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ASCITES
INTRODUCTION:
Ascites is abnormal collection of free fluid in the peritoneal cavity.
The term ascites is from greek origin ‘askos’ meaning bag or bladder.

Diagnostic features of Ascites:

1.Uniform distension of abdomen
2.Flanks full (500ml)
Shifting dullness (1000ml)
Fluid thrill =massive ascites
Other associated features:
Everted umbilicus,
umbilical hernia,
Divarication of recti,
Inguinal or epigastric hernia

Note:Absence of shifting dullness or fluid thrill or absence of both does not exclude the presence of
ascites.

Dullness in ascites
Moderate Ascites- Flanks are dull
Large ascites (500ml)- Horse shoe shaped dullness
Flanks and hypogastric regions are dull
Massive Ascites- Whole of the abdomen is dull except for a small area over the umbilical region.

Puddles sign: to detect small volume of ascetic fluid 100ml.

Method to elicit: Patient is put in knee elbow position, keeping the diaphragm of stethoscope over the
most dependent part of abdomen, flick on the flank repeatedly and lightly.
Diaphragm of stethoscope is moved gradually to the other flank.A change in the intensity and character
of the note indicates fluid.
Shifting dullness: to be elicitable requires minimum of 1000 ml of free fluid
Fluid thrill _elicitable in massive ascites

Mechanism of shifting dullness:

The ascitic fluid will flow to the most dependent portion of the abdomen,
the air filled intestine will float on top of this liquid.
The technique of shifting dullness makes use of this relationship to detect the presence of ascitic fluid.

Symptoms of ascites
Increasing abdominal girth.
Shortness of breath because of elevation of diaphragm-dypnea /orthopnea
Reflux esophagitis causing heartburn
Secondary effects of ascites:
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1.Pleural effusion Rt side:

due to defect in diaphragm allowing ascetic fluid to pass into pleural space
2.IVC obstruction:
When massive ascites presses on IVC-can lead to pedal edema
3.Distended neck veins
Elevated Rt.atrial pressure following tense ascites raising the diaphragm

COMMON CAUSES OF ASCITES

Hepatic cirrhosis
Malignant diseases (hepatic,peritoneal)
Cardiac failure
TB abdomen

LEARNING POINTS :
 Ascites is a sign of ‘decompesated ‘liver
 500ml of fluid should be present before before flank dullness is detected.
 Difficult to make out dulness in obese abdomen-diagnose by USG.
 USG can detect as little as 100 ml of fluid in peritoneum
 In ovarian masses characteristically flanks are resonant
 Ascites developing in stable chronic cirrhosis,super imposed Hepatoma to be suspected.
 Malignancy related ascites-painful
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HISTORY IN ASCITES
Chronic alcoholism
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Other Liver diseases risks-transfusion,parenteral therapy,tattoos,accupuncture

h/o alcoholic cardiomyopathy
h/o heart disease
H/o cancer- breast ,colon ,pancratic,gastric
H/o abdominal pain-malignancy related ascites,pancreatitis,infection
h/o fever ,abdominal pain-TB abdomen
h/oDM-nephrotic ascites
h/o connective tissue disease-polyserositis
h/o hypothyroidism

CLINICAL EXAMINATION
General examination: look for
Stigmata of liver disease-spider nevi,palmar erythema,jaundice,
Raised JVP,anemia,pedal edema
Virchow’s node-rt supraclavicular region
Firm umbilical nodule-Sister Mary Joseph’s nodule
Examination of abdomen
Inspection: •contour of abdomen, •movements of abdominal wall,
•Skin streched and shiny, odema of skin, •striae, •dilated veins, •position,
•shape of umbilicus(smiling umbilicus), •herniae(umbilical,epigastric)
•Transmitted pulsation in ca.stomach,,
Palpation
•Tenderness, •Rigidity,
•lump- intra abdominal/on abdominal wall •site,size,shape,surface edges
•Direction of blood flow in distended veins •viscera-liver,spleen,gall bladder,kidney
•Hernial orifices
Percussion: •Shifting dullness,fluid thrill,puddles sign
Auscul tation: •Hepatic rub, •bruit
GRADING OF ASCITES
GR1+: ONLY ON CAREFUL EXAM
GR 2: E ASILY DETECTABLE BY SMALL VOLUME
GR 3: OBVIOUS ASCITES BUT NOT TENSE
GR 4: TENSE ASCITES
ASCITES DISPROPOTIONATE TO EDEMA: CODITIONS CAUSING
1. CIRRHOSIS OF LIVER
2. CONSTRICTIVE PERICARDITIS
3. RESTRICTIVE CARDIOMYOPATHY
4. HEPATIC VENOUS OCCLUSION
5.T UBERCULOUS PERITONITIS
6.INTRA ABDOMINAL TUMOR

