University of ilorin teaching hospital presentation.

1. Management of Ascites.
Presenter: Dr. Owolabi A.A

2. Outline.
Pre-test
Introduction
Epidemiology
causes
Pathophysiology
Physical examination
Investigation
Summary
Post test
Conclusion

3. Pre-test
Ascitic fluid with total protein>1 g/dL is a high
risk for developing SBP T/F
Serum Ascites Albumin Gradient(SAAG) of
>1.1 is likely of portal hypertension aetiology
T/F
SBP is usually polymicrobial T/F
Bacterascites is the presence of PMN
<250cells/mm3 + +ve culture of a single
organism T/F
Runyon criteria is used to differentiate
Chylous Ascites from SBP T/F

4. Introduction
Ascites is derived from the greek word
“ASKOS” means bag or sac.
Acites means pathologic fluid collection within
the abdominal cavity.
Normal: Females(</=20mls).
The development of ascites is associated with
a poor prognosis and impaired quality of life in
patients with cirrhosis

5. Epidemiology
• Healthy men have little or no intraperitoneal
fluid but women normally have as much as
20ml.
• About 50% of patients with cirrhosis develop
ascites over 10years.
• The prognosis is dependent on the underlying
disorder and the response to treatment.

6. Ascites
Cirrhosis
Peritoneal Malignancy
Heart failure
peritoneal tuberculosis
others

7. Causes
Cirrhosis:Chronic hepatitis , NASH
Nephrotic syndrome
Hypoalbuminemia
Peritonitis(tuberculous, Bacterial, fungal)
Tumors:(Ovary, pancreas, colon,
mesothelioma, psudomyxoma peritonei)

8. • Ascites in heart failure can mimic ascites in
cirrhosis, and the distinction between the two
entities can be challenging.

9. Pathophysiology:
Based on three theories:
• Underfilling
• Overflow
• Peripheral Arterial vasodilation
Portal hypertension occurs as a consequence of
structural changes which involve progressive
collagen deposition within the liver in cirrhosis
and this alters vascular
architecture.(pre,sinusoidal,post)

10. • Underfilling theory: that the primary
abnormality is the pooling of fluid within the
splanchnic vascular bed of the liver due to
portal hypertension
Pooling of blood in liver  ineffective circulatory
systemic blood volume  activation of RAAS
 sodium and water retention.

11. • Peripheral arterial vasodilation: portal
hypertension, causes a compensatory
response of vasodilatation, which causes
decreased effective arterial blood volume.
Portal hypertension  NO2  Vasodilation 
effective areterial blood volume .
• The nitric oxide mediates splanchnic and
peripheral vasodilation.

12. • Overflow: innapropriate retention of sodium
and water by the kidneys in the absence of
fluid depletion.

13. Other factors:
• Other factors that contribute to the
accumulation of fluid in the peritoneal cavity:
– Elevated epinephrine and norepinephrine
– Hypoalbuminemia

14. Gradingclassification
• Uncomplicated
– Grade 1-Mild(only detectable by USS)
– Grade 2-Moderate(moderate symmetrical
abdominal distension)
– Grade 3-Large/tense(Marked abdominal
distension)

15. Clinical Presentation
• History: Abdominal distension: painless or with
abdominal discomfort, course(acute/chronic)
• Aetiology
– Alcohol
– Jaundice
– MSP
– Hepatitis status
– Blood transfusion
– Tattoos/scars/scarification marks
– Long history of Stable cirrhosis
– Gastric malignancy
– Hx of chronic medical illness.

16. Physical findings
• Abdominal distention.
• Peripheral stigmata of CLD
• Obesity/Metabolic syndrome
• Elevated JVP
• SMJ nodule
• Virchows node
Puddle sign Shifting dullness/ fluid wave
~120mls >1500mls

17. Diagnostic paracentesis
• Indications of Diagnostic tap:
– New onset ascites or at time of hospitalization
– To detect presence of cancerous cells
– When there is evidence of clinical
decompensation, such as ?secondary bacterial
peritonitis(SBP) , hepatic encephalopathy,
gastrointestinal hemorrhage, or deterioration of
renal function.
Site: Left lower abdominal quadrat

19. Contraindications
• Absolute : Acute abdomen that requires
surgery
• Relative: Severe thrombocytopenia (platelet
count < 20 x 103cells/mm3, Pregnancy,
Distended Urinary bladder, Abdominal wall
cellulitis

