Ascites in Children

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Ascites in Children

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Definition

• ? The word ascites is of Greek origin (askos) and
  means bag or sac.
• ? Ascites describes the condition of pathologic
  fluid collection within the abdominal cavity.
• ? Healthy men have little or no intraperitoneal
  fluid, but women may normally have as much as 20
  mL, depending on the phase of their menstrual
  cycle.

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Etiology of Ascites in Children

• Liver disease Cirrhosis with PHT
• Cardiac Congestive Cardiac Failure
• Renal Nephrotic syndrome
• Peritoneal diseases TB, peritoneal
  carcinomatosis, peritonitis infection
  (perforation), chemical (pancreatitis)
• Hypoproteinemic states PEM, malabsorption
  syndrome, protein losing enteropathy

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Etiology of ascites special type

• Chylous ascites lymphangiectasia,
  post-operative, trauma
• Biliary ascites spontaneous rupture or rupture
  of c. cyst, trauma
• Pancreatic ascites port-traumatic PD disruption
  or following acute or chronic pancreatitis
• Uroascites Obstructive uropathy, trauma

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Grades of ascites

• ? Grade 1 ascites mild, only visible on
  ultrasound.
• ? Grade 2 ascites detectable with flank bulging
  and shifting dullness.
• ? Grade 3 ascites directly visible, confirmed
  with fluid thrill.

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Clinical clues to the etiology

• Ascites with anasarca (periorbital puffiness) and
  oliguria

Nephrotic syndrome
Ascites with breathlessness with engorged neck
veins
CCF/constrictive pericarditis
Ascites with hepatomegaly and tortuous abdominal
wall veins
Budd-Chiari syndrome
Ascites with splenomegaly and shrunken liver
Cirrhosis
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Clinical clues to the etiology

• Ascites with abdominal pain, fever and
  lymph-adenopathy

Abdominal TB
Ascites with pain abdomen, anorexia and
abdominal lump
Malignant ascites
Ascites with diarrhea and unilateral lymphedema
of leg
Chylous ascites
Ascites with abdominal pain and bloody diarrhea
IBD (protein losing enteropathy)
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Diagnosis

• Ascites clinical diagnosis (shifting dullness,
  fluid thrill and puddle sign)
• Mild ascites (doubtful cases) abdominal
  ultrasound (as little as 10-15 ml)
• Plain radiography, CT scan, MRI also detect
  ascites but use only to detect underlying cause
  (like pancreatitis, neoplasm etc.)

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Diagnostic Abdominal Paracentesis

• Confirms the diagnosis and the most important
  investigation to find out the etiology
• Indication all cases of newly diagnosed ascites
  (OPD or in-patient) and in known cases admitted
  with deterioration
• Quick, inexpensive and safe
• Sterile gloves, iodine, disposable needle (22G)
  and LA

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Diagnostic Abdominal Paracentesis

• Complications almost nil (abdominal wall
  hematoma 1 in 100)
• Coagulopathy thrombocytopenia not a
  contraindication (avoided in frank DIC only)
• Samples
• EDTA vial cell counts
• Blood culture bottle (5-10 ml) culture
• Plain vial biochemistry (albumin)

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Diagnostic Abdominal Paracentesis

• Essential investigations TLC/DLC, Albumin, total
  protein and culture
• Optional tests glucose, LDH, amylase, ADA
• Unusual tests cytology, bilirubin, triglyceride
• Unhelpful pH, lactate, cholesterol

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Serum-Ascites Albumin Gradient

• SAAG serum albumin ascitic fluid albumin
  (g/dL)
• High gradient ( 1.1 g/dL) indicates portal
  hypertension with 97 accuracy
• Low gradient (lt 1.1 g/dL) indicates absence of
  PHT with 97 accuracy
• Replaced exudative (gt2.5 g/dL total protein) and
  transudative ascites (poor accuracy of 56)

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Serum-Ascites Albumin Gradient
High gradient
Low gradient

• Cirrhosis
• Budd-Chiari synd.
• Veno-occlusive disease
• Cardiac ascites
• Myxedema

• Tuberculosis
• Malignant
• Nephrotic synd.
• Pancreatic ascites
• Biliary ascites
• Chylous ascites

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Interpretation of ascitic fluid analysis
Etiology SAAG Other tests
Tuberculosis Low TLCgt500 (lympho), ADA
Malignancy Low Cytology
Pancreatic Low Amylase gt100 (gt5 times)
Biliary Low Bilirubin gt6 (gt serum)
Chylous Low Triglyceride gt200(gtserum)
Nephrotic Low Total protein lt2.5g/dL
Cirrhosis High Total protein lt2.5g/dL
Cardiac High Total protein gt2.5g/dL
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Ascitic fluid infection (10-27)
On the basis of neutrophil count culture

• Spontaneous bacterial peritonitis (SBP)
• Monomicrobial non-neutrocytic bacterascites (MNB)
• Culture-negative neutrocytic ascites (CNNA)
• Secondary bacterial peritonitis
• Polymicrobial bacterascites (PB)

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Ascitic fluid infection
Diagnosis PMN Culture Other
SBP 250 Positive No surgical cause
CNNA 250 Negative No antibiotics
MNB lt 250 Positive No surgical cause
Secondary 250 Polymicro Surgical cause
PB (bowel aspirate) lt 250 Polymicro No surgical cause
Secondary infection proteingt1g/dL,
glucoselt50mg/dl, LDHgt225U/L
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Ascitic fluid infection
Diagnosis Organism Antibiotics Duration
SBP Single E.coli/ Kleb/ pneumo Cefotaxime 5 days
CNNA - do do
MNB Single E.coli/ Kleb/ pneumo do do
Secondary Multiple ve, -ve, anaerobes Cefo, Amika, Metro Surgery
PB (bowel aspirate) Multiple ve, -ve, anaerobes - -
Prevention low fluid protein (lt1g/dL), previous
SBP, variceal bleed Oral Norfloxacillin od
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Treatment of ascites High gradient

