Hemolytic Disease of the Newborn (Erythroblastosis Fetalis)

What is hemolytic disease of the newborn (HDN)?

Hemolytic Disease of the Newborn (HDN), also known as Erythroblastosis Fetalis, is a condition where a fetus’ red blood cells are destroyed by maternal antibodies. This occurs when the mother and baby have incompatible blood types, typically involving the Rh factor or ABO blood group system.

The most common and severe form of HDN is caused by Rh (D) incompatibility, though it can also be caused by ABO incompatibility and incompatibilities with other minor blood group antigens

Blood Group System

ABO Blood Group System

The ABO blood group system is the most well-known and clinically important system for classifying human blood, after its discovery by Karl Landsteiner in the early 20th century. It’s based on the presence or absence of specific carbohydrate structures, called antigens, on the surface of red blood cells (RBCs), and corresponding antibodies in the blood plasma.

Antigens on Red Blood Cells

There are two primary antigens in the ABO system: A antigen and B antigen.

• Type A blood: Individuals have A antigens on their RBCs.
• Type B blood: Individuals have B antigens on their RBCs.
• Type AB blood: Individuals have both A and B antigens on their RBCs.
• Type O blood: Individuals have neither A nor B antigens on their RBCs (they only have a precursor antigen called the H antigen).

Antibodies in Plasma

Unlike the Rh system where antibodies are typically formed after exposure, antibodies against ABO antigens are naturally occurring in the plasma of individuals who lack the corresponding antigen. These antibodies are primarily IgM class, meaning they generally don’t cross the placenta easily.

• Type A blood: Has anti-B antibodies in their plasma.
• Type B blood: Has anti-A antibodies in their plasma.
• Type AB blood: Has neither anti-A nor anti-B antibodies in their plasma.
• Type O blood: Has both anti-A and anti-B antibodies in their plasma.

Inheritance

The ABO blood type is inherited and determined by a gene on chromosome 9 with three main alleles: A, B, and O.

• Alleles A and B are co-dominant, meaning if both are inherited (e.g., from an A parent and a B parent), both A and B antigens will be expressed (resulting in AB blood type).
• The O allele is recessive. To have Type O blood, an individual must inherit an O allele from both parents.

Clinical Significance (Transfusion)

The ABO system is critical for safe blood transfusions. If a patient receives blood with antigens they don’t have, their naturally occurring antibodies will quickly attack the transfused RBCs, leading to a severe and potentially fatal hemolytic transfusion reaction.

• Type O blood is considered the universal donor for red blood cells because its RBCs lack A and B antigens, so they won’t be attacked by anti-A or anti-B antibodies in a recipient’s plasma.
• Type AB blood is considered the universal recipient for red blood cells because individuals with AB blood have both A and B antigens, and therefore lack anti-A and anti-B antibodies, allowing them to receive blood from any ABO type.

Relevance to Hemolytic Disease of the Newborn (Erythroblastosis Fetalis)

While less severe than Rh-hemolytic disease of the newborn (erythroblastosis fetalis), ABO incompatibility can also cause HDN. This usually occurs when a Type O mother has a Type A or Type B fetus. The mother’s naturally occurring anti-A or anti-B antibodies (which can sometimes be IgG and thus cross the placenta, especially anti-A,B) can cause mild to moderate hemolysis in the fetus/newborn. It typically results in less severe symptoms than Rh-hemolytic disease of the newborn (erythroblastosis fetalis) and rarely leads to hydrops fetalis.

Rh Blood Group System

The Rh blood group system is a crucial classification of blood based on the presence or absence of specific proteins, called Rh antigens, on the surface of red blood cells (RBCs). It’s second only to the ABO system in clinical significance, especially in transfusion medicine and pregnancy.

Rh Antigens

While there are over 50 identified Rh antigens, the most important and clinically significant is the D antigen. This is the antigen that determines whether a person is “Rh-positive” or “Rh-negative.” Other important Rh antigens include C, c, E, and e.