INVESTIGATIONS :
1.USG ABDOMEN-Confirms ascites
2.CT Abdomen
3.Peritoneoscopy
3.LAPROSCOPY and peritoneal biopsy if undiagnosed
4.Diagnostic PARACENTESIS
5.Other routine:
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TC,DC,ESR,Xray chest,abdomen
6.Liver function tests
7.Liver biopsy-in cirrhosis/malignancy of liver
8.investigations for diagnosis of portal hypertension

Differences between transudate and exudate

Features Transudate Exudate
Appearance Clear Turbid,hemorrhagic,straw
coloured
Specific gravity Less than 1016 More than1016
Proteins Less than30gms /L More than 30gms/Litre
Serum ascetic fluid albumin >1.1/dl <1.1/dl
gradient
Total cell count low high
Differential count Mesothelial cells/lymphocytes Polymorphs.lymphocytes/RBCs

ASCITIC FLUID ANALYSIS :

Points to note:
1.Gross appearance
2.Biochemical analysis
3.Microbiological with cytology

Gross appearance
transudate
exudate
cloudy –a. Infection-raised polymorphs>5000/mm3
b. purulent if >50000 cells/mm3
c. milky-chylus TGL->200mg /dl;clears on adding ether
d.Deep yellow colour-If bilirubin increased
bile stained also when there is bile duct perforation
Blood stained fluid-RBC more than10 thousand/mm 3

Cell count
WBC >denotes inflammation/malignancy
Mainly polymorphs-Bacterial infection/SBP
In SBP->250cells/mm3 diagnostic
But in surgical peritonitis>10 thosand cells/mm 3
Lymphocyte predominance in TB peritonitis
In malignancy cell type variable;in 20% RBC and also malignant cells seen.

Biochemical analysis
Proteins >3gms/dl in exudates
SAAB-Serum albumin minus ascetic fluid albumin
Less than1.1 in exudates

More than 1.1 in transudate

SAAB is is more useful (diuresis can affect total ascetic protein concentration)
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Glucose- reduced or 0- in infected ascites

(Because it is consumed by bacteria and WBC)
Low glucose but normal cell count means intestinal contents aspiration
Enzymes-LDH normally less than 50% of serum value
In bacterial infection LDH more than serum value
It is produced by lysed WBCs.
Amylase-raised in pancreatic disease
Normal 250-1000 somayagi units per day
Bacterial tests
Gram stain-in centrifuged specimens positive in severe infection only.
SBP-not positive because count is low
Culture if done specimen must be sent to the lab immeadiately.
AFB-often negative
Cytology for malignant cells
Positive only if peritoneum is directly involved

COMPLICATIONS OF ASCITES
1. Spontaneous bacterial peritonitis:
Suspect In cirrhosis with ascites, going for fever, abdominal pain ,ileus ,hypotension, encephalopathy
Ascitic fluid PMN cell count->250/mm3
Culture positive-enterobacter, strept.pneumonia, S.viridans
Treament-Cefatoxime
2.Hepato renal syndrome
Progressive renal failure
Spontaneous or precipitated by diuresis, paracentesis, bleeding, or drugs.
?due to altered renal hemodynamics

Differential diagnosis for distension of abdomen

Fluid/Fat/flatus/foetus/Tumor in the abdominal cavity.

differential diagnosis of causes of ascites

1.Cirrhosis of liver:
.Signs of liver cell failure
signs of portal hypertension
Ascitic fluid-transudate

2.Tuberculous peritonitis
Doughy abdomen
Matted omentum and loops of intestine
Multiple palpable masses
Confirmation: peritoneal biopsy shows tuberculous granuloma

3.Bacterial peritonitis
Signs of septicemia with ascites
and a focus of infection like indwelling catheter.