20. Ascitic fluid analysis
• Inspection: Clear, turbid, bloody, green, white
• Albumin concentration: allows calculation of
the serum-ascites albumin gradient (SAAG) to
classify specimens into high- or low-gradient
categories.
• Amylase, LDH and glucose Assay
• Cell count and MCS:Lymphocytes predominate
in tuberculous pertitonitis and carcinomatosis.
• CEA >5ng/ml
• ALP >240u/l

21. • Cytology is 60-90% accurate in malignant
ascites if several hundred ml of fluid is sent
and concentration technique is used but it is
not investigation of choice in HCC.
• Amylase in pancreatic ascites
• Triglyceride in chylous ascites >1000mg/dl
• Bilirubin in post op ascites

22. SAAG
• The SAAG is the best single test for classifying
ascites into portal hypertensive and non-
portal hypertensive causes.
• The accuracy of the SAAG is approximately
97% in classifying ascites
• SAAG= serum albumin – ascitic albumin
• Previously transudate if >25g/L and exudate if
>25g/L of protein up to 30% of cirrhosis will
be exudate if we use protein to categorize.

23. SAAG

24. Chylous Ascites
• Chylous ascites: Turbid, milky or creamy
peritoneal fluid due to the presence of
thoracic or interstitial lymph, shows fat
globules when stained with sudan black
• Has a triglyceride concentration of
>1000mg/dl
• Mostly the result of lymphatic obstruction
from:trauma, tumor, tuberculosis, filariasis,
congenital abnormalities

25. Treatment goals:
• Provide comfort to patient
• Minimize ascitic volume and peripheral edema
• Avoid intravascular volume depletion
• Avoid SBP
• Improve nutrition

26. TREATMENT
• Treatment of the Underlying Disorder
• Cessation of alcohol use is vital to the management of ascites
due to alcoholic liver disease. In one study of hospitalized
patients with Child-Turcotte-Pugh class C cirrhosis due to
severe alcoholic liver disease, 75% of those who remained
abstinent were still alive at 3 years whereas most who
continued to drink alcohol were not.
• Treatment of autoimmune hepatitis and chronic hepatitis B
can also lead to significant clinical improvement and
resolution of ascites in some cases.
• Treatment of ascites in non-hepatic cases should focus on
treatment of the underlying disorder (e.g. treatment of
tuberculosis, treatment of secondary bacterial peritonitis, or
surgical resection of benign ovarian tumor).

27. Treatment-bed rest
• No clinical data to back up the finding that
upright position is asscociated with reduced
GFR and reduced Na excretion and reduced
diuretic efficacy
• Bed rest promote muscle atrophy and other
complications and extends hospital stay
• So bed rest not recommended

28. Treatment
• Sodium restriction and diuretics are the
mainstays of treatment for patients with
ascites due to portal hypertension, but
patients with low SAAG (less than 1.1 g/dL)
ascites do not respond well to these
measures, with the exception of those with
nephrotic syndrome

29. Treatment- salt restriction
• Diet: moderate restriction of salt intake is an
important component in the management of ascites
(4.6-6.9g/day 80-120mmol/day), and there has been no
data to support salt restriction in patients who have
never had ascites.
• ?water: its been found not to be necessary unless
serum sodium is less than 120-125mmol/l.
• Lowers diuretic requirement, faster resolution of
ascites and shorter hospital stay

30. Treatment- water restriction
• No role in uncomplicated ascites
• The downside is water restriction causes increase in the central effective
hypovolaemia- more ADH- more water retention and further dilutional
hyponatraemia.
• So hepatologist including the authors of the BSG guidelines suggest
further plasma expansion to inhibit ADH secretion
• Data emerging supporting use of specific vasopressin 2 receptor
antagonists.

