Ascites in Pediatric Age: Complete Case Discussion & Key Points
Model Case Presentation
Patient Demographics
Name: Master Rohan, Age: 7 years, Gender: Male, Informant: Mother (Reliable)
Chief Complaints
- Progressive abdominal distension – 3 months
- Swelling of both legs – 1 month
- Yellowish discoloration of eyes – 2 months
History Summary
Child was apparently well until 3 months ago when parents noticed progressive abdominal swelling. Swelling started around the umbilicus and gradually extended to involve the whole abdomen. Associated with decreased urine output and passage of dark-colored urine. Pedal edema appeared 1 month ago. History of jaundice 8 months ago (treated at local hospital). No history of hematemesis or melena currently. Appetite reduced; significant weight loss. Constipation present. No fever currently.
Antenatal period normal. Delivered at term via NVD. Immunization up to date. No similar illness in siblings. No family history of liver disease.
Examination Summary
| Parameter | Finding | Significance |
|---|---|---|
| Weight | 18 kg (expected 22 kg) | Weight loss / wasting |
| PR | 96/min | Mild tachycardia |
| BP | 90/60 mmHg | Low (circulatory compromise) |
| Jaundice | Present (2+) | Hepatocellular dysfunction |
| Pallor | Present (2+) | Chronic disease / hypersplenism |
| Cyanosis | Absent | — |
| Pedal edema | Bilateral, pitting (2+) | Hypoalbuminemia / portal HTN |
| Clubbing | Grade 2 | Chronic liver disease |
Abdomen: Grossly distended, flanks full. Umbilicus everted. Dilated tortuous veins over anterior abdominal wall (caput medusae). Dull note in flanks with shifting dullness positive. Fluid thrill present. Liver — 4 cm palpable below right costal margin, hard, nodular edge, non-tender. Spleen — 5 cm palpable below left costal margin. Dipping technique used. Hernial orifices normal.
Other systems: Palmar erythema. Spider angiomata (3) on anterior chest wall. Leukonychia (white nails). Parotid enlargement. No asterixis. CNS — alert, oriented.
✅ Complete Diagnosis
Chronic Liver Disease (likely Post-Hepatitic Cirrhosis — Hepatitis B/C) with Portal Hypertension, presenting as Ascites with Bilateral Pedal Edema, Hepatosplenomegaly, and Signs of Hepatocellular Failure (jaundice, spider angiomata, palmar erythema, leukonychia).
📝 History — Exam Q&A
Ascites is the pathological accumulation of free fluid in the peritoneal cavity. The word is derived from the Greek "askhos" meaning "bag" or "sack." Normally, the peritoneal cavity contains only 10–20 mL of serous fluid for lubrication. Clinically detectable ascites requires >500 mL of fluid; shifting dullness requires >1500 mL.
| Age Group | Common Causes |
|---|---|
| Neonates | Hydrops fetalis, bile/urine ascites (urinary tract obstruction, bladder perforation), intestinal perforation, congenital infections (CMV, toxoplasma), chylous ascites |
| Infants | Biliary atresia, congenital hepatic fibrosis, nephrotic syndrome, congestive heart failure, storage disorders (Gaucher, Niemann-Pick) |
| Older Children (school age) | Cirrhosis (post-hepatitic, Wilson disease, autoimmune hepatitis, alpha-1 antitrypsin deficiency), nephrotic syndrome, malignancy (lymphoma, Wilms tumor), constrictive pericarditis, tuberculosis |
| Adolescents | Same as older children + Budd-Chiari syndrome, SLE |
💡 Exam Tip
The most common cause of ascites in children overall is hepatic disease (cirrhosis/liver failure), followed by renal disease (nephrotic syndrome), and then cardiac disease (constrictive pericarditis, CCF).