4.Malignant Ascites:
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Primary-stomach,colon,ovary,or other intra abdominal tumors,

Sister Joseph nodules in umbilicus
5.Pancreatic ascites
H/o acute abdominal pain radiating to the back
In chronic pancreatitis fluid leaks from the pseudo pancreatic cyst
Serum amylase raised
Ascitic amylase>1000Iu/L
Diagnosis:ERCP

6.Constrictive Pericarditis
Pulsus paradoxus;kussmauls sign
Hepatomegaly with ascites
Pericardial knock
Calcific pericardium

7.Portal vein thrombosis

Sudden rapid development of –ascites,splenomegaly,hemetemesis and melena

8.Hepatic vein thrombosis

Large tender liver
Absent hepatojugular reflux

9.Nephrotic syndrome
Initial puffiness of face
Massive protenuria
Hypercholestrolemia

MANAGEMENT
1.daily weight chart ,IO chart,
2.Fluid restriction -1500ml/day
3.Salt restriction2gms per day –most important initial step
4.Diuretics indicated in
Gross ascites,tense ascites,before biopsy,scan or venogram
Drugs used
Spiranolactone25mg qid,increase to maximum of 400mg/day.
Frusemide20-40mg in divided doses (may combine with spiranolactone)
Amiloride10mg/day ±frusemide/thiazide
5.Paracentesis in severe distension causing respiratory distress
6.Peritoneal shunt in intractable ascites
7. Salt free Albumin infusion
8. Treatment of the cause.
KEY TAKE HOME MESSAGE
1.Assessment of SAAG helps to determine if diuretics are likely to help.
SAAG of >1.1gm/dl is associated with portal hypertension
2.About diuretic therapy
 Avoid postural hypotension or fatgue from diuretic tmt which
is likely to produce falls ;that is worse than having ascites
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3. Abstinence from alcohol

As a First step in treatment –convince patients to abstain from alcohol
Abstinence of few months greatly improves reversible component of ascites.

REFRACTORY ASCITES
Types:
I. Diuretic resistant ascites
II. Diuretic intractable ascites
Definition
I. Diuretic resistant ascites
Lack of response to high dose of diuretic i.e.
-400mg/day of spiranolactone and 160 mg/day of frusemide
-while remaining compliant with low sodium diet of 50-mmolsodium per day
- and lack of response with weight loss of less than200gm/day
This requires an observation period of weeks to ensure diuretic resistance.
Recent study shows single dose of 80 mg of IV frusemide and subsequent random
- urine sodium of less than 50mmol/l is indicates refractory ascites

II. Diueretic-intractable ascites

Development of diuretic –induced complication like severe electrolyte disturbance,
Renal impairement,hepatic encephalopathy precluding the use of an effective diuretic dose.
(put in simple terms patient who cannot tolerate diuretics because of side effects)

Conditions contributing to refractory ascites

1. Active inflammation
2. Portal or hepatic vein thrombosis
3. GI bleed
4. Infection
5. Spontaneous bacterial peritonitis
6. Malnutrition
7. Hepatoma
8. Super imposed cardiac and renal disease.
9. Hepato toxic and nephrotoxic drugs

Prognosis poor

Treatment
I. Large volume paracentesis
Removal of 5 litre or more of ascetic fluid
Total paracentesis –removal of all ascetic fluid also can be done (20L or more)
Complications of large volume paracentesis
Electrolyte imbalance ,raised serum creatinine
Spplemental Albumin infusion required
5gm albumin per each Litre above 5L tapped
Alternative to albumin – “Terlipressin”-avoids exposing patient to blood product
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II. TIPS (trans jugular intrahepatic porto systemic stent shunt)

Effective in decreasing ascetic fluid reaccumulation
A flexible metal prosthesis is used to connect a branch of hepatic vein to portal vein thus reducing
sinusoidal pressure
Demerit:
increased risk of hepatic encephalopathy.
Frequent TIPS occlusion demands careful follow up

III. Peritonio venous shunt (Nearly Abandoned therapy )

A surgically inserted tube connects peritoneal cavity to superior vena cava
Tube courses subcutaneously
Allows only one way passage of ascetic fluid to SVC and so back into circulation
Demerits
Tecchnical problems like blockage of tube and others)

IV. Recent research

Aquaretics-Vasopressin receptor antagonist

Promote excretion of electrolyte free water
Useful in patients with ascites and hyponatremia
Not yet approved by FDA
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