Approach to a pediatric patient with ascites made simplified with referrence from all standard textbooks

1. Dr Pravakar Sethi
Diagnostic
approach to ascites

2. ASCITES
Askites a Greek word which means ‘bag’ or ‘sac’.
definition
ASITES IS AN ACCUMULATION OF FREE FLUID
WITHIN THE PERITONIAL CAVITY.
In CHILDREN,hepatic,renal,and cardiac disease are the
most common causes.

3. CAUSES OF ASITES
HEPATIC
Cirrhosis
Cong.hepatic fibrosis
Fulminant hepatic failure
Budd-chiari syndrome
Lysomal storage ds.
RENAL
Nephrotic synd.
Obst.uropathy
Perforation of urinary tract
Peritoneal cyst

4. CONT.
CARDIAC
Heart failure
Constrictive pericarditis
Inferior venacaval web
INFECTION
Tuberculosis
Abscess
chlamydia
schistosomiasis

5. CONT.
GASTROINTESTINAL
Infected bowel
Perforation
NEOPLASM
Lymphoma
Neuroblastoma
GYNAECOLOGIC
Ovarian tumor
ovarian torsion,rupture
PANCREATIC
Pancreatitis
rupture pancreatic duct.

6. CONT.
MISCELLANIOUS
SLE
Ventriculo peritoneal shunt
Eosinophillic ascites
Chyllous ascitis
Hypothyroidism

7. Pathophysiology of Ascites
From: Robbins Basic Pathology

8. pathogenesis
 According to starling’s hypothesis the exchange
of fluids between the blood and tissue spaces is
controlled by the balance between two factors;
1. Capillary blood pressure
2. Osmotic pressure of plasma proteins (plasma
colloid osmotic pressure)
 capillary blood pressure / Plasma colloid
osmotic pressure Ascites

9. Mechanisms
Underfill theory
Overfill theory
Vasodilatation theory

10. UNDERFILL THEORY
HYPOVOLAEMIA
Kidney feels  Body is under filled & require more
salt and water
Stimulates JG cell to release RENIN
angiotensinogen  anginsioten-I
in lungs by ACE
Angiotensin II
Releases aldosterone from the zona glomerulosa
Increase the reabsorption of sodium and water &
excretion of potassium from the DCT ASCITES

11. Overfill theory
 The combination of portal hypertension and
circulating hypervolaemia results in ‘over flow’
from the congested portal system to the
peritoneal cavity, to produce ascites
 Decrease in vasodilatory prostaglandins like
PGE2 & PGE1deteriorates the renal
fuctionASCITES

12. NITRIC OXIDE THEORY(PERIPHERAL ARTERIAL
VASODILATATION THEORY)
Most recent theory
When a portal pressure increases above a
critical threshold, nitric oxide levels increase
leading to vasodilatation
 As the state of vasodilatation worsens 
plasma levels of vasoconstrictor, sodium
retentive hormones increase and renal
function deteriorates ASCITES

13. EVALUATION…

14. Evaluation of ascites patient
history
 Age
 child : Tuberculous ascites and nephrosis
 Middle age : cirrhosis of liver
 Old age : malignance
 Sex
 Female : meigs synd., pelvic tumours and infection and
ovarian tumours
 Order of Development of Ascites
 cardiac causes : Leg oedema precedes ascites .
 Kidney causes : Puffiness of face precedes ascites .
 Cirrhosis of liver : Ascites is the first feature .
Ascites is the part of generalised anasarca caused by
nephrosis , anaemia , hypoproteinaemia etc.

15. General examinations
 Enlarged lymph nodes : Suggestive of TB ,
leukaemia , malignancy , and lymphomas .
 Associated jaundice : Cirrhosis of liver .
 Dyspnoea , PND , orthopnoea , and oedema :
congestive cardiac failure .
 Periorbital oedema , puffiness of face and
oedema associated with ascites : acute nephritis
, nephrotic synd.
 Severe anaemia : Ascites of haematologic origin .
 Other signs of malnutrition with ascites :
Kwashiorkor .

