Fetal thrombocytopenia

What are Fetal Anemia and Thrombocytopenia?

Anemia is a lack of red blood cells in the fetal circulation. The red blood cells carry oxygen from the placenta to the fetal tissues. Thrombocytopenia is a lack of platelets in the circulation. Platelets are responsible for blood clotting.

Different conditions can cause the baby to become anemic. One of the most common disorders is rhesus immunization. In the disease, the mother forms antibodies against the red blood cells of the fetus. These antibodies are passed through the placenta into the fetal circulation and destroy the red blood cells of the fetus. Other, less common reasons for fetal anemia are fetal viral infections (parvovirus B 19), fetomaternal hemorrhage and inborn blood disorders.

Thrombocytopenia can be caused by the mother forming antibodies against the fetal platelets (fetal and neonatal alloimmune thrombocytopenia, FNAIT) or by viral infections.

Fetal anemia can be diagnosed by a specialized ultrasound that measures the speed of the blood flow in one of the vessels in the fetuses brain (middle cerebral artery). Fetal thrombocytopenia cannot be diagnosed by ultrasound. Thrombocytopenia however can sometimes be suspected when the fetus presents with a bleed in the brain or when a sibling was born with thrombocytopenia.

What is the outcome for a fetus with anemia or thrombocytopenia?

Mild and moderate anemia will not affect the fetal condition and the long-term outcome of these infants is excellent.

When a fetus is severely anemic, there will be insufficient red blood cells to sustain adequate oxygen transport to the tissues. The fetus will try to compensate for this by increasing its heart function, and circulating the available red blood cells faster. At some point however, the heart will not be able to maintain this high output and heart failure will develop. This may become evident by the accumulation of fluid under the fetuses skin, in the abdomen and in the chest (hydrops). Fetuses with this condition are very sick and may not survive.

As for anemia, mild and moderate thrombocytopenia will not affect the fetal condition, and the long-term outcome of these infants is excellent. In severe thrombocytopenia however, fetal blood clotting is severely impaired and minor trauma may lead to fetal bleeds. These will mainly occur in the brain and may cause severe long-term handicap.

What other tests should we consider?

When fetal anemia or thrombocytopenia are suspected, a detailed ultrasound at a specialized center such as the Fetal Medicine Unit at Mount Sinai Hospital is required to assess the severity of the disease. Further investigations include maternal blood work to investigate the cause of the anemia or thrombocytopenia. In certain circumstances, amniocentesis will be performed to determine the fetal karyotype and to exclude fetal infections. Fetal blood sampling allows direct determination of the fetal red blood cell  and platelet count.

What therapies are available?

Mild or moderate fetal anemia does not require any prenatal therapy. These infants may however need light therapy (phototherapy) for jaundice after birth or may require a neonatal transfusion. When severe fetal anemia is diagnosed, intrauterine fetal transfusion may be considered. In experienced hands, intrauterine transfusions are successful in over 97% of cases. The rate of severe complications is 3% per procedure and the procedure related fetal loss rate is 1.6%. Overall survival after intrauterine transfusions is 75% if the fetus is hydropic at the first transfusion and over 90% in non-hydropic fetuses. This stresses the importance of close follow-up of fetuses at risk for fetal anemia and the need for referral to a fetal therapy center if severe anemia is suspected. A large follow-up study on neurologic outcomes after intrauterine transfusions for rhesus immunization shows a cerebral palsy rate of 2.1% and an overall risk for developmental delay of 4.8%. The risk of fetal death after intrauterine transfusions for hydropic fetuses with parvovirus B 19 infection is 30% and the risk of neurologic impairment in survivors is 10%.

Fetuses at high risk for thrombocytopenia due to FNAIT are treated preventatively with weekly immunoglobulin infusions to the mother, starting in the second trimester of pregnancy. Fetal blood sampling may be considered in the third trimester to document fetal platelet levels and to adjust further treatment. This strategy has significantly reduced the need for fetal platelet transfusions. The risk for severe thrombocytopenia causing intracranial hemorrhage after such prophylactic therapy is less than 5% and long-term outcomes are generally good.

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