Ascites by_ Dr Mohammed Hussien

How to deal with Case of Ascites ( Etiology ..Diagnosis..Management)... By ..Mohammed Hussien

1. Ascites
Dr Mohammed Hussien
Assistant Lecturer of Hepatology & Gastroentrology
Kafrelsheik University

2. What is Ascites ?
•Ascites is the presence of excess fluid in the peritoneal cavity.
•It is a common clinical finding with a wide range of causes, but
develops most frequently as a part of the decompensation of
previously asymptomatic chronic liver disease.

3. 3
Cirrhotic
ascites
75%
Non cirrhotic
ascites
20%
Mixed ascites
5%
Etiology of
ascites

4. •Ascites occurs in 50% of patients within 10 years of
diagnosis of compensated cirrhosis.

• It is a poor prognostic indicator, with a 50% 2-year
survival.

• Worsening significantly to 20 - 50% at 1 year when the
ascites becomes refractory to medical therapy.

5. Mechanism of ascites
formation

6. A)Incresased hydrostatic
pressure
•Cirrhosis
•Hepatic vein occlusion (Budd- Chiari
syndrome)
•Inferior vena cava obstruction
•Constrictive pericarditis
•Congestive heart failure

7. B) Decreased colloid osmotic pressure
•End-stage liver disease with poor protein
synthesis
•Nephrotic syndrome with protein loss
•Malnutrition
•Protein-losing enteropathy
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8. C) Increased permeability of peritoneal
capillaries
•Tuberculous peritonitis
•Bacterial peritonitis
•Malignant disease of the peritoneum

9. D) Leakage of fluid into the
peritoneal
cavity
•Bile ascites
•Pancreatic ascites
•Chylous ascites
•Urine ascites

10. E) Miscellaneous causes
•Myxedema
•Ovarian disease (Meigs' syndrome)
•Chronic hemodialysis

11. Pathogenesis of
ascites in cirrhosis

12. 2004
cirrhosiscirrhosis
Hemodynamic changesHemodynamic changes . .
VC
substances
VD
substances
Favoring VD
Systemic & splanchnic VD
Decrease effective circulating
blood volume
Imbalance

13. Perceived hypovolemia activates
various VC systems
↑ RAAS , SNS , ADH
Renal VC
renal Na &
water
reabsorption
Decrease
in GFR
Ascites
Decrease in effective circulating
blood volume
↓oncotic pressure

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SNSSNS
RASRAS
ADHADH
SNSSNS
RASRAS
ADHADH
KidneyKidney
R perfusionR perfusion
& GFR& GFR
R perfusionR perfusion
& GFR& GFR
Ability toAbility to
Exc. SodExc. Sod
Ability toAbility to
Exc. SodExc. Sod
Ability toAbility to
Exc. waterExc. water
Ability toAbility to
Exc. waterExc. water
HRSHRSHRSHRS
AscitesAscitesAscitesAscites
DilutionalDilutional
HyponatHyponat
““Sod<130Sod<130””
DilutionalDilutional
HyponatHyponat
““Sod<130Sod<130””
Renal Dysfunction in CirrhosisRenal Dysfunction in Cirrhosis

15. Commonest causes
(90% of cases(
•Cirrhosis (Cirrhotic Ascites)
•Cancer (Malignant Ascites)
•Congestive Heart Failure
•Mycobacterium tuberculosis

16. Clinical Manifestations and
Diagnosis

17. Symptoms
•Small amount of ascites
•Asymptomatic
•Large amount of ascites
•Abdominal distention and discomfort
•Anorexia
•Nausea
•Early satiety
•Heartburn (Gastroesophageal Reflux)
•Flank pain
•Respiratory distress

18. Signs

•Umbilicus may evert
•Bulging flanks with patient lying supine
•Weight of ascitic fluid pushes against side walls
•Tympany at the top of the abdominal curve
•Patient lies supine
•Gas filled bowel floats upward over ascites
•Fluid Wave Test
•Shifting Dullness Test
•Puddle Sign

19. Grades of ascites
•Grade 1 :–
Mild ascites detectable only by ultrasound
examination
•Grade 2:
Moderate ascites manifested by moderate
symmetrical distension of the abdomen
•Grade 3 :
Large or gross ascites with marked abdominal
distension

20. Ultrasonography
•Ultrasound is probably the most cost-
effective
modality.
•It involves no radiation or intravenous
access, &
no risk of contrast allergy or nephropathy.
• If a computed tomographic (CT) scan is
performed, ascites is easily seen
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21. •Ultrasound findings in patients with portal
hypertension may include :
- may reveal evidence of a nodular liver.
- dilation of the portal vein to ≥13 mm,
- dilation of the splenic and superior
mesenteric
veins to ≥ 11 mm,
- reduction in portal venous blood flow velocity,
splenomegaly (diameter >12 cm), and
recanalization of the umbilical vein.
- may reveal evidence of hepatocellular
carcinoma

22. Analysis of
Ascitic Fluid

23. Investigations
Peritoneal fluid analysis
Peritoneal fluid Cell and
differential PMN count
Gram stain
Direct inoculation in
routine blood culture
bottles
Other studies of ascitic fluid Other studies of ascitic fluid

to be consideredto be consideredCytologyCytology
LactateLactate
pHpH

24. Calculated by subtracting the albumim
concentration of the ascitic fluid from
the albumin concentration of a serum
specimen obtained on the same day.

