I understand the pathophysiology of hydrops fetalis and erythroblastosis fetalis independently, but not why the edema occurs during erythroblastosis fetalis. For example, Langman's Embryology has mentioned the following in regards to erythroblastosis fetalis:

...the anemia due to the Rh antibodies in Erythroblastosis Fetalis) becomes so severe that fetal hydrops occurs.

Similarly, in Medscape for fetal hydrops:

Fluid accumulation in the fetus can result from congestive heart failure, obstructed lymphatic flow, or decreased plasma osmotic pressure. The fetus is particularly susceptible to interstitial fluid accumulation because of its greater capillary permeability, compliant interstitial compartments, and vulnerability to venous pressure on lymphatic return.

I wanted to know how fetal hydrops results from having erythroblastosis fetalis (i.e. how congestive heart failure, obstructed lymph flow or decreased plasma oncotic pressure result from erythroblastosis fetalis in the first place).

1 Answer 1


Many conditions can lead to fetal hydrops. The most significant contributing factor is the fetal homeostatic response to relative hypoxia. For a number of reasons, the fetus is more prone to the acccumulation of interstitial fluid. This can be triggered by hypoxia as the fetal circulation responds in an attempt to maintain oxygenation of the tissues.

From Pathophysiology of hydrops fetalis:

Hydrops fetalis occurs when the rate of interstitial fluid production by capillary ultrafiltration exceeds the rate of interstitial fluid return to the circulation via lymphatic vessels. Developmental differences in the microcirculation and lymphatic system of the fetus, as compared with mature subjects, renders the fetus susceptible to interstitial fluid accumulation. These differences include greater capillary permeability, more compliant interstitial compartment, and greater influence of venous pressures on lymphatic return. The balance between interstitial fluid production and removal is most commonly disrupted as a consequence of homeostatic mechanisms serving to preserve adequate systemic delivery of metabolic substrate when cardiocirculatory function is impaired. The pathophysiology of two conditions of impaired cardiocirculatory function, atrial tachycardia and severe anemia, serve as examples of the mechanisms by which these homeostatic mechanisms perturb the balance of interstitial fluid movement.

Hydrops can be immune (as in this case, due to incompatibility of fetal and maternal blood) or non-immune (e.g. cardiac, infectious, chromosomal, metabolic or non-immune haematological problems). Non-immune causes are much more common.

Haemolytic disease of the newborn occurs when there is an immune incompatibility between fetal and maternal blood (usually due to Rhesus incompatibility). This leads to breakdown of fetal red blood cells (haemolysis) which results in anaemia. This means that there is a reduced ability to carry oxygen and nutrients to the tissues. The condition is also known as fetal erythroblastosis due to the large number of erythroblasts seen in later stages.

The anaemia leads to compensatory tachycardia and eventually a high-output cardiac failure (this can also happen in adults due to anaemia).

From the Wikipedia page on high-output cardiac failure:

High-output heart failure is a heart condition that occurs when the cardiac output is higher than normal due to increased peripheral demand. There is a circulatory overload which may lead to pulmonary edema secondary to an elevated diastolic pressure in the left ventricle. These individuals usually have a normal systolic function but symptoms are those of heart failure. With time, this overload causes systolic failure. Ultimately cardiac output can be reduced to very low levels.

Compensatory erythrogenesis (red cell production) in the liver and spleen causes circulatory obstruction in the liver and portal hypertension.

These changes, coupled with the increased capillary permeability and tendency to accumulate interstitial fluid, gradually lead to the development of fetal hydrops.

There is a useful summary on fetal hydrops at perinatology.com.

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