Rh-Positive vs. Rh-Negative

• Rh-positive (Rh+): If your red blood cells have the D antigen, you are Rh-positive. This is the more common status.
• Rh-negative (Rh−): If your red blood cells lack the D antigen, you are Rh-negative.

Inheritance

Inheritance of Rh status is separate from ABO blood type. The presence of the D antigen is dominant. So, if an individual inherit at least one gene for the D antigen, then he/she will be Rh-positive. To be Rh-negative, an individual must inherit two copies of the gene that results in the absence of the D antigen (one from each parent).

Clinical Significance

The Rh factor is critically important because Rh-negative individuals do not naturally produce anti-Rh antibodies. However, if an Rh-negative person is exposed to Rh-positive blood (e.g., through a blood transfusion or during pregnancy), their immune system will recognize the D antigen as foreign and produce anti-D antibodies. These antibodies are primarily of the IgG class, which means they can cross the placenta. This is the basis of Hemolytic Disease of the Newborn (HDN) when an Rh-negative mother is sensitized to an Rh-positive fetus.

How does hemolytic disease of the newborn (HDN) happen?

Hemolytic disease of newborn (erythroblastosis fetalis) most commonly occurs when an Rh-negative mother has an Rh-positive baby. However, it can also occur when the mother and baby have different ABO blood types. 

Naturally Occurring Antibodies vs Immune Antibodies

Naturally occurring antibodies occur in the plasma of subjects who lack the corresponding antigen and who have not been transfused or been pregnant. The most important are anti-A and anti-B. They are usually IgM and react optimally at cold temperatures also known as cold antibodies.

Immune antibodies, also known as adaptive antibodies or acquired antibodies, are highly specific proteins produced by the body’s adaptive (acquired) immune system in response to a prior exposure to a foreign substance (an antigen). These antibodies are commonly IgG, although some IgM antibodies may also develop usually in the early phase of an immune response. Immune antibodies react optimally at 37^oC.

Only IgG antibodies are capable of transplacental passage from mother to foetus as IgM is too big. The most important immune antibody is the anti-D. These antibodies can cross the placenta and attack the baby’s red blood cells, causing them to break down. 

Pathophysiology of hemolytic disease of the newborn (HDN) (erythroblastosis fetalis)

In hemolytic disease of the newborn (erythroblastosis fetalis), the mother is Rh-negative while the father is Rh-positive.

During the first pregnancy, leakage of D+ fetal red cells across the placenta results in the mother becoming immunised against the D antigen as this antigen is not naturally occurring but is produced after sensitization as the fetus is Rh-positive. However, the amount of anti-D antibody that crosses the placenta into the fetal circulation following the initial exposure is too low to cause hemolysis.

During subsequent pregnancies, the mother mounts an anamnestic immunological response to D+ fetal red cells if the fetuses inherit the Rh-positive antigen from the father unless the father is heterozygous for the D antigen and there is a 50% probability that the fetus may be Rh-negative.

The IgG alloantibody produced by the mother is small enough to cross through the placenta into the fetal circulation and binds to fetal RBCs that are D+. The IgG-sensitized fetal RBCs are cleared from the circulation by macrophages in the fetal spleen. This leads to anemia and hyperbilirubinemia resulting in hemolytic disease of newborn (erythroblastosis fetalis).

What are the signs and symptoms of hemolytic disease of the newborn (HDN) (erythroblastosis fetalis)?

The severity of hemolytic disease of newborn (erythroblastosis fetalis) can vary from mild to severe.

Mild cases of hemolytic disease of newborn (erythroblastosis fetalis) may cause no symptoms, while severe cases can be life-threatening. The severity of hemolytic disease of newborn (erythroblastosis fetalis) depends on the number of antibodies that the mother has produced and the amount of time that the baby has been exposed to the antibodies. 

Antenatal (Fetal) Presentation

During pregnancy, hemolytic disease of the newborn (erythroblastosis fetalis) symptoms are typically detected through prenatal monitoring, especially in cases of known maternal sensitization.

Fetal Anemia

This is the primary consequence of red blood cell destruction.

