Ascites
(Think of CLD, Budd-Chiari, renal failure or heart failure, hypothyroidism, also
malignancy, TB)
Presentation
Sir, this patient has gross ascites.
There is presence of abdominal distension with an everted umbilicus. There is a positive
fluid thrill as well as shifting dullness. This is not associated with any abdominal
tenderness and patient is able to lie flat for the examination. There is also abdominal scar
marks suggesting abdominal tap has been done.
I am unable to palpate the liver and it has a span of 12 cm in the right mid-clavicular line.
The spleen is not palpable or percussible. The kidneys are not ballotable. There are no
other masses palpable in the abdomen.
There are no stigmata of chronic liver disease such as leukochynia, clubbing, palmar
erythema, spider naevi, gynaecomastia or loss of axillary hair. There is also no hepatic
fetor or a hepatic flap. Patient is not jaundice and there is no conjunctival pallor.
There is associated pedal edema up to the knee level with sacral edema but no periorbital
edema. There are no signs of renal failure such as a sallow appearance or uremic fetor.
Patient also does not have any features to suggest hypothyroidism such as a cream and
peaches complexion, macroglossia, hoarseness of voice or bradycardia.
He is not cachexic looking and there are no palpable cervical LNs. He is not toxic
looking.
I would like to complete my examination by
 CVS looking at the JVP with the patient seated 45 degrees to look for raised JVP
with steep x and y descent, early S3 suggestive of constrictive pericarditis
 Urine dipstick for proteinuria
 Temperature chart for fever (TB)
 Rectal examination for a rectal mass
In summary, this patient has got gross ascites that is not associated with any intraabdominal organomegaly or masses of which no apparent cause is found clinically. The
possible differential diagnoses include cirrhosis of the liver, Budd-chiari syndrome,
nephrotic syndrome or protein-losing enteropathy, congestive cardiac failure or intraabdominal malignancy or TB.
Questions
What are the causes of abdominal distention?
 Fat, fluid, flatus, faeces, fetus and organ enlargement
What is ascites?
 Pathologically accumulation of fluid in the peritoneal cavity
How much fluid must be present before there is flank dullness?
 1.5 L of ascitic fluid
How would you approach a patient with ascites clinically?
 Abdominal examination
o Liver
 Look for jaundice, spleen and stigmata of CLD – cirrhosis of liver
 Liver palpable and smooth – think of Budd-chiari
 Liver palpable and hard and nodular – think of malignancy
o Kidneys
 Look for evidence of kidney failure and anasarca
o Look for congestive cardiac failure or constrictive pericarditis
o Look for features of hypothyroidism
o If all above absent, think of
 TB peritonitis
 Intra-abdominal malignancy
 Carcinomatosis peritonei
 Secondaries
o Liver
o Colon
o Ovaries
o Pancreas
What are the causes of ascites?
 Serum ascites albumin gradient >1.1g/dl = portal hypertension (97% accuracy)
o Cirrhosis of the liver
o Budd-Chiari
o CCF
o Constrictive pericarditis
o Malabsorption
o Meig’s syndrome
o Hypothyroidism
 Serum ascites albumin gradient< 1.1g/dl
o Intra-abdominal malignancy
o TB
o Nephrotic syndrome
o Protein losing enteropathy
What is the pathophysiology of ascites in cirrhosis of the liver?
 The chief factor is splanchnic vasodilatation
 Cirrhosis leads to increased resistance to portal flow
 Leading to portal hypertension
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

Portal hypertension results in local production of vasodilators, with splanchnic
arterial vasodilatation
(1) Arterial underfilling
o Early stage – minimal effect on effective arterial volume as can be compensated
by increase in plasma volume and cardiac output
o Later stage
 splanchnic vasodilation so marked that effectve arterial pressure falls and
results in activation of vasoconstrictors and atrial natriuretic factors
 Sodium and fluid retention and expansion of plasma volume contributing
to ascites
 Impaired free water execretion leading to dilutional hyponatraemia
 Renal vasoconstriction with hepatorenal syndrome
(2) Increase in splanchnic capillary pressure with lymph formation exceeding return
therefore ascites
How would you investigate to determine the cause of the ascites?
 (Liver, renal, heart, thyroid, TB)
 Ascitic tap
o Cell count, albumin, and total protein concentration if cirrhosis and dx
 See attached
o Others
 Infection – c/s and g/s AFB
 Malignancy - cytology
o <0.1% of Cx such as hemperitoneum or bowel perforation
o 1% of abdominal wall hematoma
o 2FB cephalad and medial to the ASIS in the left lower quandrant
 Imaging
o USS/CT
 Liver – cirrhosis, budd-chiari
 Renal
o Echo and ECG
o CXR (TB, Pl effusion)
 Bloods
o LFT, Renal, TFT, FBC
How would you manage a patient with ascites secondary to cirrhosis of the liver?
 Treat the underlying cause
 Avoid alcohol or medications that are toxic to liver
 Management of ascites
o General measures
 Salt restriction <2 g/day
 Fluid restriction <1l/day (for ascites, edema with Na <130)
o Specific measures
 Diuretics (Spironolactone, frusemide initially)
 Aim to 0.5kg/day if no peripheral edema
 Aim 1kg/day if presence of peripheral edema also
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
Increase diuretics with spironolactone up to 400mg/d or frusemide
160mg/d
 Paracentesis
 If >5L then requires albumin administration (8g per L of fluid
removed)
 TIPSS (Transjugular Intrahepatic portosystemic shunt)
 High rate of shunt stenosis; up to 75% at 1 year
o Liver transplant
 5 year survival rate for cirrhosis with ascites is 30-40% vs 70-80% for post
liver transplant
 MELD score (Model for End Stage liver disease which has bilirubin,
creatinine and INR)
 Consider for those with refractory ascites, SBP or HRS
Manage other complications of cirrhosis
How do treat and prevent spontaneous bacterial peritonitis?
 Defined as >250 polymorphs per ml of ascitic fluid
 Commonly E coli, Klebsiella and pneumococci
 Translocation of bacteria from intestinal lumen to LNs then bacteremia
 Rule out secondary peritonitis
o Loculated infection or perforated viscus
o Fluid
 >1000 polymorphs
 LDH > upper limit of serum
 Low glucose
 High protein >1 g/L
 CEA > 5ng/ml
 ALP >240u/L
 Treatment
o 3rd generation cephalosporin
o IV albumin to prevent HRS
 Prevention
o Indications
 After 1 episode of SBP as recurrence as high as 70%/year
 In patients with acute variceal bleed
 Ascitic fluid protein concentration<1g/dl (controversial)
o Prophylaxis with ciprofloxacin or norfloxacin
What does development of ascites in a patient with cirrhosis of the liver means?
 Decompensation
 Occurs in 50% of patients within 10 years of diagnosing compensated cirrhosis
 Poor Px
o only 50% survive beyond 2 years
o poor quality of life
o increased risk of infection and renal failure