16. Systematic examination
Abdominal Examination
Inspection
 Abdomen is distended .
 Umbilicus is everted and slit
transversely(laughing umbilicus)
 The distance between umbilicus and
xiphisternum is more than the distance between
umbilicus and pubic symphysis .
 Flanks are full. Nearly 1500 mL of fluid is required
to make the flanks full .
Veins are dilated over the abdomen .
 Scrotal oedema indicates nephrotic synd.

17. Quantifications of ascites
1+ : Detectable only by careful examinations
2+ : Easily detectable but of relatively small
volume
3+ :obvious ascites but not tense
4+ :Tense ascites

18. Palpation of abdomen
Features Significance
Tenderness and local rise of temperature Peritonitis
Rebound tenderness or Blumberg sign Peritonitis
Doughy or rubbery feel Tuberculous peritonitis
Presence of splenomegaly , ascites , and
caput medusase
Cirrhosis of liver
Enlarged tender liver and ascites Congestive cardiac failure
Palpation of intra-abdominal masses TB
Palpation of lumps and enlarged glands TB, malignancy , leukaemia , and Hodgkin’s
lymphoma

19. Examination of veins over the abdomen
Vein obstructed Site of engorged veins Direction of flow of blood
1. Portal vein obstruction Veins around the umbilicus
and upper abdominal wall
Veins above umbilicus :
bellow upwards . Veins
bellow umbilicus : from
above down words . Veins
around umbilicus is called
caput medusae
2.Hepatic vein obstruction Lower thorax and upper
abdomen
From above downwards
3.Inferior vena cava
obstruction
Lower third of abdominal
wall and flanks
From bellow upwards

20. percussion
 Shifting dullness is an important sign of free
fluid in the peritoneal cavity . It requires nearly
500 mL of fluid to elicit this sign .
 Fluid thrill is present in tense ascites .
 If the fluid is small in amount nearly 120 mL , it
will be demonstrated by puddle sign (lawson’s
sign ) .
Ausculation
 It is not of much use in ascites .

21. Onset of ascites
SUDDEN INSIDIOUS
 Acute Budd- Chiari synd.
 Acute right heart failure
 Sudden decompensation
of previously compensated
cirrhosis
 Pancreatic ascites
 Decompensated cirrhosis
 Chro.Budd-Chiari synd.
 TB ascites
 Nephrotic synd.
 Hypothyroidism
 Constr. pericarditis

22. DEMONSTRATION OF ASCITES
FIVE CLASSICAL PHYSICAL SIGN
1. Bulging flanks  belly of a frog
2. Flank dullness or horse-shoe dullness
3. Shifting dullness  high sensitivity (85%) &
low specificity (50%)
4. Fluid wave / thrill
5. PUDDLE SIGN(Lawson’s sign)-decreased
auscultation of high freqency vibrations in
the central abd.when flicking the side of the
abd.with the patient of hands knees.

23. GRADING OF ASCITES
GRADE SEVERITY SIGNS
1 Mild Puddle signs +
USG abdomen+
2 Moderate Shifting dullness+
No fluid thrill
3 Severe Fluid thrill+
Resp. embarrassment+

24. Minimum amount of fluid required
Test Minimum fluid in ml.
Diagnostic tap
Puddle sign
Shifting dullness
Fluid thrill
Ultrasound scan
CT scan
10-20
120
500
1000-1500
100
100

26. After the diagnosis of ascites is made, its cause
should be determined by laboratory analysis.
ascitic fluid study
(diagnostic paracentesis)

27. DIAGNOSTIC PARACENTESIS
10 to 20 mL
The bladder should be emptied prior to the
procedure
Most common Site left lower quadrant
 Other site
1. In the midline between the pubic-symphysis &
umbilicus,
2. Right iliac fossa, lateral to the inf. epigastric artery
or a few cm above the inguinal lig.
Z-technique