• Increased Middle Cerebral Artery Peak Systolic Velocity (MCA-PSV): This is the most reliable ultrasound indicator of fetal anemia. As the blood becomes thinner (less viscous) due to anemia, it flows faster through the fetal cerebral arteries.
• Cardiomegaly and Heart Failure: The fetal heart has to work harder to circulate oxygen-poor blood, leading to an enlarged heart and, in severe cases, signs of heart failure.
• Hepatosplenomegaly: The fetal liver and spleen increase in size as they try to compensate for the accelerated red blood cell destruction by producing more immature red blood cells (extramedullary hematopoiesis).

Hydrops Fetalis

This is the most severe and life-threatening manifestation of fetal hemolytic disease of the newborn (erythroblastosis fetalis), occurring when the fetal body can no longer compensate for severe anemia and heart failure. It involves widespread fluid accumulation in at least two different fetal compartments.

• Ascites: Fluid buildup in the abdomen.
• Pleural Effusions: Fluid around the lungs.
• Pericardial Effusions: Fluid around the heart.
• Skin Edema: Generalized swelling, often visible as thickened skin.
• Polyhydramnios: Excessive amniotic fluid, often associated with hydrops.
• Thickened Placenta: The placenta may also appear enlarged and edematous on ultrasound.
• Decreased Fetal Movement: In severe cases, the fetus may become less active due to profound anemia and distress.

Postnatal (Neonatal) Presentation

After birth, the signs and symptoms of hemolytic disease of the newborn (erythroblastosis fetalis) become more apparent as the newborn’s immature liver struggles to clear the large amount of bilirubin produced from the rapid breakdown of red blood cells.

• Jaundice: This is the most common and often the earliest postnatal sign.
  • Early Onset: Jaundice typically appears within the first 24 hours of life, which is a key indicator of a pathological cause (as opposed to physiological jaundice, which usually appears after 24-48 hours).
  • Rapid Progression: The yellowing of the skin and whites of the eyes (sclera) progresses quickly and can be severe.
  • Orange-Yellow Color: The jaundice in HDN often has a more pronounced orange-yellow hue due to the high levels of unconjugated bilirubin.
• Pallor (Anemia): The newborn may appear pale due to the ongoing destruction of red blood cells and insufficient compensation by the bone marrow. The severity of pallor correlates with the degree of anemia.
• Hepatosplenomegaly: The liver and spleen may be enlarged upon physical examination, reflecting the increased erythropoiesis (red blood cell production) and red blood cell sequestration occurring in these organs.
• Edema: In severe cases, particularly if hydrops fetalis was present prenatally, the newborn may still exhibit generalized swelling or edema.
• Signs of Respiratory Distress: If lung development was compromised by hydrops (pleural effusions), or if the infant is severely anemic, they may present with tachypnea, grunting, or retractions.
• Signs of Kernicterus (Bilirubin Encephalopathy): This is the most dreaded complication of severe, untreated hyperbilirubinemia, where unconjugated bilirubin crosses the blood-brain barrier and deposits in brain tissue, causing damage. Early signs of kernicterus can be subtle and progress to more severe neurological damage:
  • Initial/Early Signs
    • Lethargy, extreme sleepiness, or difficulty waking.
    • Poor feeding or sucking.
    • Irritability.
    • High-pitched cry.
    • Decreased or absent startle reflex.
    • Hypotonia (floppy muscle tone).
  • Progressive/Late Signs
    • Fever.
    • Hypertonia (increased muscle tone), leading to arching of the back and neck (opisthotonus).
    • Seizures.
    • Abnormal eye movements, particularly an upward gaze (setting sun sign).
    • Apnea (pauses in breathing).
  • Long-term Sequelae of Kernicterus: If brain damage occurs, long-term complications can include:
    • Cerebral palsy (especially athetoid cerebral palsy, characterized by involuntary, uncontrolled movements).
    • Hearing loss or auditory neuropathy.
    • Intellectual disabilities.
    • Dental enamel hypoplasia.
    • Gaze palsies.

How is hemolytic disease of the newborn (erythroblastosis fetalis) tested?

