Differentials
Non-immune fetal hydrops
SIGNS / SYMPTOMS
Hydrops fetalis consists of generalised subcutaneous oedema and fluid collections in some or all serous cavities.
Placental calcification, oligohydramnios, and intrauterine growth restrictions may be associated with congenital infections.[40][41]
INVESTIGATIONS
Maternal serum antibodies are negative in non-immune fetal hydrops. There are more than 80 causes of fetal hydrops.
Non-immune hydrops carries a high rate of infant mortality, and in many patients (17%) its cause remains indeterminate after diagnostic work-up.[39]
Parvovirus infection
SIGNS / SYMPTOMS
History of environmental exposure to parvovirus may arouse suspicion of possible infection in asymptomatic people.
Symptoms include maternal fever, myalgia, coryza, headache, nausea, and erythematous, maculopapular exanthema on the trunk and limbs. Arthropathy and arthritis are also common in women and adolescents.
Progressive fetal anaemia, due to preferential destruction of immature red blood cells (RBCs) by the virus, leads to hydrops and intrauterine fetal death.[31][42]
INVESTIGATIONS
Viral-specific IgM appears about 10 to 12 days after infection. Fetal infection is confirmed by analysing amniotic fluid, cord blood, or serous fluid for viral DNA or RNA by polymerase chain reaction.[42]
Non-RhD haemolytic disease
SIGNS / SYMPTOMS
Usually transfusion-induced. The mechanism for fetal anaemia is haemolysis and erythroid suppression.
Prior obstetric history does not reliably predict occurrence in subsequent pregnancy, and maternal antibody titre does not correlate with severity.[2]
Kell alloimmunisation is the most common non-RhD haemolytic disease, with an incidence of 0.1% to 0.2% in the obstetric population.[2]
INVESTIGATIONS
Serum antibodies can be detected in the maternal blood. Although the titre is not as reliable as in RhD disease, severe disease is unusual with titres <1:32, with the exception of anti-Kell antibodies where significant fetal disease can occur at much lower titres.
Middle cerebral artery (MCA) Doppler should be performed and has been shown to be reliable for fetal anaemia detection.
Fetal haemoglobin should be assessed by cordocentesis when non-invasive testing (MCA Doppler) is abnormal.[2]
Placental chorioangioma
SIGNS / SYMPTOMS
May be present in up to 1% of pregnancies.[31]
Large placental masses of ≥5 cm may produce complications such as fetal anaemia, hydrops, and polyhydramnios, and poor perinatal outcome.[31]
INVESTIGATIONS
A solid placental mass is detected by standard 2-dimensional sonography, and colour Doppler sonography reveals a pulsatile mass.
Maternal serum alpha-fetoprotein may be high in association with a placental chorioangioma. Doppler velocimetry of the MCA may be consistent with fetal anaemia.[43]
Fetomaternal haemorrhage
SIGNS / SYMPTOMS
Severe, acute fetomaternal haemorrhage may be entirely asymptomatic or manifest as a reduction in perceived fetal movements by the mother. Clinical symptoms are usually non-specific.
INVESTIGATIONS
Peak systolic velocity on MCA Doppler may be increased.
Kleihauer-Betke test (persistence of fetal RBCs in maternal serum after denaturation by strong acid) or flow cytometry is also helpful.[31]
Twin-twin transfusion syndrome (TTTS)
SIGNS / SYMPTOMS
Develops in association with monochorionic twin placentation, usually between 15 and 26 weeks' gestation. It is found in 5.5% to 17.5% of all monochorionic pregnancies.[44]
INVESTIGATIONS
Ultrasound findings include polyhydramnios in one twin (recipient), and amniotic sac and oligohydramnios in the other (donor).
Growth of fetuses is usually discordant.[44]
Hydrops may develop in later stages of the disease, usually in the recipient co-twin.
Perinatal mortality may reach 80% to 100% when untreated.[44]
Twin anaemia-polycythemia sequence (TAPS)
SIGNS / SYMPTOMS
Develops in monochorionic twins and is characterised by a large intertwin haemoglobin difference without the abnormal amniotic fluid seen in TTTS.
Results mainly due to slow intertwin blood transfusion leading to anaemia for the donor and polycythemia for the recipient.
Can occur spontaneously (3% to 5%) or after laser surgery for TTTS (2% to 13%).[45]
INVESTIGATIONS
Absence of ultrasound finding of twin oligohydramnios (donor) and polyhydramnios (recipient) sequence.
Peak systolic velocity on MCA Doppler: donor >1.5 MoM (anaemia); recipient <1.0 MoM (polycythemia).
Use of this content is subject to our disclaimer