31. Treatment- diuretic
• Patients with grade 2 ascites should receive an
aldosterone antagonist (the diuretics of choice
in management of ascites);
• spironolactone starting at 100mg/day and
increasing stepwise to a maximum of
400mg/day

32. Treatment- diuretic
• Aldosterone antagonist acting in distal tubule to
increase natriuresis and conserve potassium
• Initial dose 100mg and increasing up to 400mg
• Lag of 3-5days
• Better natriuresis and diuresis than a loop diuretic
• Antiandrogenic effect- gynaecomastia- tamoxifen
20mg bd
• Hyperkalaemia frequently limits the use

33. Diuretics

34. Treatment- diuretic
• Frusemide can be added if response is not adequate, or
Hyperkalemia. Starting from a dose of 40mg/day to a
maximum of 160mg/day.
• In patients with recurrent ascites a combination of
Spironolactone and loop diuretics.
• Frusemide has low efficacy in cirrhosis
• Use only if 400mg of spironolactone fails to achieve
weight loss
• Start at 40mg a day and increasing by 40mg every 3rd
day to max of 160mg
• Watch out for metabolic alkalosis and electrolyte
disturbance

35. Treatment- diuretic
• If oedema is present daily weight loss should be 1.5kg per day
and 1g if edema is absent.
• Over diuresis is associated with intravascular volume
depletion, leading to renal impairment, hepatic
encephalopathy and hyponatraemia

36. Refractory Ascites:
• Refractory Ascites:Refractory ascites is an
inadequate response to sodium-restricted diet
and high-dose diuretic treatment (400 mg/day
spironolactone and 160 mg/day furosemide

37. Refractory Ascites
• There are two different subtypes:
• Diuretic-resistant ascites (lack of response to dietary
sodium restriction and intensive diuretic treatment)
• Diuretic-intractable ascites (diuretic-induced
complications such as hepatic encephalopathy, renal
insufficiency, hyponatremia, or hyperkalemia that
prevent optimization of diuretic dosing).
• Early ascites recurrence (within 4 weeks after initial
mobilization) is also considered refractory ascites.
• Excessive sodium intake, bacterial infection, occult
gastrointestinal hemorrhage, and intake nonsteroidal
antiinflammatory drugs should be excluded before
labeling patients as refractory.

38. Controversy regarding normal saline
• Give only if renal function is worsening –
creatinine >150 or 120 and rising
• Gelofusion/Haemaccel/ 4.5% albumin –all
have 153mmol of Na per L
• This will worsen salt retention but better to
have ascites than to develop HRS

39. Tx:Therapeutic paracentesis
• Paracentesis is a procedure in which a needle or
catheter is inserted into the peritoneal cavity to
drain ascitic fluid.
• Once a patient is deemed diuretic resistant,
diuretics should be discontinued, and
management may rely upon serial large volume
therapeutic paracenteses alone.
• Typically, a large volume paracentesis (up to 5 L
removed) performed every 2 weeks should
control ascites in a patient who is compliant with
dietary sodium restriction.

40. Therapeutic paracentesis
• Need for more frequent paracenteses
suggests dietary noncompliance.
• Paracentesis is associated with significant
haemodynamic changes
• Paracentesis-induced circulatory dysfunction,
defined as an increase in plasma renin activity
of more than 50% of the preparacentesis
value to a level of more than 4 ng/mL/h

41. How is paracentesis done?
• Use Z technique- puncture site on the skin does not
overlie the puncture site on peritoneum
• Left flank is preferrable to right flank
• After drain is out patient lie on opposite site
• Colostomy bag if continuous leakage ( some use
purse string suture)
• As rapidly as possible- should not be left overnight
• No upper limit of 8 litres or maximum time of 6
hours has been mentioned in the guidelines

44. TIPSS
• Highly effective treatment
• Complete resolution in 75% of cases
• No effect on survival in one study and reduced on others-
compared with therapeutic paracentesis
• HE occurs in 25% of patients , more if >60yrs
• May precipitate heart failure as increase cardiac preload
• TIPSS should be considered for patients who require frequent
paracentesis ( >3 a month)
• It also shown to resolve hepatic hydrothorax in 60-70%
• MELD was originally developed to predict survival after TIPSS
insertion

46. Peritoneovenous Shunts
(PVS)
• The use of peritoneovenous shunts for
management of ascites has fallen out of favor
due to limited
• long-term patency (less than 20% at 2 years), risk
of complications, and no improvement in survival
compared to medical therapy. It is reserved as
palliative treatment in select patients who are
not candidates for transplantation, TIPS, or serial
therapeutic paracenteses.

