Abnormal Middle Cerebral Artery Doppler

Abnormal middle cerebral artery Doppler is either a low pulsatility index (below the 5th centile), signalling cerebral vasodilatation in a hypoxic fetus, or a raised peak systolic velocity (above 1.5 multiples of the median), signalling fetal anaemia.

It is found on growth scans or in the monitoring of at risk pregnancies. It matters because it points to fetal hypoxia or anaemia that can cause stillbirth, and each needs different action.

Low pulsatility index: placental insufficiency, often with growth restriction.

Raised peak systolic velocity: alloimmunisation, parvovirus infection, fetomaternal haemorrhage, alpha thalassaemia.

Peak systolic velocity is measured at an angle of 0 degrees from the proximal vessel near the origin.

Women are often asymptomatic. Reduced fetal movements, small fundal height, rash or fever (parvovirus), previous affected baby or a sensitising event may be present.

• Features of the cause are present (hypertension for placental disease; rash or red cell antibodies for anaemia).

• Hydrops in severe anaemia.

Differential diagnosis: placental insufficiency, constitutionally small fetus, red cell alloimmunisation, parvovirus B19 infection, fetomaternal haemorrhage, fetal arrhythmia, technical error.

Complications: stillbirth, fetal acidosis, hydrops, growth restriction, preterm birth, neonatal anaemia and jaundice, neurological damage.

The approach is to measure both indices and then look for the cause.

• Middle cerebral artery pulsatility index below the 5th centile with cerebroplacental ratio below 1.08 suggests hypoxia; peak systolic velocity above 1.5 multiples of the median suggests moderate to severe anaemia.
• Umbilical artery Doppler, estimated fetal weight, liquor volume, ductus venosus Doppler and cardiotocography.
• For anaemia: maternal blood group with antibody screen and indirect Coombs test, parvovirus IgM and PCR, Kleihauer test, haemoglobin electrophoresis; fetal blood sampling for haemoglobin where available.
• For hypoxia: maternal blood pressure, urine protein, full blood count, platelets, antiphospholipid antibodies.

The principle is to treat the cause: delivery planning for hypoxia and intrauterine transfusion for fetal anaemia.

• Supportive: daily fetal movement counts; left lateral rest; Doppler and cardiotocography surveillance; deliver in a unit with neonatal intensive care; counsel before 26 weeks.
• Pharmacological: for hypoxia, betamethasone 12 mg IM twice, 24 hours apart, between 24 and 34 weeks and 6 days if delivery is likely, and magnesium sulphate 4 g IV over 20 minutes then 1 g per hour until delivery for 24 hours at most before 32 weeks; labetalol 200 mg oral every 8 to 12 hours (maximum 2.4 g daily) or nifedipine modified release 30 to 60 mg oral once daily (maximum 120 mg) for hypertension; for fetal anaemia, betamethasone 12 mg IM twice, 24 hours apart, before transfusion at 24 to 34 weeks; newborn phototherapy for bilirubin at treatment threshold, with exchange transfusion for severe hyperbilirubinaemia.
• Procedures: delivery at 37 weeks for a low middle cerebral artery pulsatility index or cerebroplacental ratio, earlier for abnormal umbilical artery or ductus venosus Doppler or pathological cardiotocography; intrauterine blood transfusion with O negative, Kell negative, cytomegalovirus screened packed cells to a fetal haematocrit of 40 to 50 percent for peak systolic velocity above 1.5 multiples of the median before 35 weeks; delivery at 37 to 38 weeks after the last transfusion.
• Special groups: red cell alloimmunisation needs maternal anti-D immunoglobulin 500 IU IM at 28 and 34 weeks in unsensitised RhD negative women only; parvovirus infection may need transfusion and has no antiviral drug.
• Red flags: hydrops, reduced fetal movements, bradycardia, absent end diastolic flow, rising peak systolic velocity, abnormal cardiotocography.
• Follow-up: peak systolic velocity every 1 to 2 weeks after transfusion; growth scans every 2 weeks; newborn blood count, bilirubin and Coombs test.