Ascites in Children: Clinical Case and Viva QnA

Clinical Case of Ascites in Children

Clinical Case: Ascites in a 7-year-old child

A 7-year-old boy is brought to the pediatric clinic by his parents with complaints of progressive abdominal distension over the past 3 weeks. The parents report that the child has been experiencing discomfort and a feeling of fullness after eating small amounts of food. They also noticed that his abdomen appears more prominent, especially when standing.

History:

• No history of fever, jaundice, or bleeding disorders
• No recent travel or exposure to contaminated water
• No family history of liver disease or autoimmune disorders
• Normal birth and developmental history
• Vaccinations up to date

Physical Examination:

• Weight: 25 kg (50th percentile), Height: 122 cm (50th percentile)
• Vital signs: Temperature 37°C, HR 90/min, RR 20/min, BP 110/70 mmHg
• Abdominal examination:
  • Distended abdomen with visible dilated superficial veins
  • Fluid thrill and shifting dullness present
  • No tenderness or organomegaly appreciated
• Mild pedal edema noted
• No signs of jaundice or pallor

Investigations:

• Complete blood count: Hb 11.5 g/dL, WBC 7,500/μL, Platelets 180,000/μL
• Liver function tests: ALT 65 U/L, AST 70 U/L, Total bilirubin 1.2 mg/dL, Albumin 2.8 g/dL
• Renal function tests: BUN 15 mg/dL, Creatinine 0.6 mg/dL
• Abdominal ultrasound: Moderate ascites, normal liver echotexture, no focal lesions, patent portal and hepatic veins
• Ascitic fluid analysis: SAAG (Serum-Ascites Albumin Gradient) 1.8 g/dL, protein 2.5 g/dL, cell count 100/μL (predominantly lymphocytes)

Diagnosis and Management:

Based on the clinical presentation, physical examination, and investigations, a diagnosis of portal hypertension secondary to liver cirrhosis is suspected. Further evaluation is needed to determine the underlying etiology, which may include autoimmune hepatitis, Wilson's disease, or other causes of chronic liver disease in children. Management will involve addressing the underlying cause, nutritional support, and symptomatic treatment of ascites.

5 Varieties of Presentations of Ascites in Children

Varieties of Presentations of Ascites in Children

1. Chronic Liver Disease-Related Ascites

   Presentation: Gradual onset of abdominal distension, often accompanied by other signs of chronic liver disease such as jaundice, spider angiomas, and palmar erythema. May have a history of failure to thrive or recurrent infections.

   Examples: Biliary atresia, autoimmune hepatitis, Wilson's disease

2. Acute Ascites in Nephrotic Syndrome

   Presentation: Rapid onset of generalized edema, including periorbital puffiness and ascites. Often accompanied by frothy urine and recent history of upper respiratory tract infection.

   Example: Minimal change disease

3. Cardiac Ascites

   Presentation: Ascites developing in the context of heart failure. Often associated with hepatomegaly, jugular venous distension, and peripheral edema. May have history of congenital heart disease or cardiomyopathy.

   Examples: Constrictive pericarditis, severe tricuspid regurgitation

4. Malignancy-Associated Ascites

   Presentation: Rapid onset of ascites, often accompanied by constitutional symptoms like weight loss, fever, and night sweats. May have palpable abdominal masses or lymphadenopathy.

   Examples: Lymphoma, ovarian tumors, hepatoblastoma

5. Infectious or Inflammatory Ascites

   Presentation: Acute onset of ascites with fever, abdominal pain, and signs of systemic inflammation. May have recent travel history or exposure to infectious agents.

   Examples: Tuberculous peritonitis, spontaneous bacterial peritonitis in a child with underlying liver disease

25 Viva Questions and Answers Related to Ascites in Children (Pediatrics)

1. Q: What is the definition of ascites?

   A: Ascites is defined as the pathological accumulation of free fluid within the peritoneal cavity. In children, any detectable free fluid in the peritoneum is considered abnormal and warrants investigation.

