Ductus Venosus (DV) Doppler during NT screening

Role of Ductus Venosus (DV) Doppler


Ductus venosus (DV) Doppler assessment is a critical part of first-trimester screening (11–13+6 weeks) for chromosomal abnormalities, congenital heart defects, and other aneuploidies.
1. To evaluate fetal hemodynamics, especially cardiac function.
2. Used in combination with NT thickness, nasal bone, tricuspid flow, and maternal serum markers (PAPP-A, β-hCG) to increase detection of trisomy 21, trisomy 18, and trisomy 13.
3. Abnormal DV flow (particularly reversed or absent 'a-wave') is associated with:
• Chromosomal anomalies
• Cardiac defects
• Fetal growth restriction (FGR)
• Poor pregnancy outcome

Timing

  • Performed between 11 weeks and 13 weeks + 6 days
  • Fetal crown-rump length (CRL) should be between 45–84 mm

  • Patient Preparation

  • Standard NT screening preparation
  • Full bladder may help with visualization in transabdominal scans

  • Technique

  • Begin with mid-sagittal view used for NT measurement.
  • Use high-frequency transabdominal probe; switch to transvaginal if needed for better resolution.

  • Obtain a Sagittal or Midline Section: Begin with mid-sagittal view used for NT measurement. Use high-frequency transabdominal probe; switch to transvaginal if needed for better resolution.
  • Identify the Ductus Venosus: Located between the umbilical vein and inferior vena cava (IVC) near the fetal heart. Appears as a narrow vessel in the fetal abdomen, coursing between the left portal vein and IVC.
  • Color Doppler Application: Apply color Doppler to visualize the aliasing jet in the ductus venosus. Narrow color box, optimize gain and PRF to detect low-volume high-velocity flow.
  • Pulse-Wave Doppler Settings: Place the sample volume (gate) in the aliasing area of the ductus venosus. Insonation angle should be <30° if possible.
    • Filter: Low
    • Sweep speed: High (50–100 mm/s) for wave analysis
  • Record Doppler Waveform: Normal DV waveform is triphasic:
    • S-wave: during ventricular systole
    • D-wave: during early diastole
    • a-wave: during atrial contraction

    Normal: Forward a-wave in triphasic waveform. (Forward flow during all phases (especially a-wave))
    Abnormal: Reversed or absent a-wave.
    Indicates: Trisomy 21, 18, 13, congenital heart defects, fetal cardiac compromise.

  • Normal doppler value

    Ductus Venosus Doppler Measurement Table (11–13+6 Weeks)

    Parameter Measured Value Normal Range / Interpretation
    Ductus Venosus PI 1.2 < 95th percentile (~1.0–1.5 at 11–13w)
    Ductus Venosus RI 0.6 0.5 – 0.8
    Ductus Venosus PSV 35 cm/s 30 to 60 cm/s
    Ductus Venosus A-wave Positive Forward flow (Normal) / Reversed or Absent (Abnormal)

    Implications of High Ductus Venosus PI (>95th percentile)

    Condition Explanation
    Chromosomal Abnormalities Strongly associated with Trisomy 21 (Down Syndrome), Trisomy 18, and Trisomy 13.
    Fetal Cardiac Defects May indicate congenital heart disease, especially when combined with abnormal tricuspid flow or reversed a-wave.
    Fetal Growth Restriction (FGR) Suggests impaired placental perfusion or fetal hypoxia, particularly in high-resistance placentas.
    Increased Perinatal Mortality Risk High PI, especially with reversed a-wave, is associated with poor fetal outcomes or IUFD.
    Twin-to-Twin Transfusion Syndrome (TTTS) In monochorionic twins, high PI may signal early hemodynamic imbalance between fetuses.