Laboratory investigations for Hemolytic Disease of the Newborn (HDN) (erythroblastosis fetalis) are crucial for diagnosis, assessment of severity, monitoring, and guiding treatment decisions. These investigations are performed at different stages: antenatally (on the mother and fetus) and postnatally (on the newborn).

Maternal Investigations (Antenatal Screening)

These tests are routinely performed on all pregnant women to identify those at risk of developing hemolytic disease of the newborn (erythroblastosis fetalis).

• ABO and Rh Blood Typing: Determines the mother’s ABO blood group (A, B, AB, or O) and Rh (D) status (positive or negative). An Rh-negative mother is a key indicator of risk for Rh-HDN, especially if the father is Rh-positive.
• Antibody Screen (Indirect Antiglobulin Test – IAT / Indirect Coombs Test): To detect the presence of “atypical” (non-ABO) red blood cell antibodies in the mother’s serum that could potentially cross the placenta and cause hemolytic disease of the newborn (erythroblastosis fetalis).
  • Positive IAT: Indicates the mother has developed antibodies against red blood cell antigens (e.g., anti-D, anti-Kell, anti-c).
  • Antibody Titer: If a positive IAT is found, the specific antibody is identified, and its concentration (titer) is measured. A “critical titer” (e.g., usually 1:8, 1:16, or 1:32 depending on the lab and specific antibody) indicates a significant risk of severe hemolytic disease of the newborn (erythroblastosis fetalis) and necessitates closer fetal monitoring. For certain antibodies like anti-Kell, even low titers can be significant due to their mechanism of action (suppression of erythropoiesis in addition to hemolysis).

Fetal Investigations (Monitoring Sensitized Pregnancies)

Once a mother is identified as sensitized (positive antibody screen/IAT), these investigations are used to assess the severity of fetal anemia.

Doppler Ultrasonography of Middle Cerebral Artery Peak Systolic Velocity (MCA-PSV)

This is the current gold standard non-invasive method for detecting and monitoring fetal anemia.

• Mechanism: In anemic fetuses, the blood viscosity is reduced. To maintain oxygen delivery, the fetal heart pumps harder, increasing blood flow velocity, particularly in the middle cerebral artery.
• Interpretation: An elevated MCA-PSV (measured in cm/sec) above a certain “multiple of the median” (MoM) for gestational age indicates fetal anemia. A value of 1.5 MoM or greater is highly predictive of moderate to severe anemia.
• Advantage: Non-invasive, widely available, and has largely replaced invasive procedures like amniocentesis for assessing fetal anemia.

Amniocentesis for Bilirubin Levels (Spectrophotometric analysis of delta OD450)

Historically used to assess the severity of fetal hemolysis by measuring the bilirubin concentration in amniotic fluid. Bilirubin in amniotic fluid originates from fetal urine. Largely replaced by MCA-PSV due to its invasive nature and associated risks (e.g., feto-maternal hemorrhage, infection, rupture of membranes), unless MCA-PSV is equivocal or other information is needed.

Cordocentesis (Percutaneous Umbilical Blood Sampling – PUBS):

Direct sampling of fetal blood from the umbilical vein. This is an invasive procedure, usually reserved for cases where precise fetal blood parameters are needed (e.g., before an intrauterine transfusion or when MCA-PSV is inconclusive).

• Tests Performed on Fetal Blood:
  • Hemoglobin (Hb) and Hematocrit (Hct): Direct measurement of fetal anemia.
  • Blood Type and Rh Status: Confirms the fetal blood type.
  • Direct Antiglobulin Test (DAT / Direct Coombs Test): Detects maternal antibodies already bound to fetal red blood cells (see below for more detail). A positive result indicates sensitization and hemolysis.
  • Bilirubin Levels: Measures direct and indirect bilirubin in fetal blood.
  • Reticulocyte Count: An elevated count indicates the fetus is actively producing new red blood cells in response to hemolysis.

Neonatal Investigations

These tests are performed on the newborn, usually on cord blood, immediately after birth if HDN is suspected or diagnosed antenatally.

ABO and Rh Blood Typing of Newborn

Confirms the baby’s blood group and Rh status.