2. Q: What are the main pathophysiological mechanisms leading to ascites formation?

   A: The main mechanisms are: 1) Portal hypertension leading to increased hydrostatic pressure 2) Hypoalbuminemia causing decreased oncotic pressure 3) Lymphatic obstruction 4) Increased capillary permeability (e.g., in inflammation) 5) Fluid overload states (e.g., renal failure, heart failure)

3. Q: How do you clinically assess for ascites in a child?

   A: Clinical assessment includes: 1) Inspection for abdominal distension and visible veins 2) Palpation for fluid thrill 3) Percussion for shifting dullness 4) Measurement of abdominal girth 5) Assessment of peripheral edema

4. Q: What is the most sensitive method to detect small amounts of ascites?

   A: Ultrasonography is the most sensitive method for detecting small amounts of ascites, capable of identifying as little as 100 mL of free fluid in the peritoneal cavity.

5. Q: What is the SAAG, and how is it useful in the evaluation of ascites?

   A: SAAG stands for Serum-Ascites Albumin Gradient. It's calculated by subtracting the albumin concentration of the ascitic fluid from the serum albumin concentration. A SAAG ≥1.1 g/dL suggests portal hypertension as the cause of ascites, while a SAAG <1.1 g/dL suggests other causes like malignancy or infection.

6. Q: What are the common causes of ascites in children?

   A: Common causes include: 1) Liver diseases (cirrhosis, hepatitis) 2) Nephrotic syndrome 3) Congestive heart failure 4) Malignancies (e.g., lymphoma, ovarian tumors) 5) Infections (e.g., tuberculosis) 6) Protein-losing enteropathy 7) Chylous ascites (lymphatic disorders)

7. Q: How does ascites in portal hypertension differ from cardiac ascites?

   A: In portal hypertension, ascites is typically isolated or associated with splenomegaly. Cardiac ascites is usually accompanied by other signs of heart failure such as jugular venous distension, hepatomegaly, and peripheral edema. The SAAG is typically high in both conditions, but cardiac ascites may have a higher protein content.

8. Q: What investigations would you perform in a child presenting with ascites?

   A: Investigations should include: 1) Complete blood count 2) Liver function tests 3) Renal function tests 4) Serum albumin and total protein 5) Abdominal ultrasound 6) Diagnostic paracentesis with ascitic fluid analysis 7) Additional tests based on suspected etiology (e.g., echocardiogram, liver biopsy)

9. Q: What are the indications for diagnostic paracentesis in a child with ascites?

   A: Indications include: 1) New-onset ascites of unknown etiology 2) Suspected spontaneous bacterial peritonitis 3) Refractory ascites 4) Ascites in the setting of fever or abdominal pain 5) To guide management in known chronic liver disease

10. Q: What parameters should be analyzed in ascitic fluid?

    A: Ascitic fluid analysis should include: 1) Appearance and color 2) Cell count and differential 3) Total protein 4) Albumin (for SAAG calculation) 5) Glucose 6) LDH 7) Gram stain and culture 8) Cytology (if malignancy is suspected) 9) Additional tests as indicated (e.g., adenosine deaminase for TB, triglycerides for chylous ascites)

11. Q: How is spontaneous bacterial peritonitis (SBP) diagnosed in children with ascites?

    A: SBP is diagnosed when the ascitic fluid absolute neutrophil count is ≥250 cells/mm³ in the absence of an intra-abdominal, surgically treatable source of infection. A positive bacterial culture supports the diagnosis but is not required.

12. Q: What is the initial management of a child with newly diagnosed ascites?

    A: Initial management includes: 1) Identifying and treating the underlying cause 2) Sodium restriction (1-2 mEq/kg/day) 3) Fluid restriction if hyponatremia is present 4) Diuretics (typically spironolactone ± furosemide) 5) Monitoring of weight, urine output, and electrolytes 6) Nutritional support 7) Treatment of complications (e.g., SBP prophylaxis in cirrhotic ascites)

13. Q: What are the complications of ascites in children?

    A: Complications include: 1) Spontaneous bacterial peritonitis 2) Respiratory compromise due to diaphragmatic elevation 3) Umbilical or inguinal hernias 4) Malnutrition and growth failure 5) Electrolyte imbalances 6) Renal dysfunction (hepatorenal syndrome in cirrhotic patients) 7) Increased risk of infections