28. DIAGNOSTIC PARACENTESIS

29. CONTRAINDICATIONS
Severe Coagulopathy
Abdominal wall hematoma
Local infecction
Relative
Repeated surgeries

30. complications
1. Infection & peritonitis
2. Bladder or bowel perforation
3. Hypovolaemia & shock (>1 lit. remove
rapidly), especially if the patient does not
have oedema
4. Blockage of needle

31. Tests on Ascitic Fluid
Routine Optional Unusual
Cell count and differential Glucose concentration Tuberculosis smear and
culture, adenosine
deaminase
Albumin concentration LDH concentration Cytology
Total protein concentration Gram stain Triglyceride concentration
Culture in blood culture
bottles
Amylase concentration Bilirubin concentration

32. Colour / appearance of ascitic fluid
Straw coloured
/ Transparent
Bloody fluid Opaque /
milky
Dark -brown Black / tea
colour
normal
Cirrhosis
TB
Malignancies
Trauma
TB peritonitis
Pancreatitis
Perforated
viscus
Traumatic tap
Chylous
ascites
Billiary
ascites
Deep
jaundice
Pancreatic
ascites
(pigment
ascites)
Malignant
melanoma

33. CELL
NORMAL UNCOMPLICAT
ED CIRRHOTIC
ASCITES
SBP IN
CIRRHOTIC
ASCITES
TB ASCITES
WBC count
Cell
RBC
< 250 / cc
Lymphocytic
< 500 / cc
ANC < 250 cells
> 500 / cc
PMN > 250
High
Lymphocytic
predominance
> 50,000 cells
Also in trauma ,
malignancy

34. cytology
 At least 50 ml of fluid
 50 – 80% accurate –diagnosis of malignant
ascites
 Differentiate malignant cells from atypical
mesothelial cells

35. GRAM STAINING/CULTURE
Gram stain – 10 % sensitive
--approximately 10,000 bacteria /
ml are required
Culture in blood culture bottle 92 % yield

36. TOTAL PROTEIN
 Low sensitivity in differentiating exudate
from transudate.
 Elevated TP ( ≥2.5 g ) + high SAAG
hepatic congestion
 Elevated TP + low SAAG malignancy

37. Differences bet. exudative & transudative ascites
Features Exudative ascites Transudative
ascites
Protein in g%
Sp gravity
LDH
Fibronectin
Cholesterol
Hyaluronic acid
ADA
>3 g%
>1015
High
75 mg%--(malignant
ascites)
>48 mg%--(malignant
ascites)
>0.25 mg%
(mesothelioma)
High in TB ascites
<3 g%
<1015
Low
Low
Low
Low
Normal

38. SERUM-ASCITES ALBUMIN GRADIENT (SAAG)
 SAAG= serum albumin – ascitic fluid albumin
 The gradient correlates directly with portal
pressure.
 A gradient > 1.1 g/dL, ascitic is due to portal
hypertension (high gradient or transudative
ascites or portal hyper tensive)
 A gradient < 1.1g/dL (low gradient / exudative or
non potal hyper tensive) suggests that the
ascites is not due to portal hypertension .
 The specificity & sensitivity of SAAG around 97%
 SAAG-Is far superior to the old exudate-transudate
concept .
 SAAG does not explain the pathogenesis of PTN

39. ERRORS IN SAAG
Timing of collection
Arterial hypotension
Chylous ascites
Serum hyperglobulinemia

40. Classification of ascites based on SAAG
SAAG
≥1.1gm/dl
Ascitic protein<3gm/dl
Cirrhosis
Late Budd-chiary synd.
Massive liver metastasis
Ascitic protein ≥3gm/dl
CHF/Constr. Pericarditis
Early Budd-chiary synd.
IVC Obstr.
Sinusoidal obstr. Synd.
≤1.1gm/dl
Biliary Leak
Nephrotic synd.
Pancreatitis
Peritonial carcinomatosis
TB