Direct Antiglobulin Test (DAT / Direct Coombs Test) on Cord Blood

This is the cornerstone test for diagnosing hemolytic disease of the newborn (erythroblastosis fetalis) in the newborn. It directly detects whether maternal antibodies (IgG) are already attached to the surface of the newborn’s red blood cells in vivo.

A Positive DAT indicates that maternal antibodies are coating the newborn’s red blood cells, confirming alloimmune hemolysis. A positive DAT is expected in Rh-HDN and is often positive in ABO-HDN, although it can be negative in some cases of ABO-HDN due to fewer antibody binding sites or rapid elution of antibodies.

While a positive DAT indicates the presence of coating antibodies, the strength of the reaction does not always directly correlate with the severity of hemolysis, especially in ABO-HDN.

Complete Blood Count (CBC) with Reticulocyte Count

• Hemoglobin (Hb) and Hematocrit (Hct): Measures the degree of anemia. Low values indicate significant red blood cell destruction.
• Reticulocyte Count: Measures the percentage of immature red blood cells. An elevated reticulocyte count (reticulocytosis) indicates the newborn’s bone marrow is actively attempting to compensate for the hemolysis by producing more red blood cells.
• Peripheral Blood Smear: May show abnormal red blood cell characteristic features such as polychromasia (immature red blood cells), spherocytes (in ABO-HDN), and nucleated red blood cells (erythroblastosis), especially in severe cases, reflecting increased erythropoiesis.

Serum Bilirubin Levels (Total and Direct/Conjugated)

To monitor the level of bilirubin, a breakdown product of heme from destroyed red blood cells. Unconjugated (indirect) bilirubin is toxic to the brain.

• Interpretation: Elevated total bilirubin, particularly a rapidly rising unconjugated bilirubin, is a key indicator of ongoing hemolysis and risk of kernicterus. Direct bilirubin should also be monitored as its elevation could indicate liver dysfunction or other causes of jaundice.
• Serial measurements: Bilirubin levels are typically monitored every few hours in affected newborns to guide phototherapy or exchange transfusion decisions.

How is hemolytic disease of the newborn (erythroblastosis fetalis) treated?

The treatment and management of hemolytic disease of the newborn (erythroblastosis fetalis) are multifaceted, focusing on prevention, monitoring during pregnancy, and interventions for both the fetus and the newborn, depending on the severity of the condition. Mild cases of hemolytic disease of newborn (erythroblastosis fetalis) may not require any treatment. More severe cases of hemolytic disease of newborn (erythroblastosis fetalis) may require phototherapy (light therapy) or blood transfusions. 

Antenatal Management (During Pregnancy)

The primary goal antenatally is to prevent sensitization and, if sensitization has occurred, to monitor the fetus closely and intervene to prevent severe anemia and its complications like hydrops fetalis.

Prevention of Rh Sensitization: Rho(D) Immune Globulin (RhIg / RhoGAM)

Routine use of RhIg has dramatically reduced the incidence of severe Rh-HDN.

• Mechanism of Action: RhIg is a solution of IgG antibodies against the D antigen. When administered to an Rh-negative mother, these pre-formed antibodies bind to any Rh-positive fetal red blood cells that may enter the maternal circulation (e.g., during feto-maternal hemorrhage). This binding “coats” and clears the fetal red blood cells from the mother’s system before her own immune system can recognize them as foreign and produce its own, potentially harmful, anti-D antibodies. It essentially provides passive immunity to prevent active sensitization.
• Indications and Timing of Administration:
  • Routine Antenatal Prophylaxis: A dose of RhIg is typically given to all unsensitized Rh-negative pregnant women at 28 weeks of gestation. This is to cover any small, asymptomatic feto-maternal hemorrhages that might occur in the third trimester.
  • Post-Event Prophylaxis: RhIg is also administered within 72 hours after any event that could cause feto-maternal hemorrhage, potentially exposing the mother to Rh-positive fetal red blood cells. These events include:
    • Delivery of an Rh-positive baby (a higher dose may be needed if a large feto-maternal hemorrhage is suspected, determined by a Kleihauer-Betke test).
    • Miscarriage or abortion (spontaneous or induced).
    • Ectopic pregnancy.
    • Amniocentesis, chorionic villus sampling (CVS), or cordocentesis.
    • External cephalic version.
    • Abdominal trauma during pregnancy.
    • Threatened abortion with vaginal bleeding.