14. Q: How do you manage refractory ascites in children?

    A: Management of refractory ascites may include: 1) Large volume paracentesis with albumin replacement 2) Consideration of transjugular intrahepatic portosystemic shunt (TIPS) in selected cases 3) Evaluation for liver transplantation if due to end-stage liver disease 4) Trialing of alternative diuretics or higher doses 5) Sodium and fluid restriction 6) Nutritional support and addressing any underlying cause

15. Q: What is chylous ascites and how is it diagnosed?

    A: Chylous ascites is the accumulation of lipid-rich lymph in the peritoneal cavity, often due to disruption or obstruction of the lymphatic system. It's diagnosed when the ascitic fluid triglyceride level is >200 mg/dL or when chylomicrons are present on lipoprotein electrophoresis.

16. Q: How do you manage chylous ascites in children?

    A: Management includes: 1) Treating the underlying cause (e.g., lymphoma, congenital lymphatic malformation) 2) Dietary modification with medium-chain triglycerides 3) Total parenteral nutrition in severe cases 4) Octreotide to reduce lymph production 5) Paracentesis for symptomatic relief 6) Surgical intervention if conservative measures fail

17. Q: What is the role of albumin infusion in the management of ascites?

    A: Albumin infusion is used in: 1) Large volume paracentesis (>5 L) to prevent post-paracentesis circulatory dysfunction 2) Treatment of spontaneous bacterial peritonitis to reduce the risk of renal impairment 3) Management of hepatorenal syndrome 4) Severe hypoalbuminemia causing refractory ascites It helps maintain intravascular volume and oncotic pressure.

18. Q: How does ascites in nephrotic syndrome differ from that in liver disease?

    A: In nephrotic syndrome: 1) Ascites is typically part of generalized edema 2) SAAG is usually <1.1 g/dL 3) Ascitic fluid protein content is higher 4) There's often associated massive proteinuria and hypoalbuminemia 5) Response to diuretics may be more dramatic 6) Underlying liver function is typically normal

19. Q: What are the key features of tuberculous peritonitis in children?

    A: Key features include: 1) Gradual onset of ascites 2) Constitutional symptoms (fever, weight loss, night sweats) 3) Abdominal pain and tenderness 4) Lymphadenopathy (abdominal or peripheral) 5) Ascitic fluid with lymphocytic predominance 6) High adenosine deaminase levels in ascitic fluid 7) Positive TB skin test or interferon-gamma release assay 8) Omental and peritoneal thickening on imaging

20. Q: How do you differentiate between transudate and exudate in ascitic fluid?

    A: The traditional criteria (Light's criteria adapted for ascites): 1) Transudate: fluid protein <2.5 g/dL 2) Exudate: fluid protein ≥2.5 g/dL However, the SAAG is now considered more useful than the transudate/exudate classification: 3) SAAG ≥1.1 g/dL suggests portal hypertension (regardless of protein content) 4) SAAG <1.1 g/dL suggests other causes (e.g., malignancy, infection) Additional parameters that may help: 5) Exudates typically have higher LDH levels 6) Exudates may have a fluid:serum LDH ratio >0.6 7) Cell counts are usually higher in exudates

21. Q: What is the significance of portal hypertension in pediatric ascites?

    A: Portal hypertension is a significant cause of ascites in children. Its importance includes: 1) It's often associated with chronic liver disease or cirrhosis 2) It leads to the formation of portosystemic collaterals (e.g., esophageal varices) 3) It increases the risk of spontaneous bacterial peritonitis 4) It may cause hypersplenism and pancytopenia 5) It can lead to hepatopulmonary syndrome or portopulmonary hypertension 6) Management often requires both medical therapy and consideration of surgical interventions (e.g., shunts, transplantation)

22. Q: How does one calculate the Pediatric End-stage Liver Disease (PELD) score, and what is its significance in children with ascites due to liver disease?