• Salt restriction sodium 2 mEq/kg/day (max.
  2g88 mEq/day) 1g table salt17mEq Na
• Diuretics Spironolactone (2- 6mg/k/day)
  Furosemide (2.51 ratio, once daily)

• Therapeutic Paracentesis (LVPgt50ml/kg)
• TIPS transjugular intrahepatic porto-
• systemic shunt
• Liver transplantation

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Treatment of ascites Diuretics

• Spironolactone T1/2 24h, 5 days to reach steady
  state (slow acting), more than once daily dose is
  unnecessary
• Site distal convoluted tubules k sparing
• Furosemide Short T1/2 (100 min), fast acting,
  loop of Henle, k losing
• Combination synergistic, two different sites,
  counter-balance electrolytes, fast response
• Ratio 100mg sprio 40mg fruse or 2.5 1

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Treatment of ascites Diuretics

• Efficacy of diuretics combo therapy 90
• Target weight loss
• - Without edema 1 of body weight (max.
  500g/d)
• - With edema as much as possible
• Compliance check 24h urine Na (gt78 mEq/d with
  2g salt/d) or urine Na/K ratio (gt1)

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Treatment of ascites High gradient

• Mild to moderate ascites Salt restriction and
  diuretics
• Tense ascites Therapeutic paracentesis followed
  by diuretics and salt restriction

• Therapeutic Paracentesis Large volume
• paracentesis (gt50ml/kg) or single total
• paracentesis, speed quickly (up to 4L/h)
• Albumin infusion Not compulsory

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Treatment of ascites Albumin

• Paracentesis induced circulatory dysfunction
  asymptomatic change in electrolytes, plasma renin
  creatinine. No increase in morbidity or
  mortality
• Can be prevented with albumin replacement (10g/L
  of fluid removed), ½ at the end ½ after 6h of
  paracentesis
• Albumin infusions increase degradation, decrease
  synthesis of albumin and cost
• Up to 5L No, gt5L albumin as optional

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Treatment of ascites Low gradient

• Nephrotic syndrome Diuretics useful
• Other causes No role of diuretics, treatment of
  etiology like TB,CCF, pancreatitis etc.

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Refractory Ascites

• ? The term Refractory Ascites was introduced in
  the 1950s as a general term defining ascites that
  could not be satisfactorily managed by medical
  therapy.
• ? A proposed definition of Refractory Ascites is
  ascites that cannot be mobilized or the early
  recurrence of which (ie, after therapeutic
  paracenteses) cannot be satisfactorily prevented
  by medical therapy.

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Types of Refractory Ascites

• ? Diuretic-Resistant Ascites Failure of
  mobilization or the early recurrence of ascites
  which cannot be prevented because of a lack of
  response to sodium restriction and diuretic
  treatment.
• ? Diuretic-Intractable Ascites Failure of
  mobilization or the early recurrence of ascites
  which cannot be prevented because of the
  development of diuretic-induced complications.

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• ? Treatment duration Patients must be on
  intensive diuretic therapy (spironolactone 400
  mg/day and furosemide 160 mg/day) for at least 1
  wk and on a salt-restricted diet of less than 90
  mmol/day.
• ? Lack of response Mean weight loss of less than
  0.8 kg over 4 day and urinary sodium output less
  than the sodium intake.

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• ? Early ascites recurrence There is a
  reappearance of grade 2 or 3 ascites (clinically
  detectable) within 4 week of initial
  mobilization.
• ? However, it is important to notice that in
  patients with severe peripheral edema,
  reaccumulation of ascites within 2-3 days of
  paracentesis must not be considered as early
  ascites recurrence because it represents a shift
  of interstitial fluid to the intraperitoneal
  space.

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• ? Diuretic-induced complications
  Diuretic-induced HE is the development of
  encephalopathy in the absence of any other
  precipitating factor.
• ? Diuretic-induced renal impairment is indicated
  by an increase of serum creatinine by gt 100 to a
  value of gt 2 mg/dL in patients with ascites
  otherwise responding to treatment.

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• ? Diuretic-induced hyponatremia is defined as a
  decrease of serum sodium by gt 10 mEq/L to serum
  sodium of lt 125 mEq/L.
• ? Diuretic-induced hypo- or hyperkalemia is
  defined as a change in serum potassium to lt 3
  mEq/L or gt 6 mEq/L despite appropriate measures.

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Conclusions

• Ascites clinical diagnosis, elaborate
  investigations (AXR, USG, CT) not required
• Diagnostic paracentesis
• The best in finding etiology
• Coagulopathy/thrombocytopenia not a
  contraindication
• Basic tests cell count (EDTA), albumin/TP,
  culture (blood c/s bottle)
• SAAG replaced exudate/transudate, 97 accuracy
  in differentiating PHT vs non-PHT

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Conclusions

• Ascites fluid infection (SBP) PMN 250 c/s
  positivity, Cefotaxime for 5 days.
• Treatment of ascites
• Salt restriction (2 mEq/kg/day of Na)
• Diuretics combination of spironolactone
  frusemide at 2.5 1 ratio
• Therapeutic paracentesis
• No restriction of volume or speed of removal
• Albumin replacement optional

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