Presenting complaints:
- Progressive abdominal distension — onset, duration, progression
- Pedal edema — bilateral/unilateral, pitting/non-pitting
- Decreased urine output (oliguria → suggests hypoalbuminemia or renal cause)
- Breathing difficulty (diaphragm elevation in massive ascites)
Etiological clues:
- Jaundice history — duration, color of urine/stools (hepatic cause)
- Hematemesis/melena — portal hypertension with variceal bleed
- Frothy urine — nephrotic syndrome
- Prolonged fever, weight loss, lymphadenopathy — TB, malignancy
- Joint pains, rash — SLE
- Blood transfusion history — Hepatitis B/C
- Drug/toxin exposure — drug-induced hepatitis
Family history: Wilson disease, alpha-1 antitrypsin deficiency, Budd-Chiari (hypercoagulable states)
- No facial puffiness on waking — Rules out nephrotic syndrome (nephrotic edema is worse in mornings)
- No frothy urine — Against significant proteinuria/nephrotic syndrome
- No exertional dyspnea/orthopnea — Against cardiac cause
- No cough, evening fever, contact with Koch's — Against tubercular peritonitis
- No pain abdomen — Cirrhotic ascites is usually painless; malignant ascites may be painful
- No polyuria/polydipsia — Against diabetes (rare cause of liver disease in children)
| Feature | Nephrotic Syndrome | Cirrhosis |
|---|---|---|
| Onset of edema | Periorbital/facial first (morning worse) | Pedal first (evening worse) |
| Urine | Frothy, reduced output | Dark (jaundice), normal or reduced output |
| Jaundice | Absent | Usually present |
| Abdominal veins | Absent | Caput medusae (portal HTN) |
| Organomegaly | Absent or mild hepatomegaly | Hepatosplenomegaly |
| Malnutrition | Mild | Marked |
Chylous ascites results from accumulation of chyle (lymphatic fluid rich in triglycerides) in the peritoneal cavity due to disruption of the lymphatic system.
Causes in children:
- Congenital lymphatic malformations (most common in neonates)
- Post-surgical (after abdominal/retroperitoneal surgery)
- Trauma to the thoracic duct
- Malignancy (lymphoma causing lymphatic obstruction)
- Tuberculosis (lymph node obstruction)
- Intestinal lymphangiectasia
Clue on aspiration: Ascitic fluid is milky white; triglycerides >200 mg/dL (usually >1000 mg/dL).
The most accepted theory is the "Peripheral Arterial Vasodilation Hypothesis":
- Portal hypertension → increased sinusoidal pressure → local release of vasodilators (notably nitric oxide)
- Splanchnic vasodilatation → effective arterial blood volume decreases
- Compensatory activation of RAAS, sympathetic nervous system, and ADH → sodium and water retention
- Hypoalbuminemia (reduced hepatic synthesis) → decreased plasma oncotic pressure
- Combined effect: fluid transudates from splanchnic capillaries into peritoneal cavity → ascites
💡 Key Concept
Sodium retention (not water retention) is the primary driver. Hence, sodium restriction is more important than fluid restriction in management.
🩺 Examination — Exam Q&A
Inspection:
- Generalized abdominal distension (fullness in all quadrants)
- Fullness/bulging of flanks
- Everted (smiling/inverted) umbilicus
- Dilated anterior abdominal veins (caput medusae)
- Tense, shiny skin with stretched striae
- Hernias: umbilical, inguinal, incisional (increased intra-abdominal pressure)
Percussion:
- Dull note in flanks (flanks dull to percussion)
- Shifting dullness — positive (83% sensitive, 56% specific; needs >1500 mL fluid)
Palpation:
- Fluid thrill — positive in massive ascites (needs >3000–4000 mL)
- Dipping technique for organ palpation in tense ascites
Technique:
- Patient supine. Percuss from umbilicus to left flank — note transition from tympanic (center) to dull (flank).
- Keep finger at the dullness-tympany transition point.
- Ask patient to turn to right lateral decubitus; wait 30–60 seconds.
- Repeat percussion at the same point — if dullness shifts to tympany, shifting dullness is positive.
Principle: Free fluid gravitates to the dependent side; the gas-filled bowel floats to the top. The transition point shifts accordingly.
Significance: Positive shifting dullness confirms free fluid in the peritoneal cavity. Minimum 1500 mL required.