48. • Contraindications: The absolute
contraindications to placement of TIPS include
• congestive heart failure (particularly right-sided
heart failure), severe tricuspid regurgitation,
• severe pulmonary hypertension (mean
pulmonary pressure greater than 45 mmHg),
• extensive polycystic liver disease, and
uncontrolled infection or biliary obstruction

49. Cirrhosis liver transplant
Intrahepatic resistance
Portal hypertension  TIPS
Splanchnic/systemic vasodilation
Effective arterial blood volume Albumin
Activation of neurohumoral systems 
Sodium retention spironolactone/fruse
Ascites paracentesis-LVP/ PVS

50. Complications
The absence of the following qualifies ascites as
uncomplicated.
• SBP(fever):
• HRS:The hepatorenal syndrome occurs in patients with
advanced liver failure and portal hypertension. It is a
functional renal failure caused by intrarenal
vasoconstriction resulting from arterial vasodilatation in
the splanchnic circulation and severe reflex activation of
the endogenous vasoconstrictive systems.
Hepatorenal syndrome can be divided into two types:
Type I HRS
Type 2 HRS
Clinical presentation is acute renal failure.

52. Other terms
• Hepatic hydrothorax(-cardiac,pulmonary and
pleural cause)
• SBP: PMN >250cells/mm3 + +ve culture
• Culture negative neutrocytic ascites: PMN
>250cells/mm3 + -ve culture
• Bacterascites: PMN <250cells/mm3 + +ve
culture.
• Polymicrobial Bacterascites: PMN
<250cells/mm3 + +ve polymicrobial culture

53. Risk factors for SBP

54. • Secondary bacterial peritonitis should be suspected when ascitic
fluid analysis shows two or three of the following criteria (Runyon
criteria):
• Total protein more than 1 g/dL
• Glucose less than 50 mg/dL
• LDH more than 225 mU/mL (or more than the upper limit of
normal for serum).
• These criteria were recently validated and shown to have a
sensitivity of 66.6% and specificity of 89.7%.
• When combined with the presence of a polymicrobial ascitic fluid
culture, specificity improved to 95.6%.
• Most of the ascitic fluid cultures in patients with secondary
bacterial peritonitis are polymicrobial, whereas in patients with SBP
the infection is usually monomicrobial

55. Which subgroups of patients with liver disease
should receive prophylaxis against bacterial
infection?
• Gastrointestinal hemorrhage (ceftriaxone 1
g/day or norfloxacin 400 mg twice daily or
ceftri) or
• Prior episodes of SBP (norfloxacin 400
mg/day)
• Low ascitic fluid protein (norfloxacin 400
mg/day) and
• Fulminant hepatic failure (norfloxacin 400
mg/day)

56. Prognosis
• The prognosis for patients with ascites depends
on the underlying disease, the degree of
reversibility of the disease and response to
treatment.
• Ambulatory patients with an episode of cirrhotic
ascites have a 3 year survival rate of 50%.
• Development of refractory ascites has a poor
prognosis with a 1 year survival rate of <50%
• Time for referral to transplant centre as
paracentesis and TIPSS does not improve long
term survival except improving quality of life

57. Pre-test
Ascitic fluid with total protein>1 g/dL is a high
risk for developing SBP T/F
Serum Ascites Albumin Gradient(SAAG) of
>1.1 is likely of portal hypertension aetiology
T/F
SBP is usually polymicrobial T/F
Bacterascites is the presence of PMN
<250cells/mm3 + +ve culture of a single
organism T/F
Runyon criteria is used to differentiate
Chylous Ascites from SBP T/F

58. Conclusion
• Ascites is the most common decompensating
event in cirrhosis

59. References
• Kumar and clark’s clinical medicine, 8th ed.
• Harrison’s principle of internal medicine, 19th ed.
• Angeli P, Fasolato S, Mazza E, et al. Combined versus
sequential diuretic treatment of ascites in non-
azotaemic patients with cirrhosis: results of an open
randomised clinical trial. Gut. 2010;59:98-104.
• Ginès P, Arroyo V, Quintero E, et al. Comparison of
paracentesis and diuretics in the treatment of cirrhotics
with tense ascites. Results of a randomized study.
Gastroenterology 1987;93:234-41.
• Heuman DM, Abou-Assi SG, Habib A, et al. Persistent
ascites and low serum sodium to identify patients with
cirrhosis and low MELD scores who are high risk for
early death.Hepatology. 2004;40