Table 3.

Clinicopathological details and outcomes of cases with isolated fetal ascites presenting after >24 gestational weeks

Case	Antenatal ultrasound findings	Ascitic tap evaluation	Chromosomal analysis	Genetic testing	Maternal infection screen	Postnatal outcome	Postnatal diagnosis
1	Distended bowel loops, polyhydramnios? Hirschsprung’s disease	-	Normal	-	-ve	Ileostomy Surgery, alive and well	Hirschsprung’s disease confirmed on HPE
2	Distended echogenic bowel, polyhydramnios	-	Normal	-	-ve	PTD at 33 weeks (reduced fetal movements), NND day 7 postbilious vomiting (postnatal ultrasound not done)	Intestinal malformation
3	Intestinal perforation with meconium pseudocyst, polyhydramnios	-	Normal	-	-ve	Ileostomy for long segment ileal atresia, alive and well	Ileal atresia with perforation
4	Polyhydramnios	Ascitic fluid cytology - mainly lymphocytes, no vacuolated cells	Normal	CF common mutation negative, enzyme assay on cord blood for beta-glucosidase, beta-glucuronidase, beta-galactosidase, sphingomyelinase was within normal range	-ve	Postnatal ascitic tap - LDH - 415 U/L, glucose - 22 mg/dL, protein - 2.0 g/L Surgery, alive and well. Postnatal detailed workup for CF was negative as well	Rectal shelf
5	Genitourinary? Hydrocolpos	Not done, hydrocolpos was drained	Normal	-	-ve	Postnatal ascitic tap - LDH - 251 U/L, glucose - 15 mg/dL, protein - 0.1 g/dL Surgery, alive and well	Hydrocolpos
6	Genitourinary Hydronephrotic kidneys - distended urinary bladder followed by collapsed bladder with ascites	Beta 2 microglobulin - 6 mg/L	Normal	-	-ve	Surgery, alive and well (cystoscopy, fulguration of PUV)	PUV
7	Echogenic bowel + cardiomegaly (hypertrophied ventricular walls) + hepatomegaly	-	Normal	CF (comm.-on mutation, -ve, Clinical exome sequencing revealed 2 mutations of unknown significance correlating with familial hypertrophic cardiomyopathy	-ve	Neonatal demise	Hypertrophic cardiomyopathy
8	CHAOS + complex heart disease	-	Normal	-	-ve	Delivery at term, stillbirth	CHAOS
9	Hepatosplenomegaly, oligoamnios	Dark yellow ascitic fluid, Glucose - 64 mg/dL, protein - 2.4 g/dL, LDH - 1639 U/L, cytology - 100% lymphocytes	Could not be done due to paucity of cells in ascitic fluid	Negative for CF common mutation	-ve	LSCS for fetal distress, neonatal Hb 4 g, maternal hemorrhagic dengue fever diagnosed postoperative, neonatal death day 4	Storage disease most likely Niemann-Pick or lethal Gaucher disease on PAS stain on liver HPE
10	CHAOS+B/L renal agenesis	-	Not done	-	-ve	Delivered at 30 weeks, died immediately upon birth	Fraser syndrome on autopsy - additional findings - cryptophthalmos, syndactyly, and ambiguous genitalia
11	Isolated	Hemorrhagic ascitic tap	Normal		-ve	IUFD at 33 weeks	Idiopathic
12	Congenital heart block secondary to maternal SLE	Done to relieve thoracic compression	Normal		-ve	Alive and well At 10 years on medication	Congenital heart block
13	Isolated	Done to relieve thoracic compression	Normal		-ve	One postnatal tap, mild hepatomegaly at birth, alive and well at 5 years	Idiopathic
14	Isolated	Done to relieve thoracic compression	Normal		-ve	Alive and well at 3 years	Idiopathic
15	Isolated	-	Normal		-ve	Alive and well at 3 years	Idiopathic
16	Ascites in Recipient twin of MCDA pair, with DV changes, TTTS Stage IV	-	-		-	Neonatal death	MCDA complication
17	Echogenic bowel? meconium pseudocyst	Done, predominant-l year lymphocytes	Normal		-ve	Alive and well at 3 years	Ileal atresia with perforation repaired at day 16 of life

PTD: Preterm delivery, -ve: Negative, NND: Neonatal death, HPE: Histopathological examination, CHAOS: Congenital high airway obstruction syndrome, LDH: Lactate dehydrogenase, PUV: Posterior urethral valve, LSCS: Lower segment cesarean section, Hb: Hemoglobin, PAS: Periodic acid-Schiff, SLE: Systemic lupus erythematosus, MCDA: Monochorionic diamniotic, TTTS: Twin-twin transfusion syndrome, IV: Intravenous, CF: Cystic Fibrosis