The puddle sign detects minimal ascites (120–150 mL) — smallest amount detectable clinically.
Technique: Patient is in knee-elbow position. Examiner flicks one flank gently and auscultates over the dependent umbilical area — a "ripple" sound indicates free fluid pooling. The sound changes in intensity as the examiner moves the stethoscope away from the umbilicus.
Use: Detection of small-volume ascites not detectable by shifting dullness or fluid thrill.
💡 Sensitivity Comparison
Puddle sign: ~120–150 mL | Shifting dullness: ~1500 mL | Fluid thrill: ~3000–4000 mL | Ultrasound: ~100 mL
| System | Signs |
|---|---|
| Hands | Palmar erythema, Leukonychia (white nails), Clubbing, Dupuytren's contracture (adults), Asterixis (flapping tremor — hepatic encephalopathy) |
| Face | Jaundice, Parotid enlargement, Fetor hepaticus (musty/sweet smell), Spider telangiectasias on malar area |
| Trunk/Skin | Spider angiomata (upper body), Gynecomastia (males), Caput medusae, Loss of body hair, Scratch marks (pruritis) |
| Eyes | Kayser-Fleischer rings (Wilson disease), Jaundice |
| Lower limbs | Pedal edema, Testicular atrophy (males) |
💡 Spider Angioma
A spider angioma consists of a central arteriole with radiating vessels. On pressing the center, it blanches completely and refills from the center. More than 5 spider angiomata is pathological. They occur above the nipple line (distribution of SVC) due to estrogen excess.
Technique (Empty vein test): Place two fingers on the vein, slide them apart to empty the segment. Release one finger and observe from which end the vein fills — that is the direction of flow. Repeat by releasing the other finger.
| Flow Direction | Cause |
|---|---|
| Away from umbilicus (upward above, downward below) — Caput medusae | Portal hypertension (obliterated umbilical vein recanalization) |
| Upward (all veins) | IVC obstruction (Budd-Chiari) |
| Downward (all veins) | SVC obstruction |
In tense ascites, normal palpation fails to feel organomegaly because fluid interposes between the examining hand and the organ. The dipping/ballottement technique is used instead:
Place fingers over the area of organ, then give a quick short pressure (dip) — this displaces the fluid momentarily and the organ "floats up" to meet the fingertips, which is felt as a distinct tap (ballottement). Used especially to palpate the liver and spleen in tense ascites.
| Feature | Ascites | Gaseous Distension | Large Mass (e.g., Wilms tumor) | Obesity |
|---|---|---|---|---|
| Flanks | Full, bulging | Not full | Asymmetric fullness | Full |
| Umbilicus | Everted | Normal/everted | May be displaced | Deep/inverted |
| Percussion | Flanks dull, center tympanic | Uniformly tympanic | Solid dullness localized | Normal |
| Shifting dullness | Positive | Negative | Negative | Negative |
| Fluid thrill | Positive (massive) | Negative | Negative | Can be positive (fat thrill) |
💡 Obese child
In obese children, a false fluid thrill may be transmitted through fat. To differentiate, an assistant places the edge of the hand firmly in the midline to prevent fat wave transmission — the true fluid thrill persists in ascites but disappears in obesity.
🔬 Investigations — Exam Q&A
Abdominal Ultrasonography is the most useful bedside investigation. It can:
- Detect as little as 100 mL of ascitic fluid (vs 500 mL clinically)
- Confirm free fluid in peritoneal cavity (echogenic floating debris, layering)
- Assess liver texture (nodular = cirrhosis), liver size
- Assess portal vein diameter (>12 mm = portal hypertension)
- Demonstrate splenomegaly
- Guide safe paracentesis (loculated fluid)
- Detect hepatocellular carcinoma or mass lesions
CT/MRI abdomen: For localizing small amounts, detecting malignancies, and evaluating portal/hepatic veins (Budd-Chiari).
