow.

Hydrops fetalis is a condition in the fetus characterized by an accumulation of fluid, or edema, in at least two fetal compartments. By comparison, hydrops allantois or hydrops amnion is an accumulation of excessive fluid in the allantoic or amniotic space, respectively.

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.

Ballantyne syndrome has several characteristics:

- edema, always a key feature

- albuminuria of the mother, usually mild

- preeclampsia, unusual

The fetal symptoms are related to fluid retention, including ascites and polyhydramnios.

Fetal hydrops suggests the presence of an important and probably fatal fetal pathology.

It can be associated with twin-to-twin transfusion syndrome.

Fetal disease refers to disorders originating in utero.

Examples include hydrops fetalis and chorioamnionitis

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.

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

Types of breech depend on how the baby’s legs are lying.

- A frank breech (otherwise known as an extended breech) is where the baby’s legs are up next to its abdomen, with its knees straight and its feet next to its ears. This is the most common type of breech.

- A complete breech (flexed) breech is when the baby appears as though it is sitting crossed-legged with its legs bent at the hips and knees.

- A footling breech is when one or both of the baby’s feet are born first instead of the pelvis. This is more common in babies born prematurely or before their due date.

In addition to the above, breech births in which the sacrum is the fetal denominator can be classified by the position of a fetus. Thus sacro-anterior, sacro-transverse and sacro-posterior positions all exist, but left sacro-anterior is the most common presentation. Sacro-anterior indicates an easier delivery compared to other forms.

Hemolytic disease of the newborn, also known as hemolytic disease of the fetus and newborn, HDN, HDFN, or erythroblastosis fetalis, is an alloimmune condition that develops in a fetus, when the IgG molecules (one of the five main types of antibodies) produced by the mother pass through the placenta. Among these antibodies are some which attack antigens on the red blood cells in the fetal circulation, breaking down and destroying the cells (hemolysis). The fetus can develop reticulocytosis and anemia. This fetal disease ranges from mild to very severe, and fetal death from heart failure (hydrops fetalis) can occur. When the disease is moderate or severe, many erythroblasts (immature red blood cells) are present in the fetal blood, and so these forms of the disease can be called "erythroblastosis fetalis" (or "erythroblastosis foetalis").

HDFN represents a breach of immune privilege for the fetus or some other form of impairment of the immune tolerance of pregnancy. Various types of HDFN are classified by which alloantigen provokes the response. In order of incidence, the types include ABO, anti-RhD, anti-RhE, anti-Rhc, anti-Rhe, anti-RhC, multiantigen combinations, and anti-Kell.

A breech birth occurs when a baby is born bottom first instead of head first. Around 3-5% of pregnant women at term (37–40 weeks pregnant) will have a breech baby.

Most babies in the breech position are born by a caesarean section because it is seen as safer than being born vaginally.

As most breech babies are delivered by caesarean section in developed countries, doctors and midwives may lose the skills required to safely assist women giving birth to a breech baby vaginally. Delivering all breech babies by caesarean section in developing countries may be very difficult to implement or even impossible as there are not always resources available to provide this service.

Signs of hemolytic disease of the newborn include a positive direct Coombs test (also called direct agglutination test), elevated cord bilirubin, and hemolytic anemia. It is possible for a newborn with this disease to have neutropenia and neonatal alloimmune thrombocytopenia as well.Hemolysis leads to elevated bilirubin levels. After delivery bilirubin is no longer cleared (via the placenta) from the neonate's blood and the symptoms of jaundice (yellowish skin and yellow discoloration of the whites of the eyes) increase within 24 hours after birth. Like other severe neonatal jaundice, there is the possibility of acute or chronic kernicterus, however the risk of kernicterus is higher because of the rapid destruction of blood cells. It is important to note that isoimmunization is a risk factor for neurotoxicity and lowers the level at which kernicterus can occur. Untreated profound anemia can cause high-output heart failure, with pallor, enlarged liver and/or spleen, generalized swelling, and respiratory distress.

HDN can be the cause of hydrops fetalis, an often-severe form of prenatal heart failure that causes fetal edema.

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.

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.

Any condition that affects bone growth, most notably rickets (from vitamin D deficiency), marasmus, syphilis, or thalassemia, can cause craniotabes if present during a time of rapid skull growth (most especially during gestation and infancy). It can be a "normal" feature in premature infants. It is the first sign in children and infants with rickets.

Temporary hypoglycemia in the first three hours after birth is a normal finding. Most of the time it resolves without medical intervention. The lowest blood sugars occur one to two hours after birth. After this time, lactose begins to be available through the breast milk. In addition, gluconeogenesis occurs when the kidneys and liver convert fats into glucose..

Hemoglobin Lepore syndrome or Hb Lepore syndrome (Hb Lepore) is typically an asymptomatic hemoglobinopathy, which is caused by an autosomal recessive genetic mutation. The Hb Lepore variant, consisting of two normal alpha globin chains (HBA) and two deltabeta globin fusion chains which occurs due to a "crossover" between the delta (HBD) and beta globin (HBB) gene loci during meiosis and was first identified in an Italian family in 1958. There are three varieties of Hb Lepore, Washington (Hb Lepore Washington, AKA Hb Lepore Boston or Hb Lepore Washington-Boston), Baltimore (Hb Lepore Baltimore) and Hollandia (Hb Hollandia). All three varieties show similar electrophoretic and chromatographic properties and hematological findings bear close resemblance to those of the beta-thalassemia trait; a blood disorder that reduces the production of the iron-containing protein hemoglobin which carries oxygen to cells and which may cause anemia.

