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Dr Pravakar Sethi 
Diagnostic 
approach to ascites
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.
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
CONT. 
CARDIAC 
Heart failure 
Constrictive pericarditis 
Inferior venacaval web 
INFECTION 
Tuberculosis 
Abscess 
chlamydia 
schistosomiasis
CONT. 
GASTROINTESTINAL 
Infected bowel 
Perforation 
NEOPLASM 
Lymphoma 
Neuroblastoma 
GYNAECOLOGIC 
Ovarian tumor 
ovarian torsion,rupture 
PANCREATIC 
Pancreatitis 
rupture pancreatic duct.
CONT. 
MISCELLANIOUS 
SLE 
Ventriculo peritoneal shunt 
Eosinophillic ascites 
Chyllous ascitis 
Hypothyroidism
Pathophysiology of Ascites 
From: Robbins Basic Pathology
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
Mechanisms 
Underfill theory 
Overfill theory 
Vasodilatation theory
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
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
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
EVALUATION…
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.
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 .
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.
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
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
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
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 .
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
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.
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+
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
After the diagnosis of ascites is made, its cause 
should be determined by laboratory analysis. 
ascitic fluid study 
(diagnostic paracentesis)
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
DIAGNOSTIC PARACENTESIS
CONTRAINDICATIONS 
Severe Coagulopathy 
Abdominal wall hematoma 
Local infecction 
Relative 
Repeated surgeries
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
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
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
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
cytology 
 At least 50 ml of fluid 
 50 – 80% accurate –diagnosis of malignant 
ascites 
 Differentiate malignant cells from atypical 
mesothelial cells
GRAM STAINING/CULTURE 
Gram stain – 10 % sensitive 
--approximately 10,000 bacteria / 
ml are required 
Culture in blood culture bottle 92 % yield
TOTAL PROTEIN 
 Low sensitivity in differentiating exudate 
from transudate. 
 Elevated TP ( ≥2.5 g ) + high SAAG 
hepatic congestion 
 Elevated TP + low SAAG malignancy
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
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
ERRORS IN SAAG 
Timing of collection 
Arterial hypotension 
Chylous ascites 
Serum hyperglobulinemia
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
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
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
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
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
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.
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)
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
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.
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
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.
Cont.. 
Is most often the result of lymphatic 
obstruction from 
Trauma/ surgeries 
Tumor 
Tuberculosis 
 Filariasis 
Congenital abnormalities 
Nephrotic syndrome
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
MUCINOUS ASCITIC FLUID 
Pseudomyxoma peritonei 
Colloid carcinoma of the stomach or colon 
with peritoneal implants.
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
TREATMENT
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
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
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
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
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
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
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
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 .
Theraputic options in refractory ascites 
 Chronic outpatient paracentesis 
 Ascites ultra filtration and re-infusion 
 Le Veen shunt 
 TIPS-(Transjugular Intrahepatic Peritonial Shunt ) 
 Liver transplantation
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.
Transjugular intrahepatic portosystemic shunt 
(TIPS)
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 .
 Current therapeutic strategies include 
repeated large –volume paracentesis with the 
use of plasma expanders and transjugular 
intrahepatic portosystemic shunts
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
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 .
Approach to ascites

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Approach to ascites

  • 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
  • 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
  • 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
  • 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
  • 42.
  • 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 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.
  • 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 .