SAAG = Serum albumin − Ascitic fluid albumin (both measured on the same day)
| SAAG | Category | Causes |
|---|---|---|
| ≥ 1.1 g/dL (High) | Portal hypertension | Cirrhosis, Budd-Chiari, Congestive heart failure, Constrictive pericarditis, Portal vein thrombosis |
| < 1.1 g/dL (Low) | Non-portal hypertension | Nephrotic syndrome, Tuberculosis, Malignancy, Pancreatitis, Chylous ascites, Protein-losing enteropathy |
💡 SAAG vs Old Transudate/Exudate Classification
SAAG has replaced the old transudative/exudative classification for ascites (based on total protein). SAAG is superior because it is based on oncotic-hydrostatic balance, reflecting portal pressure. Its accuracy is ~97% for diagnosing portal hypertension.
| Test | Normal/Interpretation |
|---|---|
| Appearance | Straw-colored (transudate); turbid/cloudy (infection/inflammatory); milky (chylous); bloody (trauma/malignancy) |
| Total protein | <2.5 g/dL = transudate; >2.5 g/dL = exudate (old classification) |
| Albumin (for SAAG) | See SAAG interpretation above |
| Cell count and differential | PMN count >250 cells/mm³ = Spontaneous Bacterial Peritonitis (SBP) |
| Gram stain and culture | Inoculate into blood culture bottles at bedside; identifies organism in SBP |
| Glucose | Low (<50 mg/dL) = SBP, secondary peritonitis, TB |
| LDH | Elevated in malignancy and secondary peritonitis |
| Triglycerides | >200 mg/dL (usually >1000 mg/dL) = Chylous ascites |
| Cytology | Malignant cells in peritoneal carcinomatosis/lymphoma |
| AFB smear + culture | Tubercular peritonitis (culture is gold standard but takes weeks) |
SBP is the infection of ascitic fluid without an identifiable intra-abdominal source (i.e., no perforation or adjacent abscess).
Diagnostic criterion: Ascitic fluid PMN count >250 cells/mm³
Clinical features: Fever, abdominal pain/tenderness, altered mental status (encephalopathy), unexplained clinical deterioration. Up to 13% may be asymptomatic.
Organisms: Gram-negative (E. coli — 50%, Klebsiella), Gram-positive (Streptococcus, Staphylococcus). Almost always monomicrobial (polymicrobial infection suggests perforation).
Culture-negative neutrocytic ascites: PMN >250/mm³ but culture negative — treat as SBP.
🚨 Important Distinction
SBP = PMN >250/mm³ + single organism (or culture negative). Secondary bacterial peritonitis = PMN >250/mm³ + polymicrobial + total protein >1 g/dL + glucose <50 mg/dL + LDH above normal → requires CT/surgery.
Baseline: CBC (anemia, thrombocytopenia from hypersplenism), LFT (bilirubin, AST, ALT, ALP, albumin, globulin), PT/INR (synthetic function), serum electrolytes, BUN/creatinine (hepatorenal syndrome), blood sugar.
Etiological: HBsAg, Anti-HCV, Ceruloplasmin + serum copper + 24-hr urinary copper (Wilson disease), Alpha-1 antitrypsin level, ANA + Anti-dsDNA (SLE, autoimmune hepatitis), Anti-smooth muscle antibody (AIH), urine protein (nephrotic), throat culture/ASO titre (post-streptococcal), serum ferritin (metabolic liver disease).
Imaging: USG abdomen with Doppler (portal vein, hepatic veins), Chest X-ray (pleural effusion, cardiomegaly).
The International Club of Ascites (ICA) classifies ascites into three grades:
| Grade | Description | Detection |
|---|---|---|
| Grade 1 (Mild) | Minimal ascites — only detectable on ultrasound | USG only |
| Grade 2 (Moderate) | Moderate, symmetric distension of abdomen | Clinical (shifting dullness +) |
| Grade 3 (Tense/Large) | Marked distension, tense abdomen | Clinical (fluid thrill +) |
Refractory ascites: Ascites that does not respond to maximum doses of diuretics (spironolactone 400 mg/day + furosemide 160 mg/day in adults) — requires large-volume paracentesis or TIPS.