41. Classification of ascitesbased on SAAG
High-gradient
ascites(SAAG>1.1 gm/dl)
Low gradient ascites(SAAG<1.1
gm/dl)
 Cirrhosis
 Veno-occlusive disease
 Budd-chiari syndrome
 Fulminant hepatic failure
 Cardiac ascites
 Mixed ascites
 Massive liver metastasis
 Tuberculous ascites
 Nephrotic synd.
 Pancreatic ascites
 Chylous ascites
 Biliary ascites
 Serositis in collagen disease
 Peritoneal carcinomatosis
 Postoperative lymphatic leak
 Bowel obstr./infarction

43. X RAY
Non specific
Direct signs
 Elevation of diaphragm
 Diffuse abdominal
haziness
 Bulging of flanks
 Indistinct psoas margins
 Separation of small bowel
loops
 Centralization of floating
bowel
 Hellmer’s sign
 ‘Dog’s ear’ or ‘Mickey
Mouse’
 Medical displacement of
cecum and ascending
colon
 Lateral displacement of
properitoneal fat line

44. USG
 Extreamly sensitive, can detect as little as 100 mL,
 “lollipop”/arcuate appearance of small bowel loops
 Coarse internal echoes blood
 Fine internal echoes chyle
Multiple septa TB , pseudomyxoma peritonei
Matting or clumping of bowel loops, thickning of fluid-wall
interface
 Tethering of bowel along post .abd. wall with loculated
fluid in between malignancy
 Gall bladder thickening cirrhosis

45. CT
 Can differentiate malignant from benign
 Lymph nodes
 Focal liver , spleenic lesions
 Pancreatic and colonic masses
Malignant ascites fills greater & lesser sac
 More useful than USG in detecting hepatic lesions ,
primary or secondary
 Detect up to 100 ml of fluid

46. Complications of ascites
1. Spontaneous bacterial peritonitis ( SBP)
2. Hydrothorax
3. Gastro-oesophageal reflux
4. Respiratory distress and atelectasis due to
elevation of diaphragm
5. Inguinal / umbilical / femoral hernia
6. Scrotal oedema
7. Collection of fluid in the pleural sac
8. Mesenteric venous thrombosis
9. Functional renal failure.

47. Spontaneous bacterial peritonitis
 Characterized by the spontaneous infection of
ascitic fluid in the absence of an intra-abdominal
source of infection
 Prevalence 10-30 %
 Sex  M = F
 Age  Before 6 year age – most common
Most cases occure in children with ascites
nephrotic synd.
cirrhosis
infection.
WBC >250 cells / mm3 (>50 % PMN)

48. Cont…
 Organisim- Pneumococci (most common)
Gr. A strept. , Enterococci , Staph.
Gr. –ve enterobiacteria  E. coli,
Klebsella pneu.
 Involves the translocation of bacteria from the
intestinal lumen to the lymph nodes, with
subsequent bacteremia and infection of ascitic
fluid .
 Third – generation cephalosporins (cefotaxime) +
Aminoglycoside . Duration  10-14 days
 Amoxicicillin + clavulanic acid  also effective
 Vancomycin  resistant pneumococci

49. Sbp recurrence
 70 % probability of recurrence at one year
 Long – term antibiotic prophylaxis with
quinolones reduces the rate of recurrence
 Cotrimoxazole may be an alternative to
quinolones.

50. Complication of sbp
 The most severe is the hepato-renal syndrome,
which occurs in up to 30 % of patients and carries
a high mortality rate
 Intravenous albumin (1.5 gm /kg at diagnosis and
1gm/kg 48 hours later ) helps to prevent the
hepato-renal syndrome and improves the
probability of survival

51. CHYLOUS ASCITES
 Turbid, milky, or creamy peritoneal fluid due to
the presence of thoracic or intestinal lymph.
 Shows staining fat globules with sudan black Oil
red
 Opaque milky fluid usually has a triglyceride
concentration of >1000 mg/dL.

