- Fetal Upturned Nose
- IgA Nephropathy in Pregnancy
- Umbilical vein varix
- Timing of Cranial Markers in Open NTD
- Real world experience Open Neural tube defect and Brain Signs
- Real world experience First Trimester Megacystis – Management
- Real world experience Fetal Megacystis
- Abnormal facial profile
- Azygous Vein & ARSA
- Blakes Pouch Cyst
- Absent nasal bone (ANB)
- Choroid plexus cysts
- Chronic placental abruption
- Fetal Alcohol Syndrome
- Placenta-First Risk Stratification
- AVSD
- Blakes Pouch Cyst
- Confined Placental Mosaicism
- Echogenic Bowel
- Fetal Anemia
- Fetal Club Foot
- Fetal Mild Micromelia
- Hypochondroplasia – Mild Micromelia
- Hypoplastic Nasal Bone
- IgM IgG IgG Avidity
- Increased Nuchal Translucency
- Isotretinoin in Pregnancy
- Partial agenesis of corpus callosum
- PGT A
- PGT-A Mosaicism to CPM
- Placenta First - CPM
- Radiation exposure during pregnancy
- Real world Chorionic bump experience
- Real world Fetal Isotretinoin exposure
- Real world Increased Nuchal Translucency & Genetic RISK
- Real world Renal Pyelectasis
- Real world Transient NT & Cystic Hygroma
- Real world Transient NT
- Renal Pyelectasis or Extra Renal Pelvis
- Right And Double Aortic Arch
- Short Femur Length Foot FL ratio
- Y Microdeletion
- CCAM CPAM
- Coffin–Siris syndrome
- Congenital CMV Infection
- Increased NT and Localized CHAOS
- Indomethacin and Reduction for AFI
- Atrioventricular septal defect (AVSD)
- Choledochal cyst & Cystic biliary atresia
- Duodenal Atresia
- Fetal atrial bigeminy
- Fetal Dilated stomach
- Mutation Types in DMD
- Risk of rubella in nonimmune pregnant woman
- Salt-losing nephropathy
- Syndromic Cystic biliary atresia
- TGA DORV TOF CCTGA
- Unilateral echogenic kidney with polyhydramnios
- Unilateral renal agenesis, Ectopic, Cross fused kidney
Congenital cytomegalovirus infection
Most common congenital viral infection worldwide.
Maternal infection types
| Type | Risk to fetus |
|---|---|
| Primary infection | Highest risk |
| Reinfection | Lower risk |
| Reactivation | Lowest risk |
Transmission risk by gestational age
| Trimester of maternal infection | Fetal transmission risk | Severity risk |
|---|---|---|
| 1st trimester | ~30–40% | Most severe |
| 2nd trimester | ~40–50% | Moderate |
| 3rd trimester | ~60–70% | Usually mild |
Timing of embryopathy vs fetopathy
Infection at 6–12 weeks - This is the highest-risk period.
Major effects:
- Neuronal migration defects
- Cortical malformations
- Microcephaly
Infection at 12–20 weeks
- Ventriculomegaly
- Intracranial calcifications
- White matter injury
Infection after 20–24 weeks
- Milder CNS involvement
- Hepatosplenomegaly
- Growth restriction
Fetal pathophysiology
CMV primarily affects: developing brain
Mechanisms:
- Neuronal destruction
- Impaired migration
- Calcification
- Gliosis
Also affects:
- Liver
- Bone marrow
- Placenta
Ultrasound timeline after infection
0–2 weeks after fetal infection - No ultrasound findings
3–6 weeks after infection
Early signs:
- Echogenic bowel
- Mild ventriculomegaly
- Hepatomegaly
6–10 weeks after infection
Progressive findings:
- Intracranial calcifications
- Ventriculomegaly
- Microcephaly emerging
>10 weeks
Late-stage features:
- Cortical malformations
- Severe brain injury
- Growth restriction
Major long-term complications
Especially neurological.
- Hearing loss (most common)
- Developmental delay
- Cerebral palsy
- Epilepsy
Prognostic ultrasound features
Poor prognosis indicators
- Microcephaly
- Ventriculomegaly
- Cortical malformations
- Cerebellar hypoplasia
- Hydrops
Placental involvement
CMV affects placenta significantly.
Findings:
- Thick placenta
- Calcifications
- Inflammation
Placental dysfunction contributes to: fetal growth restriction.
Diagnosis — maternal and fetal
Maternal testing
- CMV IgM
- CMV IgG
- IgG avidity
Avidity interpretation
| Avidity | Meaning |
|---|---|
| Low | Recent infection |
| High | Old infection |
Fetal diagnosis
Most definitive: Amniotic fluid PCR
- Timing:
- ≥21 weeks
- ≥6–8 weeks after maternal infection
CMV classic cluster
- Ventriculomegaly
- Intracranial calcifications
- Echogenic bowel
- Hepatosplenomegaly
This combination is very characteristic.
Congenital CMV severity is determined mainly by gestational age at infection, with early infection causing severe neuronal migration defects and later infection producing milder systemic findings, and ultrasound abnormalities typically appearing 3–10 weeks after fetal infection.