- Appearance: Straw-colored or turbid, sometimes hemorrhagic
- SAAG: <1.1 g/dL (low — exudative, non-portal hypertensive)
- Total protein: >2.5 g/dL (exudate)
- Cell count: Lymphocytic pleocytosis (lymphocytes predominant)
- Glucose: Low
- Adenosine deaminase (ADA): >30–40 U/L — sensitive marker for TB peritonitis
- AFB smear: Low sensitivity (~0–5%). Culture: Gold standard but slow (weeks).
- Peritoneal biopsy: Caseating granulomas — highest diagnostic yield
- Laparoscopy: "Millet seed" white nodules on peritoneum
💊 Management — Exam Q&A
- Treat the underlying cause — Antiviral therapy for hepatitis B/C, steroids for autoimmune hepatitis, D-penicillamine/zinc for Wilson disease, antituberculous therapy for TB peritonitis
- Sodium restriction — 1–2 mEq/kg/day (no added salt diet) — more important than fluid restriction
- Fluid restriction — Only if serum sodium <125 mEq/L
- Diuretic therapy — Spironolactone ± Furosemide
- Large-volume paracentesis — For tense/refractory ascites
- Nutritional support — High-protein, high-calorie diet
- Treat complications — SBP, hepatic encephalopathy, hepatorenal syndrome
- Liver transplantation — Definitive treatment for end-stage liver disease
| Drug | Dose (Children) | Mechanism | Notes |
|---|---|---|---|
| Spironolactone | 1–3 mg/kg/day (max 200 mg/day) | Aldosterone antagonist → Na excretion in distal tubule | First-line; preferred as hyperaldosteronism drives Na retention in cirrhosis |
| Furosemide | 1–2 mg/kg/day (max 80 mg/day) | Loop diuretic → blocks Na-K-2Cl cotransporter | Added to spironolactone for inadequate response |
Ratio in adults: Spironolactone:Furosemide = 100 mg:40 mg (5:2 ratio maintains normokalemia). In children, adjust by weight.
Goal: Weight loss of 0.5 kg/day (with edema), 0.25 kg/day (without peripheral edema) to avoid dehydration and precipitating hepatorenal syndrome.
🚨 Monitor
Monitor serum electrolytes, creatinine, urine output regularly. Diuretics must be stopped if serum Na <120 mEq/L, serum creatinine rises significantly, or hepatic encephalopathy worsens.
Therapeutic paracentesis is the removal of large volumes of ascitic fluid via needle or catheter to relieve symptoms.
Indications:
- Tense (Grade 3) ascites causing respiratory distress or discomfort
- Refractory ascites not responding to maximum diuretics
- Rapidly accumulating ascites
Preferred site: Left lower quadrant — 2 finger-breadths medial and cephalad to the anterior superior iliac spine. Avoids epigastric arteries and cecum (right side risk).
Albumin replacement (Large Volume Paracentesis >5L in adults): 6–8 g of albumin IV per liter of ascitic fluid removed beyond 5 L — prevents post-paracentesis circulatory dysfunction (PPCD). In children: 1 g/kg IV albumin if removing large volumes.
Contraindications: Coagulopathy (relative), bowel obstruction, skin infection at site.
Empirical Antibiotic Therapy (start immediately on diagnosis — PMN >250/mm³):
- First-line: IV Cefotaxime 50 mg/kg/day 8-hourly (children) OR IV Ceftriaxone for 5–7 days
- For nosocomial/hospital-acquired SBP or prior antibiotic exposure: Piperacillin-tazobactam ± meropenem
Albumin infusion: 1.5 g/kg at diagnosis, 1 g/kg at 48 hours — significantly reduces incidence of hepatorenal syndrome and decreases mortality (Sort et al., NEJM 1999).
Assess response: Repeat paracentesis at 48 hours — PMN should decrease by >25%. If not → consider secondary peritonitis/resistant organism.
Long-term secondary prophylaxis: Norfloxacin 400 mg/day (adults) or Co-trimoxazole in children — SBP recurs in 50–70% within 1 year without prophylaxis.