    Implications of Low Ductus Venosus PI (<5th percentile)

    Condition Explanation
    Normal Variant Often a benign finding, especially if other fetal parameters are normal.
    High-Output Cardiac States May be seen in conditions with increased fetal cardiac output, such as anemia or AV malformations.
    Twin Anemia-Polycythemia Sequence (TAPS) Recipient twin may show lower resistance in venous flow in early stages of TAPS.
    Fetal Heart Failure Rarely, low PI can precede signs of heart failure or hydrops fetalis in high-output states.
    Condition/Concern Explanation
    Chromosomal Abnormalities High DV RI is associated with Trisomy 21 (Down syndrome), Trisomy 18 (Edwards), and Trisomy 13 (Patau) — especially when combined with increased NT or absent/reversed A-wave.
    Fetal Cardiac Defects Reflects possible structural heart defects or ventricular dysfunction (e.g., AV canal defects, HLHS).
    Impaired Venous Return / Cardiac Load Suggests elevated pressure in the right atrium or reduced cardiac compliance due to hypoxia or fluid overload.
    Fetal Hypoxia or Acidemia May be an early sign of compromised oxygenation or fetal metabolic imbalance.
    Fetal Growth Restriction (FGR) Associated with placental dysfunction, which can later lead to intrauterine growth restriction.
    Twin-to-Twin Transfusion Syndrome In monochorionic twins, high RI may be an early marker of donor twin circulatory stress.
    Increased Risk of IUFD Persistently high RI and/or reversed A-wave are linked to poor perinatal outcomes and increased risk of intrauterine fetal demise (IUFD).

    Clinical Implications of High Ductus Venosus PSV (>60 cm/s)

    Condition/Concern Explanation
    Fetal Anemia or Hyperdynamic State High PSV may reflect increased cardiac output, often seen in fetal anemia, parvovirus infection, or twin anemia–polycythemia sequence (TAPS).
    Arteriovenous Malformations Conditions like vein of Galen malformation or cardiac tumors may increase preload and cause elevated venous return velocities.
    Maternal Conditions (e.g., Diabetes) Increased PSV has been reported in maternal diabetes mellitus, possibly due to altered fetoplacental hemodynamics.
    Fetal Tachyarrhythmia or Stress Elevated fetal heart rate or stress may transiently increase venous return velocity.
    Normal Variant (Early Gestation) Occasionally, high PSV can occur as a normal physiological variant, especially if all other findings (NT, A-wave, RI, PI) are normal.

    Clinical Implications of Low Ductus Venosus PSV (<30 cm/s)

    Condition/Concern Explanation
    Fetal Cardiac Dysfunction May reflect reduced systolic function or ventricular outflow obstruction (e.g., aortic stenosis, HLHS).
    Chromosomal Abnormalities In combination with abnormal A-wave and increased NT, low PSV may be associated with Trisomy 21, 18, or 13.
    Impaired Placental Perfusion Reduced preload due to placental insufficiency may lead to lower velocities in venous return.
    Fetal Hypoxia or Acidemia Sluggish flow may indicate hypoxic or acidotic fetal status, especially if A-wave is reversed or absent.
    High Central Venous Pressure May suggest increased right atrial pressure, leading to dampened DV waveforms.
    Increased Risk of IUFD Persistently low PSV with reversed A-wave is linked to poor fetal prognosis or intrauterine fetal demise (IUFD).
    Condition/Concern Explanation
    Chromosomal Abnormalities Strongly associated with Trisomy 21, Trisomy 18, Trisomy 13, and Turner syndrome, especially when combined with increased NT.
    Congenital Heart Defects Suggests possible structural cardiac anomalies like AV canal defects, hypoplastic left heart, or outflow tract obstruction.
    Impaired Cardiac Function Reversed A-wave may reflect ventricular diastolic dysfunction or elevated central venous pressure.
    Fetal Growth Restriction (FGR) An early marker of placental insufficiency and may precede signs of intrauterine growth restriction.
    High Risk of Fetal Demise (IUFD) Abnormal A-wave is linked to increased risk of miscarriage or fetal death, especially if combined with low PSV or high RI.
    Twin-to-Twin Transfusion (TTTS) In monochorionic twins, absent/reversed A-wave may signal donor twin cardiovascular strain in early TTTS.
    Transient/Benign Variant Occasionally seen in normal fetuses, particularly when NT is normal and no structural abnormalities are detected. Requires follow-up.

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