The homozygous state for Hb Lepore is rare. Patients of Balkan descent tend to have the most severe presentation of symptoms including severe anemia during the first five years of life. They also presented with significant splenomegaly, hepatomegaly, and skeletal abnormalities identical to those of homozygous beta-thalassemia. The amount of Hb Lepore in the patients blood ranged from 8 to 30%, the remainder being fetal hemoglobin (Hb F) which is present in minute quantities (typically<1 percent) in the red blood cells of adults. Known as F- cells they are present in a small proportion of overall RBCs.

Homozygous Hb Lepore is similar to beta-thalassemia major; however, the clinical course is variable. Patients with this condition typically present with severe anemia during the first two years of life. The heterozygote form is mildly anemic (Hb 11-13 g/dl) but presents with a significant hypochromia (deficiency of hemoglobin in the red blood cells) and microcytosis.

Pulmonary hypoplasia is incomplete development of the lungs, resulting in an abnormally low number or size of bronchopulmonary segments or alveoli. A congenital malformation, it most often occurs secondary to other fetal abnormalities that interfere with normal development of the lungs. Primary (idiopathic) pulmonary hypoplasia is rare and usually not associated with other maternal or fetal abnormalities.

Incidence of pulmonary hypoplasia ranges from 9–11 per 10,000 live births and 14 per 10,000 births. Pulmonary hypoplasia is a relatively common cause of neonatal death. It also is a common finding in stillbirths, although not regarded as a cause of these.

Anisopoikilocytosis is a medical condition illustrated by a variance in size (anisocytosis) and shape (poikilocytosis) of a red blood cell. The underlying cause can be attributed to various anemias, most often; beta thalassemia major, a form of microcytic anemia. In β thalassemia major the beta hemoglobin chain is completely absent, rendering an increase in fetal hemoglobin (HbF).

The symptoms and signs of congenital dyserythropoietic anemia are consistent with:

- Tiredness (fatigue)

- Weakness

- Pale skin

Craniotabes is softening or thinning of the skull in infants and children, which may be normally present in newborns. It is seen mostly in the occipital and parietal bones. The bones are soft, and when pressure is applied they will collapse underneath it. When the pressure is relieved, the bones will usually snap back into place.

Gray platelet syndrome (GPS), or platelet alpha-granule deficiency, is a rare congenital autosomal recessive bleeding disorder caused by a reduction or absence of alpha-granules in blood platelets, and the release of proteins normally contained in these granules into the marrow, causing myelofibrosis.

GPS is primarily inherited in an autosomal recessive manner, and the gene that is mutated in GPS has recently been mapped to chromosome 3p and identified as "NBEAL2". "NBEAL2" encodes a protein containing a BEACH domain that is predicted to be involved in vesicular trafficking. It is expressed in platelets and megakaryocytes and is required for the development of platelet alpha-granules. "NBEAL2" expression is also required for the development of thrombocytes in zebrafish.

GPS is characterized by "thrombocytopenia, and abnormally large agranular platelets in peripheral blood smears." The defect in GPS is the failure of megakaryocytes to package secretory proteins into alpha-granules. Patients with the GPS are affected by mild to moderate bleeding tendencies. Usually these are not major bleeds but there has been some life threatening cases. Also Women will tend to have heavy, irregular periods. Myelofibrosis is a condition that usually comes with the Gray Platelet syndrome.

The diagnosis of Hb Lepore syndrome may be performed antenatally or postnatally via the use of a variety of tests

- Complete blood count (CBC)

- Cation Exchange High-performance liquid chromatography (CE-HPLC): a chromatographic technique used to separate and quantify various normal and abnormal hemoglobin components in blood.

- Hemoglobin electrophoresis

- DNA analysis:

The presentation of individuals with alpha-thalassemia consists of:

CDA may be transmitted by both parents autosomal recessively or dominantly and has over four different subtypes, but CDA Type I, CDA Type II, CDA Type III, and CDA Type IV are the most common. CDA type II (CDA II) is the most frequent type of congenital dyserythropoietic anemias. More than 300 cases have been described, but with the exception of a report by the International CDA II Registry, these reports include only small numbers of cases and no data on the lifetime evolution of the disease.

ATR-16 syndrome affects the blood, development, and brain; symptoms vary based on the specific genes deleted on chromosome 16. Because it is so rare, it is difficult to determine the "core" symptoms of the disease. People with ATR-16 have alpha-thalassemia, a blood disorder where there is less normal hemoglobin in the blood than there should be, and the red blood cells are smaller than they should be (microcytic anemia). Affected children have various characteristic physical features, including clubfoot, "locked" little fingers, microcephaly (small head), hypertelorism (widely spaced eyes), broad, prominent nose bridge, downward-slanted palpebral fissures, small ears, retrognathia, and short neck. Children with ATR-16 syndrome also have mild to moderate intellectual disabilities, developmental delays/growth delays, and speech delays. Some children with ATR-16 have seizures, cryptorchidism (undescended testes), or hypospadias.