- Spontaneous Bacterial Peritonitis (SBP) — most common serious complication; mortality 20–30%
- Hepatorenal Syndrome (HRS) — functional renal failure in cirrhosis; type 1 (acute) and type 2 (chronic)
- Hepatic Hydrothorax — ascitic fluid tracks through diaphragmatic defects into the pleural cavity (usually right-sided)
- Hyponatremia — dilutional (free water retention); poor prognosis marker
- Abdominal hernias — umbilical, inguinal (increased intra-abdominal pressure)
- Respiratory distress — diaphragm elevation in massive ascites
- Malnutrition — early satiety, anorexia from abdominal distension
- Protein loss — repeated paracentesis leads to protein depletion
HRS is a functional, potentially reversible form of acute kidney injury occurring in advanced cirrhosis with ascites, in the absence of structural kidney disease. It results from intense renal vasoconstriction secondary to splanchnic vasodilation and decreased effective circulating volume.
| Feature | HRS Type 1 (HRS-AKI) | HRS Type 2 (HRS-CKD) |
|---|---|---|
| Onset | Rapid (<2 weeks) | Gradual |
| Prognosis | Very poor (weeks) | Better (months) |
| Trigger | Often SBP, bleed, large-volume paracentesis | Refractory ascites |
| Creatinine | Doubles to >2.5 mg/dL | Moderate, stable rise |
Treatment: Terlipressin + albumin (preferred); norepinephrine + albumin; liver transplant (definitive).
- Post-large-volume paracentesis: 6–8 g per liter removed (>5 L) — prevents post-paracentesis circulatory dysfunction
- SBP treatment: 1.5 g/kg at diagnosis + 1 g/kg at 48 hours — reduces HRS and mortality
- Spontaneous prophylaxis against SBP: Long-term albumin infusions in high-risk cirrhosis (recent trial ANSWER study — showed reduction in complications)
- HRS management: Combined with terlipressin (vasopressin analogue) for HRS-AKI
🔭 Recent Advances — Exam Q&A
TIPS is a radiologically placed stent between the portal vein and hepatic vein within the liver, creating a direct portosystemic shunt that reduces portal hypertension.
Indications for TIPS in ascites:
- Refractory ascites (not responding to maximum diuretic therapy)
- Recurrent large-volume paracentesis requirement (>2–3 per month)
- Hepatic hydrothorax refractory to diuretics
- Bridge to liver transplantation
Contraindications: Severe hepatic encephalopathy, advanced heart failure, severe hepatic dysfunction (Child-Pugh >11, bilirubin >3 mg/dL), hepatic vein obstruction (Budd-Chiari — relative).
Complications: Hepatic encephalopathy (most common), shunt dysfunction/stenosis, heart failure.
Note: TIPS is used less frequently in children than adults but is performed in select pediatric cases at specialized centers.
- Rifaximin: Non-absorbable antibiotic — reduces gut bacterial translocation, emerging as an alternative/adjunct to quinolone prophylaxis; may reduce risk of SBP and hepatic encephalopathy
- Leucocyte esterase dipstick test on ascitic fluid: Rapid bedside test for SBP diagnosis — results in minutes (vs hours for cell count); reduces time to antibiotic therapy
- Ascitic calprotectin: Novel biomarker; correlates with PMN count and may allow rapid non-laboratory SBP screening
- Long-term albumin infusions (ANSWER trial, 2018): Monthly albumin infusions in cirrhotic patients reduced complications including SBP, hospitalizations, and mortality
Liver transplantation is the definitive treatment for end-stage liver disease with refractory ascites in children. All children with cirrhosis and ascites should be referred for transplant evaluation, as the development of ascites marks the onset of decompensated cirrhosis.
Common indications in children: Biliary atresia (most common pediatric liver transplant indication), Wilson disease, Alagille syndrome, autoimmune hepatitis, alpha-1 antitrypsin deficiency, metabolic liver diseases.
PELD score (Pediatric End-stage Liver Disease): Used to prioritize children under 12 years on the transplant waiting list (analogous to MELD in adults). Parameters: albumin, bilirubin, INR, growth failure, age <1 year.
