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
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
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 & PGE1deteriorates the renal
fuctionASCITES
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
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 .
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
25.
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
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
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
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
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
Goalwt 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
TbATT
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 ascitesChemotherapy
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.
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 .