Fetal anemia is a medical condition where a developing baby does not have enough red blood cells or sufficient hemoglobin while still in the womb. Red blood cells carry oxygen throughout the body, and hemoglobin is the protein within these cells that binds to oxygen. If these oxygen-carrying components fall below the normal range, the fetus becomes deprived of the necessary oxygen supply. This requires immediate medical attention and specialized management during pregnancy.
Defining Fetal Anemia and Its Impact
Red blood cells transport oxygen from the placenta to all fetal tissues. Anemia, a deficit in these cells or their hemoglobin content, forces the fetal body to activate compensatory mechanisms. The blood becomes thinner and less viscous due to the lower concentration of red blood cells, resulting in a hyperdynamic state of circulation.
The fetal heart attempts to compensate for the reduced oxygen-carrying capacity by increasing its output, pumping faster and harder to move the thinner blood rapidly. This sustained workload can eventually lead to heart failure. The consequence of this cardiac strain is the accumulation of fluid in at least two different body compartments.
This pathological fluid buildup is known as Hydrops Fetalis. It involves fluid accumulating around the lungs (pleural effusion), the heart (pericardial effusion), or in the abdomen (ascites). Hydrops Fetalis is an advanced stage of untreated fetal anemia and is associated with a high risk of stillbirth or neonatal death. Early diagnosis and intervention are necessary to prevent progression to this life-threatening state.
Primary Causes and Contributing Factors
Fetal anemia arises from various underlying conditions, categorized into Alloimmune and Non-Immune causes. Alloimmune anemia occurs when the pregnant person’s immune system produces antibodies against the fetus’s red blood cells. This typically happens when the mother lacks a specific red blood cell antigen the fetus inherited from the father, such as in Rhesus (Rh) incompatibility.
Maternal antibodies cross the placenta and target the fetal red blood cells for destruction, causing hemolysis. While Rh-D alloimmunization was historically the most common cause, routine preventative treatment has significantly reduced its incidence. Sensitization to other red blood cell antigens, known as minor blood group antigens, can still lead to this immune-mediated anemia.
Non-Immune causes are diverse and do not involve maternal antibodies attacking the fetal blood cells. Infections are a frequent contributor, most commonly Parvovirus B19, which temporarily halts the production of new red blood cells. Other non-immune factors include genetic disorders like alpha-thalassemia, where hemoglobin production is impaired.
Complications in multiple gestations, such as Twin-to-Twin Transfusion Syndrome (TTTS) or Twin Anemia Polycythemia Sequence (TAPS), can result in anemia in one twin due to abnormal blood flow across shared placental vessels. Additionally, fetomaternal hemorrhage, a large bleed of fetal blood into the maternal circulation, can cause a sudden drop in the fetal red blood cell volume.
Methods of Detection During Pregnancy
Screening for fetal anemia involves non-invasive maternal blood tests that check for red blood cell antibodies. If antibodies are detected, or if another risk factor like Parvovirus infection exists, monitoring begins. The primary non-invasive diagnostic tool is the Doppler ultrasound, which measures the flow velocity of blood in a major artery in the fetal brain, the Middle Cerebral Artery (MCA).
When a fetus is anemic, the blood is less viscous, and the body prioritizes blood flow to the brain, causing the blood to move faster. This increased speed, specifically the peak systolic velocity (PSV) in the MCA, is a reliable indicator of anemia. An MCA-PSV measurement greater than 1.5 times the median for that gestational age suggests moderate to severe fetal anemia.
If the MCA-PSV reading is significantly elevated, an invasive procedure called cordocentesis, or percutaneous umbilical cord blood sampling (PUBS), may be performed to confirm the diagnosis. This procedure involves inserting a fine needle, guided by ultrasound, into the umbilical vein to withdraw a small sample of fetal blood. The sample is analyzed to measure the hemoglobin level and hematocrit, confirming the severity of the anemia before treatment begins.
Treatment Options and Monitoring
The definitive intervention for moderate to severe fetal anemia is an Intrauterine Blood Transfusion (IUT). This procedure involves transfusing donor red blood cells directly into the fetus. The transfusion is performed under continuous ultrasound guidance, with a needle inserted through the mother’s abdomen into the umbilical vein, which is the preferred site for delivery.
The transfused blood is specially prepared, typically O-negative, and cross-matched with the mother’s serum to ensure compatibility. A small blood sample is often taken immediately before the transfusion to confirm the degree of anemia and calculate the precise volume needed. The goal is to raise the fetal blood count to a safe level, typically achieving a post-transfusion hematocrit of at least 40.
Following the procedure, the fetus is monitored for several hours. The need for subsequent transfusions is assessed through serial MCA-PSV Doppler measurements. Repeat transfusions may be necessary every two to four weeks until the fetus reaches a gestational age for safe delivery. The management strategy focuses on sustaining the fetus in utero until the risks of prematurity are lower than the risks of continued treatment.