Monitoring Sensitized Pregnancies

For mothers who are already sensitized (have anti-D or other significant antibodies), regular monitoring of the fetal status is crucial using Doppler ultrasonography of the Middle Cerebral Artery Peak Systolic Velocity (MCA-PSV). This non-invasive method is the primary tool for assessing the degree of fetal anemia.

Monitoring frequency increases as the pregnancy progresses and depends on antibody titers and previous pregnancy outcomes.

Intrauterine Fetal Transfusion (IUT)

This procedure is performed when severe fetal anemia (indicated by high MCA-PSV or direct fetal blood sampling via cordocentesis) is detected, often before hydrops fetalis develops. The goal is to provide enough red blood cells to sustain the fetus until it is mature enough for early delivery.

Under ultrasound guidance, a needle is inserted through the mother’s abdomen and uterus into the umbilical cord vein (intravascular transfusion, IVT) or, less commonly, into the fetal abdominal cavity (intraperitoneal transfusion, IPT). Compatible, O-negative, CMV-negative, irradiated, and concentrated red blood cells are slowly transfused into the fetus.

Risks of complications include fetal bradycardia, fetal distress requiring emergency C-section, premature labor, premature rupture of membranes, infection, and rarely, fetal death or exacerbation of maternal sensitization. Multiple transfusions may be needed throughout the pregnancy.

Early Delivery

If the fetus reaches adequate lung maturity (typically around 34-37 weeks, sometimes confirmed by amniocentesis for lung maturity), or if fetal anemia is severe and unresponsive to IUT, early delivery may be considered to prevent further intrauterine damage. Delivery method (vaginal or C-section) depends on obstetric indications.

Postnatal Management (After Birth)

The focus after birth is to manage hyperbilirubinemia and anemia resulting from ongoing hemolysis.

Phototherapy for Hyperbilirubinemia

Phototherapy uses specific wavelengths of blue-green light (420-490 nm). This light is absorbed by bilirubin in the skin and converts it into water-soluble photoisomers and oxidation products (lumirubin) that can be excreted in bile and urine without requiring liver conjugation. This prevents the accumulation of toxic unconjugated bilirubin.

Treatment is initiated based on the newborn’s total serum bilirubin (TSB) levels plotted on hour-specific nomograms, considering gestational age, postnatal age, and risk factors (like positive DAT, rapid rise in bilirubin, prematurity). Intensive phototherapy is used for higher bilirubin levels.

Exchange Transfusion

This is a more invasive procedure reserved for severe hyperbilirubinemia when phototherapy is insufficient or for significant anemia at birth. It is indicated if:

• TSB levels reach a critical threshold, despite intensive phototherapy, and are approaching levels associated with kernicterus.
• Signs of acute bilirubin encephalopathy (kernicterus) are present.
• Severe anemia is present at birth (Hb < 10-12 g/dL, depending on the clinical scenario).

A “double volume” exchange transfusion is typically performed, where small aliquots of the newborn’s blood are incrementally removed and replaced with an equal amount of compatible donor blood (usually O-negative packed red blood cells suspended in AB plasma). This process aims to remove sensitized red blood cells, circulating maternal antibodies, and excess bilirubin, while correcting anemia.

While effective, it carries risks including electrolyte imbalances (hypocalcemia, hyperkalemia, hypoglycemia), acid-base disturbances, infection, vascular complications (e.g., thrombosis, air embolism), cardiac arrhythmias, necrotizing enterocolitis, and even death.

