This document discusses non-immune hydrops fetalis (NIH), which causes fetal swelling. NIH has many potential causes including cardiovascular anomalies, chromosomal abnormalities, and infections. Ultrasound is used to diagnose NIH by identifying signs such as skin thickness over 5mm, placental thickness over 4cm, and fluid accumulations. The prognosis is poor, with mortality rates of 50-90%. While the underlying cause should be determined, the outcome depends on the specific condition and potential for treatment.

1. NON IMMUINE HYDROPS
FETALIS UNIT IV
DR VARSHA DESHMUKH
KAY

2. HISTORY
• 25 Yrs. Old
• 7 Months Amenorrhoea
• Swelling of Feet 1 month
• Headache 3 days
OBST. HISTORY
• G5 P4 L1 A0
• First 3 Preterm deliveries all died.
• 4th
FTND 3 year old female live KAY

3. GENERAL EXAMINATION
• GC Moderate, afebrile, pulse 96 /min.,
BP – 150/110 mm.Hg.
• Pallor +, Edema +
• CVS, RS wnl
• Per abdomen
• Ut over distended, tense, fetal parts
not felt, FHS CNL
• Per Vaginum Cx 1 Fl, 60 % Effaced,
Membranes + breech at – 2 St.
• Pelvis adequate
• Provisional Diagnosis G5 P4 L1 A0,
Sev. PIH, ? Twins ? Hydramnios
• Ultrasonography KAY

4. Ultrasonography
KAY1. Placental Oedema 2. Scalp Oedema

5. Ultrasonography
KAY1. Ascitic Fluid 2. Liver 3. Peri. Effusion

6. LABOUR NOTES
• Preterm Vaginal Delivery
on 11/7/2003 (within 7 hrs.of active
labour)
• Female child 2200 gm., MSB,
e/o Hydrops Fetalis +
• Hyperplacentosis +, WT 1500 gm
KAY

7. KAY

8. KAY

9. INVESTIGATIONS
• Bld gr Orh+ve
• Hemogram Normal
• LFTs, KFTs Wnl
• BSL Normal
• Urine Exam. Normal
• Findings of neonatal autopsy :
• Macerated baby, distension of abd, edema all over body,
peeling of skin.
• Pericardial effusion, fluid in peritoneal cavity 200 cc.
• Congested liver, lungs, spleen, kidneys
• diagnosis – non immunize hydrops fetalis
KAY

10. INTRODUCTION
Potter in 1943 described clinical entity, that
affected non-Rh sensitised pregnancies,
NIH –
1) Fetal ansarca.
2) Placental oedema
3) Fetal serous effusions
NIH does not represent a specific
disease. “Late manifestation of many
severe diseases”. KAY

11. ETIOLOGY
• Cardiovascular anomalies -
tachyarrhythmia, Anatomic defects
• Chromosomal - Down syndrome, Turner
Syndrome.
• Malformation syndrome
• Twin pregnancy- Twin transfusion
syndrome
• Hematologic - Arteriovenous shunt
• Genitourinary - Congenital nephrosis
KAY

12. ETIOLOGY
• Respiratory - Pulmonary hypoplasia
• Gastrointestinal
• Liver
• Maternal - Severe diabetes mellitus,
severe anemia, Hypoproteinemia
• Placenta-umbilical cord - Chorionic vein
thrombosis
• Medications - Antepartum indomethacin
• Infectious - Parvovirus B 19, TORCH
• Miscellaneous KAY

13. DIAGNOSIS
• Ultrasound evaluation.
• Skin thickness more than 5 mm.
• Placental thickness more than 4 cm
• Ascitis, pericardial effusion, pleural
effusion.
• Polyhydramnios. KAY

14. MANAGEMENT
All NIH should be referred to a unit where
facilities exist for detailed anomaly scans
including - echocardiography, fetal blood
sampling and tertiary neonatal care.
Principles of Management
• If detected at <20 wks option for
termination of pregnancy given.
• Establish underlying cause
• Determine appropriate therapy & optimal
timing of therapy.
Prognosis :Overall mortality ranges 50% - 90% .

15. CONCLUSION
• USG has a pivotal role in diagnosis.
• Generalised lymphoedema has a poor
prognosis
• Cardiovascular anomalies is the most
identifiable cause. Arrhythmias are
amenable to therapy.
• Knowledge of etiology and fetal karyotype
will determine whether aggressive
management is warranted.
• Parent’s of affected child, need counselling
regarding accurate diagnosis and prognosis.