52. Cont..
Is most often the result of lymphatic
obstruction from
Trauma/ surgeries
Tumor
Tuberculosis
 Filariasis
Congenital abnormalities
Nephrotic syndrome

53. PSEUDOCHYLOUS
A turbid fluid due to leukocytes or tumor
cells may be confused with chylous fluid.
TESTS CHYLOUSASCITES PSEUDOCHYLOUS
ASCITES
Fat globules by Sudan red
stain
present absent
Ether test Top thick layer becomes
clear, as fat dissolves in ether
Remains turbid
Alkali test No change in colour Becomes clear , as alkali
dissolves cellular proteins

54. MUCINOUS ASCITIC FLUID
Pseudomyxoma peritonei
Colloid carcinoma of the stomach or colon
with peritoneal implants.

55. Ascitic fluid
study
CIRRHOS
IS
TB PYOGEN
IC
PERITON
ITIS
CCF NEPH.
SYND.
PANCRE.
ASCITES
NEOPLA
SMS
COLOR STRAW /
BILE
STAINED
Clear,
turbid,
hmgic or
chylous
Turbid or
purulent
Straw Straw /
chylous
Turbid ,
hmgic or
chylous
Straw,
Hmgic,ch
ylous,mu
cinous
PROTEIN < 2.5 g/dl >2.5 g/dl < 2.5 g/dl Variable <2.5 g/ dl Variable /
>2.5 g /dl
>2.5 g /dl
Very high
SAAG >1.1 g/dl <1.1 g/dl < 1.1 g/dl >1.1 g /dl <1.1 g /dl <1.1 g /dl <1.1 g/ dl
RBC
( / μl)
>10,000
- 1%
>10,000
- 7%
>10,000
Unusual
>10,000 >10,000
unusual
>10,000
Blood
stain
>10,000
- 20%
WBC
( / μl)
< 250 >1000
lymph
70 %
Definit Δ
periton
ial biopsy
Predom.
Polymorp
hs
Gram
stain +ve
<1000
Usually
mesotheli
al
mononucl
ear
< 250
mesotheli
al or
mononucl
ear
Variable
Increase
am ylase
(>2000 u/
l )
>1000

56. TREATMENT

57. Management of ascites
 GOAL-To achieve ascites-free status
-To maintain it thereafter
INDICATION FOR HOSPITALIZATION
1. If there is no response to outpatient management
for 4-6 weeks.
2. Tense (grade III) ascites with respiratory
embarrassment
3. Spontaneous bacterial peritonitis
4. Diuretic – induced complications like ;
 Hyponatraemia, Na < 125 mEq /L
 Hypokalaemia, K < 3 mEq /L
 Hyperkalaemia, K > 6 mEq /L
 Hepatorenal synd.
 Hepatic encephalopathy
5. Refractory ascites

58. TREATMENT OF HIGH SAAG ASCITES
Bed rest
Salt restriction
Fluid restriction
Diuretics
Therapeutic
paracentesis
Albumin
Peritoneovenous
shunt
TIPS
transplantation
1 gm / D in smallar
children,2 - 3 gm / D in
adolescents.
1000 ml / day
Goalwt loss to prevent renal
failure of prerenal origin is 300-
500 g per day in patients
without peripheral edema and
800 - 1000 g per day in those
with peripheral edema

59. TREATMENT OF LOW SAAG ASCITES
 Peritoneal carcinomatosis therapeutic Paracentesis
 Ovarian tumours  surgery + chemo
 TbATT
 Pancreatic ascites endoscopic stenting, surgery, or
respond to somatostatin , octrotide therapy.
 Lymphatic leak after surgery peritoneovenous
shunting
 Chlamydia peritonitis tetracycline,doxycycline.
 Lupus steroid
 Dialysis related ascites  aggressive dialysis
 Nephrotic syndrome steroid
 Malignant ascitesChemotherapy