    A: The PELD score is calculated using: 1) Bilirubin 2) INR 3) Albumin 4) Growth failure 5) Age (<1 year or not) Its significance: 1) Used for liver transplant allocation in children <12 years 2) Higher scores indicate more severe disease and higher priority for transplantation 3) Helps in prognostication and management decisions 4) Ascites, being a sign of decompensation, often correlates with higher PELD scores

23. Q: What are the principles of nutritional management in children with ascites due to chronic liver disease?

    A: Principles include: 1) High calorie intake (130-150% of recommended daily allowance) 2) Adequate protein intake (2-3 g/kg/day) unless hepatic encephalopathy is present 3) Sodium restriction (typically 1-2 mEq/kg/day) 4) Fluid restriction only if serum sodium <125 mEq/L 5) Supplementation of fat-soluble vitamins (A, D, E, K) 6) Medium-chain triglyceride supplementation if fat malabsorption is present 7) Zinc supplementation 8) Frequent small meals and late evening snacks to prevent catabolism 9) Enteral nutrition preferred; parenteral nutrition if enteral route is inadequate

24. Q: How do you manage hepatorenal syndrome in a child with ascites?

    A: Management of hepatorenal syndrome includes: 1) Identification and treatment of precipitating factors (e.g., GI bleeding, SBP) 2) Discontinuation of nephrotoxic drugs 3) Volume expansion with albumin (1 g/kg/day for 2 days) 4) Vasoconstrictors: Terlipressin (if available) or Norepinephrine 5) Midodrine and Octreotide as an alternative if Terlipressin is unavailable 6) Avoidance of diuretics and large volume paracentesis 7) Renal replacement therapy as a bridge to liver transplantation 8) Evaluation for liver transplantation, which is the definitive treatment

25. Q: What is the role of transjugular intrahepatic portosystemic shunt (TIPS) in managing pediatric ascites, and what are its limitations?

    A: Role of TIPS: 1) Used in refractory ascites not responding to medical management 2) Can be effective in reducing portal pressure and controlling ascites 3) May serve as a bridge to liver transplantation Limitations: 1) Technical challenges in small children 2) Risk of hepatic encephalopathy 3) Potential for shunt dysfunction or thrombosis 4) May complicate future liver transplantation 5) Limited long-term data in pediatric population 6) Contraindicated in severe liver failure, pulmonary hypertension, and uncontrolled infection

26. Q: How do you diagnose and manage eosinophilic ascites in children?

    A: Diagnosis: 1) Ascitic fluid eosinophil count >10% of total nucleated cells 2) Peripheral eosinophilia often present 3) Exclude parasitic infections, particularly in endemic areas 4) Consider associated conditions like eosinophilic gastroenteritis, hypereosinophilic syndrome, or allergic reactions Management: 1) Treat underlying cause if identified 2) Dietary elimination if food allergy is suspected 3) Corticosteroids (e.g., prednisolone 1-2 mg/kg/day) as first-line therapy 4) Consider second-line immunosuppressants (e.g., azathioprine) in refractory cases 5) Supportive care including nutritional support 6) Montelukast or ketotifen may be beneficial in some cases

27. Q: What are the indications for liver transplantation in a child with ascites?

    A: Indications include: 1) Refractory ascites despite optimal medical management 2) Recurrent spontaneous bacterial peritonitis 3) Hepatorenal syndrome 4) Progressive liver failure (elevated PELD/MELD score) 5) Intractable pruritus or recurrent cholangitis in cholestatic liver diseases 6) Hepatopulmonary syndrome or portopulmonary hypertension 7) Failure to thrive despite optimal nutritional support 8) Significant portal hypertension with recurrent variceal bleeding 9) Poor quality of life due to complications of end-stage liver disease

28. Q: How do you manage ascites in a child with Budd-Chiari syndrome?

    A: Management includes: 1) Anticoagulation to prevent further thrombosis 2) Diuretics and sodium restriction for ascites control 3) Consider thrombolysis in acute cases 4) Angioplasty or stenting of hepatic vein stenosis if present 5) TIPS for refractory ascites or failed angioplasty 6) Surgical shunts (e.g., mesoatrial shunt) in selected cases 7) Liver transplantation for end-stage liver disease 8) Investigate and manage underlying prothrombotic conditions 9) Nutritional support and management of complications (e.g., SBP prophylaxis)