Intravenous Immunoglobulin (IVIG)

IVIG may be used in moderate to severe cases of ABO or Rh-HDN (often in conjunction with phototherapy) to reduce the need for exchange transfusion. IVIG is a preparation of pooled antibodies from human plasma. It is thought to work by saturating the Fc receptors on the newborn’s macrophages and reticuloendothelial cells, thereby blocking the destruction of antibody-coated red blood cells and reducing the rate of hemolysis.

Supportive Care

• Correction of Anemia: Besides exchange transfusion, some newborns with less severe anemia may require simple top-up blood transfusions during the first few weeks or months of life as maternal antibodies persist and continue to cause hemolysis.
• Fluid Management: Adequate hydration is important, especially during phototherapy, to facilitate bilirubin excretion.
• Respiratory Support: For newborns with hydrops fetalis or severe anemia leading to heart failure, respiratory support (oxygen, mechanical ventilation, surfactant) may be necessary.

Long-term Follow-up

Newborns treated for hemolytic disease of the newborn (erythroblastosis fetalis) require careful follow-up due to potential long-term complications.

• Anemia: May persist for several weeks or months due to ongoing hemolysis and suppression of erythropoiesis, requiring repeat CBCs and potentially further transfusions.
• Hearing Assessment: Due to the risk of bilirubin neurotoxicity, especially to the auditory pathway, all infants with severe hyperbilirubinemia should have auditory brainstem response (ABR) testing to screen for hearing loss.
• Neurological Development: Follow-up for neurological development is crucial to detect any signs of kernicterus sequelae (e.g., cerebral palsy, developmental delays).
• Liver Function: Monitoring for any persistent effects on liver function.

Frequently Asked Questions (FAQs)

What happens to mother in erythroblastosis fetalis?

Erythroblastosis fetalis primarily affects the fetus, but it can also have implications for the mother. While the mother’s immune system is responsible for producing the anti-D antibodies that cause the condition, she typically doesn’t experience severe symptoms.

However, the mother’s body may respond to the excessive breakdown of fetal red blood cells by:

• Anemia: In severe cases, the mother’s blood may become anemic due to the loss of red blood cells from the fetus.
• Jaundice: If the mother’s liver cannot process the breakdown products of red blood cells efficiently, she may develop jaundice, characterized by yellowing of the skin and eyes.
• Other complications: In rare cases, severe hemolysis (the breakdown of red blood cells) can lead to complications like kidney failure or liver damage.

It’s important to note that these complications are uncommon and typically occur only in severe cases of erythroblastosis fetalis. Modern prenatal care and preventive measures like Rh immunoglobulin (RhIg) have significantly reduced the risk of severe maternal complications.

What happens if mother is Rh positive and baby is Rh negative?

If a mother is Rh-positive and her baby is Rh-negative, there is no risk of Rh incompatibility.

Rh incompatibility only occurs when the mother is Rh-negative and the baby is Rh-positive. In this case, the mother’s immune system may produce antibodies against the Rh-positive blood cells, which can cross the placenta and harm the baby.  

If both mother and baby are Rh-positive or both are Rh-negative, there is no risk of Rh incompatibility.

How long does hemolytic disease of the newborn last?

The duration of hemolytic disease of the newborn (HDN) can vary depending on its severity.

In mild cases, hemolytic disease of the newborn (erythroblastosis fetalis) may resolve within a few days or weeks with supportive care, such as phototherapy to reduce jaundice. However, in more severe cases, hemolytic disease of the newborn (erythroblastosis fetalis) can last for several weeks or even months.

Disclaimer: This article is intended for informational purposes only and is specifically targeted towards medical students. It is not intended to be a substitute for informed professional medical advice, diagnosis, or treatment. While the information presented here is derived from credible medical sources and is believed to be accurate and up-to-date, it is not guaranteed to be complete or error-free. See additional information.

References

1. Anemia: Diagnosis and Treatment (Willis, 2016).
2. Management of Anemia: A Comprehensive Guide for Clinicians (Provenzano et al., 2018)
3. Goldberg S, Hoffman J. Clinical Hematology Made Ridiculously Simple, 1st Edition: An Incredibly Easy Way to Learn for Medical, Nursing, PA Students, and General Practitioners (MedMaster Medical Books). 2021.