- Diagnosis Of IUGR.

 Diagnosis Of  IUGR

A.    Establishing gestational age.

B.    Fetal assessment:

                        I. Ultrasonography (may be as often as 1– 2 times per week).

1.     Estimated fetal weight:  4 biometric measures are commonly used: biparietal diameter, head circumference, abdominal circumference, and femur length. The biometric measurements can be combined to generate an EFW. The estimate may deviate from the birthweight by up to 20%. The liver is the first organ to suffer the effects of growth restriction due to redistribution of ductus venosus blood flow to the heart and a decrease in glycogen deposition in the liver. Reduced growth of the abdominal circumference (<5 mm/wk) is the earliest sign of asymmetric growth restriction and diminished glycogen storage.

2.     Ratio of head circumference to abdominal circumference. This ratio normally changes as pregnancy progresses. In the second trimester, the head circumference is greater than the abdominal circumference. At about 32 to 36 weeks’ gestation, the ratio is 1:1, and after 36 weeks, the abdominal measurements become larger. Persistence of a head-to-abdomen ratio <1 late in gestation is predictive of late-onset FGR.

3.     Femur length: Serial measurements of femur length are as effective as head measurements for detecting early-onset FGR.

4.     Placental volume measurements may be helpful in predicting subsequent fetal growth. Placental weight and/or volume is decreased before fetal growth decreases. FGR with decreased placental size is more likely to be associated with fetal acidosis. Placental volume correlates with placental flow indices.

                      II.Doppler measurements:

Doppler assessment of the various fetal vasculature provides important clinical information on the circulatory changes that are occurring within the fetus and also indirectly provides some evidence of fetal hypoxia or acidemia.

                                               i.          Umbilical artery Doppler

                                              ii.          Middle cerebral artery Doppler

                                            iii.          venosus Doppler

                                            iv.          Cerebroplacental ratio.

                    III.   Biophysical profile score.

                    IV.   Cardiotocography (may be daily).

                      V.   Placental MRI: can assess the severity of FGR on the basis of decreased placental volume and changes in placental thickness-to- volume ratio. Fetal demise can also be predicted by abnormal signal intensity.

C. Diagnosing compensated versus decompensated fetus.

Persistence of uteroplacental insufficiency results in fetal adaptation to maintain adequate cerebral oxygenation and growth.

1.     Uteroplacental insufficiency results in increased placental vascular resistance and fetal hypoxemia by reducing umbilical blood flow. The fetus responds by redistribution of blood to the brain (brain sparing) through cerebral vasodilatation, mesenteric vasoconstriction, preferential shunting through the foramen ovale, increased fractional extraction of oxygen, polycythemia, and a relative decrease in fetal oxygen consumption. Fetal growth velocity and weight gain are decreased. Nonstress test (NST), BPP, and cardiotocography are normal. Decreased diastolic flow in the UA and increased diastolic component in the MCA may be seen. The fetus is hypoxemic but does not have cerebral hypoxemia at this stage. 

2. With worsening placental dysfunction, fetal compromise may occur with cerebral hypoxemia and acidemia associated with no fetal weight gain, oligohydramnios, decreased fetal heart rate variability, and abnormal NST, cardiotocography, and BPP. UAs show AEDV followed by REDV. Deep “a” wave is seen in the DV, suggestive of ventricular dysfunction. With severe acidosis, MCA PI and MCA PSV decrease, suggesting the imminent collapse of the fetus.

 3. Acute fetal decompensation. AEDV/REDV in UAs in early-onset FGR babies can be present up to 1 week before acute decompensation. Approximately 40% of fetuses with acidosis have AEDV/REDV pattern. MCA vasodilation with abnormal PI may be present for up to 2 weeks before acute deterioration in 50% to 80% of infants. MCA vasodilation may be independently associated with abnormal outcomes in late-onset FGR. Oligohydramnios develops in 20% to 30% of FGR infants about 1 week before acute deterioration.