CME

2. DEFINITION:
Ascites is the accumulation of excess fluid
in the peritoneal cavity, (there is little
amount of serous fluid normally in the
peritoneal cavity for lubrication & easy
movement of the abdominal organs(.
Ascites is clinically detectable when the
fluid volume exceeds 500 ml,but U/S can
detect smaller volumes.

3. The PATHOGNOMONIC clinical sign of
ascites is shifting dullness on percussion.

4. CLASSIFICATION OF ASCITES;
The new classification system of
ascitesis called (Serum-Ascites Albumin
Gradient/SAAG(has replaced the
Exudatve-Transudative classification.
-SAAG:is of 2 types
1-High(more than 1.1gm/dl(.
2-Low(less than 1.1gm/dl(.
-High SAAG signifies P.H.T.

5. Causes of Ascites:
1-High SAAG;
a.Cirrhosis,around 75 % of ascites.
b.Chronic hep.cong.;ex;R.V.F,Budd
Chiari Synd.,Consrictive pericarditis.
c.Nephrotic Synd.
d.Massive liver metastasis.
e.Myxoedema.
f.Mixed ascites.

6. 2-Low(less than 1.1 gm/dl(;
a. Peritoneal carcinomatosis.
b.Peritoneal TB.
c.Pancreatic &Biliary Disease.
d.Nephrotic Synd.

7. Mechanism of developing Ascites:
It is still debated, but there are two
main theories:
1-Overflow theory.
2-Underflow theory.

8. Overflow theory:
1-P.H.T.
2-Splanchnic vasodilatation.
3-Renal Na & water retention.
All these lead to Overflow of fluids into
the peritoneal cavity.

9. Under flow theory:
Systemic vasodilatation leads to;
Hypovolaemia ,leads to;
Activation of Neuro-Hormonal system
)Renin-Angiotensin-Aldosteron Syst.(
R.A.A.S ,leads to;
Renal Na & water Retention.

10. In other sources it is stated that,
P.H.T.+Low Oncotic pressure+ High
Aldosteron,All together share in
Ascites.
NB;
-PHT due to cirrhosis.
-low oncotic pr.due to low albumin in
impaired liver function.
-High Aldosteron level due to
impaired hepatic metabolism of Ald.

11. Treatment of Ascites:
1-Na restriction to less than 2 gm/day.
2-Fluid restriction esp. if Na less than
125 meq./l.
3-Frusemide;which is eff.in 90% of pt.
Other 10% belong to Refractory
Ascites.
4-Spironolacton)Aldosteron antagonist(

12. Refractory Ascites; is:
1-Persistent Ascites despite use of
maximal daily dose of diuretics)400 mg
spironolacton+160 mg frusemide.
2-or it is the development of Azotaemia
&electrolyte disturbance during sub-
maximal dose of diuretics.

13. Treatment of Refractory Ascites:
1-Repeated large volumes paracentesis.
)L.V.P.(
2-Transjugular Intrahepatic
Portosystemic Shunt.TIPSS.
3-Liver Transplantation.
4-Peritoneo-Venous shunt.
NB;some clinicians prefer to give IV
Albumin 6-8 gms with every Littre of
Ascitic fluid aspirated.

14. Aquaretics:
These are the promising type of diuretics
which have been proved by different
studies to be effective in the treatment of
moderately severe ascites due to liver
cirrhosis.
They act as a vasopressin receptor
antagonists.
By this they will lead to loss of water
strictly without sodium loss. which will
help to avoid hyponatraemia in those
patients.

15. The need for Aquaretics for patients who
have borderline Serum sodium levels of
115-130 meq/l.They reduce the ascites
volume and delay the time of recollection.
Ex. of Aquaretics:
1-SATAVAPTAN.
2-TOLVAPTAN.
They are usually used in combination with
frusemide or spironolacton or both
according to pt.response & need.

16. Thank You!