Q. While doing some reproductive medicine practice questions in a boards question bank I came across one I couldn’t reason through and was hoping you could help:

A 32 year-old schoolteacher in her first trimester of pregnancy is concered about a student in her class who develops a bright red rash on her cheeks. Two days later, the student’s shoulders, upper thorax, and arms become red, and develop a lacy, reticulated appearance. The physician should monitor this pregnancy closely for the development of which of the fetal conditions?

A.      Congenital heart disease
B.      Cutaneous scarring
C.      Hemolytic anemia
D.      Hydrocephalus
E.      Non-immune hydrops

E. Non-immune hydrops, was the correct answer. I selected C., hemolytic anemia. I was able to pick up on the likely parvovirus B-19 infection of the student and knew that it could cause an aplastic crisis. I think the main problem is that I can’t distinguish the difference between a hemolytic anemia and an aplastic crisis or what non-immune hydrops is.

A. You were correct in your identification of parvovirus B19 (the slapped-cheek disease) as the causative agent in this question. It’s a virus you worry about both in pregnancy and in patients with chronic hemolytic anemias, because parvovirus arrests red cell maturation at the late pronormoblast stage. It also affects platelets, but the main sequelae have to do with red cells.

In patients with chronic hemolytic anemias (like hereditary spherocytosis, or thalassemia) you worry about parvovirus infection because these patients are already maxing out their bone marrows (to compensate for the red cells that are being destroyed in the blood). This type of patient doesn’t have a ton of red cell “reserve” – red cell production is operating at full capacity already. So if a patient with a chronic hemolytic anemia gets parvovirus, all the red cells will be arrested at the pronormoblast stage – and it will take longer than usual to make new ones. Dangerous situation.

In pregnant women, there isn’t a chronic hemolysis going on (unless the patient just so happens to also have sickle cell anemia or some other hemolytic anemia). However, if you knock out a ton of red cells (by arresting their maturation), it’s pretty much the same as having a severe anemia (in both mom and baby). And one of the consequences of severe anemia in the fetus is something called “non-immune hydrops.”

“Hydrops” is just a term meaning edema in the fetus. It can be due to immune causes (like Rh incompatibility) or non-immune causes (there are a bunch of these – from tumors to infections to severe anemia). In the case of parvovirus, the problem in the fetus is that with so few red cells, the heart works extra hard to compensate for the oxygen deficiency (like it would in any severe anemia). Over time, the heart can fail (“high-output cardiac failure”) and blood can back up behind the heart, leading to peripheral edema. Also, if there is circulatory failure, the liver is likely not working so well, and if the liver isn’t making as much protein as it normally would, there will be a loss of oncotic pressure in the blood, which will make the edema worse. This can be fatal in the fetus.

This is the worst case scenario, obviously. Much of the time (about 70% of the time, depending on what source you look at) parvovirus does not end up being transmitted from mom to fetus. The riskiest time for transmission is in the first trimester; infections transmitted later have fewer complications.

So, looking at the other answers: congenital heart disease is wrong, as is cutaneous scarring and hydrocephalus. Some sources say that in addition to arresting red cells at an early stage, parvovirus can also cause some hemolysis. So I suppose you could argue that choice c could possibly be correct. The best choice, however, is non-immune hydrops.