Neonatal Ascites Case Report and Discussion

Neonatal ascites is a rare entity. It means the accumulation of fluid in the intraperitoneal cavity. Normally it should not happen. There are many reasons for neonatal ascites. Obstructive uropathy is the most common cause. We had found a case of neonatal ascites in our NICU. Here is the case report and discussion.

Case Summary

The baby of A 3130gm birth weight male preterm admitted just after birth due to severe abdominal distension and respiratory distress. The baby was born by LUCS at 36th weeks of gestation at 4 pm, 17.7.19. The baby cried immediately after birth but had meconium-stained liquor.

Mother Mrs. A, 29 years old primi gravidae nondiabetic normotensive having blood group A Negative was under regular antenatal checkup. An antenatal fetal anomaly ultrasound scan revealed Pleural effusion, pericardial effusion, huge ascites, and bilateral hydronephrosis.

On Admission the baby was ill-looking, Cyanosed, and signs of respiratory distress were present. The abdomen was hugely distended and tensed. The abdominal girth was 38 cm. Regarding Vital signs HR 152 b/min, RR 48/min, Temp 98.6F, SpO2 90% with nasal oxygen therapy. Spine and back were normal. There were no other congenital malformations.

The baby was admitted soon after birth and managed accordingly with Oxygen therapy, IV fluid, IV Antibiotics, and other supportive treatment. Oxygen therapy was reduced gradually. Feeding started by nasogastric tube and as feed tolerated amount was increased. Relative investigations were done and USG guided paracentesis was performed. Ascitic fluid was sent for study.

As the baby was improved, the baby was shifted to the cabin for further treatment and follow up plan.

Neonatal Ascites Case Report and Discussion

Investigations:

NameResults
CBC: Hb17.3
Total Count WBC7000
Neutrophil52%
Lymphocyte37%
Monocyte4%
Platelet267000/cmm
CRP0.3gm/l
S Electrolyte: Na+133 mmol/l
K+5.1 mmol/l
S. Creatinine0.8 mg/dl
S. Total Protein47 gm/l
S. Albumin33 gm/l
S. Calcium10.6 mg/dl
Coombs TestNegative
Urine R/E:
Color:Straw, Clear
Sp. Gravity1.004
AlbuminNil
SugarNil
Pus Cells0-2/HPF
RBCNil
Epithelial Cells1-2/HPF
CastsNil
Blood C/SNo Growth
Urine C/SNo Growth
Ascitic Fluid C/SNo Growth

Ascitic Fluid Study:

Appearance: Straw Color

Protein: 23 gm/l

Sugar: 75 mg/dl

Microscopy:

Total Count of Nucleated Cells: 700/cmm
Leishman’s stain: Mononuclear cells: 80%
Polymorph: 20%
RBC: A few

Grams Stain: No Microorganism

Z N Stain: No AFB has seen

Cytology: No Malignant Cell Identified

ADA (adenosine deaminase): 12.2 (Normal up to 30 u/l)

USG: 1. The appearance was suggestive of possible changes due to bladder outlet obstruction which is possibly due to the presence of Posterior Urethral Valve.
2. Gross Ascitis with echogenic debris.
3. Mild Hepatomegaly with normal texture.

Echo: Normal

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Causes of Neonatal Ascites:

Ascites is an excessive amount of fluid in the peritoneal cavity and in the neonate, it is usually urinary, biliary, or chylous. Other causes are less common.

Urinary Ascites: Causes are posterior urethral valves, ureteral stenosis, urethral stenosis/atresia, neurogenic bladder, urogenital sinus, congenital nephrotic syndrome, bladder neck obstruction.

Biliary Ascites: Perforation of the bile duct, Choledochal cyst.

Chylous Ascites: Congenital lymphatic abnormality or injury.

Hepatocellular Ascites: Neonatal hepatitis, Viral hepatitis, Congenital hepatic fibrosis, Budd-Chiari syndrome.

Gastrointestinal: Necrotizing enterocolitis, Meconium peritonitis, Atresia, Malrotation, Volvulus, Gastroschisis, Omphalocele, Postabdominal surgery, or Intussucsception.

Infections: Congenital (CMV, Toxoplasmosis, Syphilis)

Inborn errors of metabolism: Glycogen storage disorders, Lysosomal storage disorders, Galactosemia, Cystic fibrosis.

Chromosomal: Turner syndrome and trisomy 21

Posterior Urethral Valve

Posterior urethral valve (PUV) is a congenital anomaly of proximal urethral development of male children. Aberrant folds of tissue that extend from verumontanum to the external sphincter, creating a urethral obstruction with varying degree of urinary tract dysfunction.

It is the leading cause of bladder outlet obstruction and renal insufficiency in male children.

Neonatal Ascites Case Report and Discussion

Spontaneous bladder perforation is a rare entity in a neonate and occurs secondary to obstructive uropathy, most commonly Posterior urethral valve  (PUV).

1 of every 5000 to 8000 male births are affected.

Read Also: Baby with Multiple Congenital Birth Defects [Case History]

Clinical Presentation of Neonatal Ascites

Its presentation depends on the degree of urinary obstruction which is determined by the severity and orientation of the valves, from mild bladder outlet obstruction to severe obstructive uropathy.

Antenatal:

  1. Bilateral hydronephrosis.
  2. Distended and thickened bladder.
  3. Dilated prostatic urethra.
  4. Oligohydramnios – accounts for co-presentation of pulmonary hypoplasia.

Newborn:

  1. A palpable abdominal mass. The bladder may feel like a small walnut in the suprapubic area.
  2. Urinary ascites due to perforation of the ureter, intrarenal collecting system, or Bladder (intraperitoneal).
  3. Respiratory distress from pulmonary hypoplasia.
  4. Poor stream and dribbling of urine after birth.

In obstructive uropathy, the upper tracts are subjected to high pressures in the intrauterine life. As a result vesicoureteral reflux, bladder diverticula and urine extravasation or urinary ascites may occur.

neonatal-ascites

Diagnosis

Prenatal diagnosis is done by Ultrasound scanning. Findings are

  1. Thickened, dilated bladder along with bilateral hydronephrosis.
  2. Oligohydramnios
  3. Dilated posterior urethra.

Postnatal Diagnosis is confirmed by Voiding cystourethrogram (VCUG).

Management of Neonatal Ascites

In cases diagnosed prenatally, in utero decompression of the bladder can be done but with limited success.

The aim of the management is achieving decompression of the urinary tract. This may be accomplished by abdominal paracentesis, catheter drainage, or surgical exploration and repair of the bladder wall.

Postnatal treatment consists of placement of an indwelling catheter, initiating antibiotic prophylaxis, and elective cystoscopic ablation of the valves.

Catheter drainage by urethral route with or without vesicostomy achieves healing in most patients in  10-14  days following which the fulguration of the  PUV  is  attempted.

Intervention when antenatal sonography detects evidence of

  1. Oligohydramnios
  2. Dilated bladder
  3. Severe Hydro-ureteronephrosis—without renal cortical cystic lesions—in a fetus with a normal karyotype.

Vesicoamniotic shunting to treat oligohydramnios offers a potential improvement on pulmonary function.

Thanks

Download PDF Neonatal Ascites Case Report

Relative Readings:

Neonatal Urinary Ascites: A Report of Three Cases

Neonatal Ascites Springer LInk

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