60. diuretics
 Are the mainstay of treatment and should be used
liberally but carefully
 All diuretics are best given in a single dose in the
morning- maximizes the compliance
A. Potassium-sparing diuretics
 Aldosterone antagonists
 Spironolactone- DOC in cirrhotic ascites, 1- 6 mg/kg/D
 Carninone, Potassium canrenoate
 Amiloride (10 mg /kg) or triamterene can be used if
spironolactone is not effective
B. Loop diuretics (high-cilling diuretics)
 Furosemide, Torsemide, azosemide, tripamide,
bumetanide, piretanide, Muzolimine, Ethacrynic acid
C. Thiazides –hydroclorothiazide,dose 2- 3 mg / kg/D

61. Response to diuretic theraphy
Relief of abdominal distension
 Relief of respiratory distress
 Decrease in abdominal girth
 Achieving a negative sodium balance (when
sodium excretion is more than intake) indicates a
good diuretic response
Monitoring during diuretic therapy
 Patient should be assessed 1 week after starting
therapy & than every 2 week
Weight & abdominal girth should be measured,
 Look for oedma, grade of ascites and subtle sign of
SBP

62. Therapeutic paracentesis
 Indications
 Tense ascites that causes respiratory embarrassment
 Intractable ascites not responding to the usual
treatment
 To release intra abdominal pressure in moderate to
severe ascites
 Large volume paracentesis, up to 200- 400 ml/
kg/D can be removed slowly over 4 – 6 hours if
the patient has peripheral oedema
 Large volume tap(>5 l) ,I.V. colloid replacement
with albumin 6-8 gm /L
 Dextran 70 is less effective than albumin

63. Criteria for discharge of the ascitic child
1. Adequate weight loss and natriuresis
2. Absence of of infection/peritonitis
3. Absence of diuretic- induced complications

64. REFRACTORY ASCITES
 5 to 10 %
 Defined as a lack of response to high doses of
diuretics (400 mg of spironolactone per day + 160
mg of furosemide per day).
 Patients in whom there are recurrent side effect
(e.g, hepatic encephalopathy , hyponatremia,
hyperkalemia, or azotemia) when lower doses
are given are also considered to have refractory
ascites .

65. Theraputic options in refractory ascites
 Chronic outpatient paracentesis
 Ascites ultra filtration and re-infusion
 Le Veen shunt
 TIPS-(Transjugular Intrahepatic Peritonial Shunt )
 Liver transplantation

66. TIPS(TRANSJUGULAR INTRAHEPATIC
PORTOSYSTEMIC SHUNT)
 TIPS consists of an intrahepatic stent inserted
between one hepatic vein and the portal vein by a
transjugular approach
 Effective in preventing recurrence in patients
with refractory ascites
 Decreases the activity of sodium – retaining
mechanisms and improves the renal response to
diuretics.

67. Transjugular intrahepatic portosystemic shunt
(TIPS)

68. disadvantage
 High rate of shunt stenosis (up to 75 % after 6 to
12 months )
 Lead to recurrence of ascites ;hepatic
encephalopathy
 High cost
 Lack of availability in some centers .

69.  Current therapeutic strategies include
repeated large –volume paracentesis with the
use of plasma expanders and transjugular
intrahepatic portosystemic shunts

70. Peritoneovenous Shunt
Ascitic fluid is shunted from the high pressure peritoneal cavity to
the low pressure superior vena cava by
1 . Le Veenshunt
2 .Denver shunt
3 . Minnesota shunt
Denver Shunt
(Similar to LaVeen Shunt)
Contraindications
•Protein > 4.5 g/l (occlusion)
•Loculated ascites
•Coagulopathy
•Advanced renal/cardiac disease
•GI malignancy
Complications
•Infection
•DIC
•Pulmonary edema
•Pulmonary emboli
•Shunt occlusion
•Malfunction
•Air embolism
•Congestive cardiac failure
•Variceal haemorrhage

71. Prognosis of ascites
 Despite the recent advances in the treatment of
ascites, the prognosis is always grave after
ascites develops in a cirrhotic patient .
Only a change of 40 % being alive 2years later .
 The presence of hepatocellular failure, evidenced
by jaundice and encephalopathy is a very bad
prognostic factor .
 The prognosis may be better if ascites develops
rapidly , especially if there is a well defined
precipitating factor such as GI bleed .