Living donor liver transplantation (LDLT): Common in India and Asia due to shortage of deceased donors; uses a portion of a living related donor's liver.
IPCs (e.g., PleurX catheter) allow repeated drainage of ascitic fluid at home without repeated hospital visits. They consist of a tunneled catheter placed into the peritoneal cavity.
Indication: Reserved for malignant ascites (e.g., peritoneal carcinomatosis, intra-abdominal lymphoma) where repeated large-volume paracentesis is required and no curative treatment exists.
NOT recommended for cirrhotic ascites — high risk of infection, protein depletion, and mortality in this group. Serial large-volume paracentesis (every 2 weeks) is preferred for cirrhotic refractory ascites.
Non-invasive tools to assess liver fibrosis have reduced the need for liver biopsy:
- Transient elastography (FibroScan): Measures liver stiffness (kPa). Values >12.5 kPa suggest cirrhosis. Also correlates with portal pressure; liver stiffness measurement (LSM) >20–25 kPa strongly predicts development of ascites.
- Acoustic Radiation Force Impulse (ARFI)/shear wave elastography: Ultrasound-based; useful in children due to absence of radiation.
- Serum fibrosis panels: APRI (AST-to-Platelet Ratio Index), FIB-4 score — easy to calculate from routine blood tests.
These tools help identify patients at high risk of developing ascites who require closer follow-up and early intervention.
⚡ Key Points — Quick Revision
One-Liners for Exam
- Definition: Pathological fluid accumulation in peritoneal cavity
- Most common cause in children: Hepatic disease (cirrhosis/CLD)
- Causes mnemonic (3 H's): Hepatic, Heart (CCF, constrictive pericarditis), Hypoproteinemia (nephrotic, malnutrition)
- Minimum fluid for shifting dullness: 1500 mL | Fluid thrill: 3000–4000 mL | Puddle sign: 120–150 mL | USG: 100 mL
- Gold standard investigation: Diagnostic paracentesis + SAAG
- SAAG ≥1.1: Portal hypertension (cirrhosis, CCF, Budd-Chiari) | SAAG <1.1: Non-portal HTN (nephrotic, TB, malignancy)
- SAAG supersedes old transudate/exudate classification
- SBP diagnosis: Ascitic PMN >250 cells/mm³ (monomicrobial)
- SBP treatment: IV Cefotaxime/Ceftriaxone + Albumin infusion
- Polymicrobial SBP: Think secondary peritonitis (perforation) → CT abdomen
- First-line diuretic for ascites: Spironolactone (aldosterone antagonist)
- Pathophysiology: Peripheral arterial vasodilation hypothesis — splanchnic vasodilation → RAAS activation → Na retention
- Sodium restriction is more important than fluid restriction (unless Na <125 mEq/L)
- Chylous ascites: Triglycerides >200 mg/dL in fluid; milky appearance
- TB ascites: SAAG <1.1, lymphocytic exudate, ADA >30–40 U/L
- Caput medusae: Dilated veins radiating from umbilicus — portal HTN (flow away from umbilicus)
- Hepatorenal syndrome: Functional AKI in cirrhosis — Terlipressin + Albumin
- TIPS: Used for refractory ascites (reduces portal pressure)
- Definitive treatment: Liver transplantation (PELD score used in children <12 years)
- Large volume paracentesis >5L: Replace albumin 6–8 g/L removed
- Dipping technique: Used to palpate organs in tense ascites
- Caput medusae flow direction: Away from umbilicus (contrast IVC obstruction — all flow upward)
🚨 Must-Know Comparisons
- Cirrhotic ascites: Painless, SAAG ≥1.1, straw-colored, PMN <250, low protein
- Malignant ascites: May be painful/hemorrhagic, SAAG <1.1, high LDH, positive cytology
- TB peritonitis: SAAG <1.1, lymphocytic exudate, ADA elevated, peritoneal biopsy (granulomas)
- Nephrotic ascites: SAAG <1.1, massive proteinuria, periorbital edema, low albumin
- Cardiac ascites: SAAG ≥1.1, high total protein (>2.5 g/dL — exception to rule), JVD present