25. Serum Ascites Albumin
Gradient (SAAG(

26. SAAG
•It is the best single test for classifying ascites into portal
hypertensive (SAAG
>1.1 g /dL) and non–portal hypertensive (SAAG <1.1
g /dL) causes.
•Calculated by subtracting the ascitic fluid albumin value
from the serum albumin value,
•It correlates directly with portal pressure.
•The accuracy is approximately 97% .

27. •This phenomenon is the result of Starling's
forces between the fluid of the circulatory
system and ascetic fluid.
•Under normal circumstances the SAAG
is < 1.1 because serum oncotic pressure
(pulling fluid back into circulation) is exactly
counterbalanced by the serum hydrostatic
pressure (which pushes fluid out of the
circulatory system).

28. •This balance is disturbed in certain diseases
(such as the Budd-Chiari syndrome , heart
failure, or liver cirrhosis) that increase the
hydrostatic pressure in the circulatory
system.
•The increase in hydrostatic pressure causes
more fluid to leave the circulation into the
peritoneal space (ascites).

29. •The SAAG subsequently increases because
there is more free fluid leaving the
circulation, diluting the albumin in the
ascitic fluid.
•The albumin does not move across
membrane spaces easily because it is a
large molecule.
DR.Mohammed Hussien
29

30. 2004
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SAAG
Helpful diagnostically, as well as Helpful diagnostically, as well as
therapeutically in decision makingtherapeutically in decision making
Low SAAG
>1.1
High SAAG
<1.1
Non –portal
hypertensive cases
Portal hypertensive
cases
Does not respond to salt
restriction nor Diuretics
Respond to salt
restriction & Diuretics

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high-albumin high-albumin
gradientgradient
> 1.1g/dl> 1.1g/dl
low-albumin low-albumin
gradientgradient
< < 1.11.1 g/dlg/dl
TransudativeTransudative ExudativeExudative
Terms should be replaced

33. Types of ascites according to
SAAG
High Gradient
) < or = 1.1 g/dl)PHT
Portal vein thrombosis
Cirrhosis
Cardiac Failure
Budd Chiari syndrome
Alcoholic hepatitis
Fulminant hepatic failure
Massive hepatic metastasis
Fatty liver of pregnancy
Myxedema
Mixed ascites
Low Gradient
) > 1.1 g/dl(
Non PHT
Peritoneal Carcinomatosis
Pancreatic ascites
Biliary ascites
Peritoneal Tuberculosis
Nephrotic Syndrome
Serositis
Bowel obstruction or
infarction
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34. High gradient
( SAAG > 1.1(
•A high gradient (> 1.1 g/dL) indicates that ascites
is due to portal hypertension with 97% accuracy.
•This is due to increased hydrostatic pressure
within the blood vessels of the hepatic portal
system, which in turn forces water into the
peritoneal cavity but leaves proteins such as
albumin within the vasculature.
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35. Important causes of high SAAG ascites (>
1.1 g/dL) include:
- High protein in ascitic fluid (> 2.5(:
Heart failure & Budd Chiari syndrome
- Low protein in ascitic fluid (< 2.5(:
- Liver cirrhosis

36. Low gradient
( SAAG <1.1)
•Indicates causes of ascites not associated
with increased portal pressure.
•Examples include :
  - Tuberculosis
- Pancreatitis . 
- Nephrotic syndrome
•Various types of peritoneal cancer.

37. 2. The amylase concentration
which is elevated in
pancreatic ascites.

3. The triglyceride concentration
which is elevated is chylous
ascites.

38. 4. White cell count :
- When greater than 250/microliter is
suggestive of infection.
- If most cells are PMNLs , bacterial
infection should be suspected.
- When mononuclear cells predominated
tuberculosis or fungal infection is likely.

39. 5.Red cell count :
•When greater than 50.000/microliter
denotes hemorrhagic ascites, which usually
is due to :
- malignancy
- tuberculosis
- Pancreatitis
- or trauma.

40. 6.Gram stain and culture :
which can confirm the diagnosis of
bacterial infection.
7.pH :
when less than 7 suggests bacterial infection
8.Cytology :
can be positive in malignancy.

41. Ascites Fluid: Cell Count with
Differential
RBCs elevated
• Malignant ascites
•Tuberculous peritonitis

•Pancreatitis
WBC elevated
>1000
•Neoplasm (>50%
Lymphocytes)
•TB peritonitis (>70%
Lymphocytes)
•Bacterial peritonitis
(WBC > 10,000)
•Spontaneous Bacterial
Peritonitis (PMN > 250)

42. Management
of ascites

43. 2016
43
Treatment ofTreatment of
ascitesascites
Bed restBed rest
Water restriction
Diuretics
Refractory ascites
Reversible CausesReversible Causes
Na+ restriction

44. Role of bed rest
no controlled trials to support this practice.
Upright posture may aggravate plasma renin
Bed rest may lead to muscle atrophy, stasis, and extended hospital stay.
Bed rest is NOT recommended for treatment of ascites.
Low Sodium diet
Sodium restriction has been associated with lower diuretic requirement, faster
resolution of ascites, and shorter hospitalization.
But, it is less palatable and may further worsen the malnutrition.
when given a choice, most patients would prefer to take some diuretics and have a
more liberal sodium intake than take no pills and have a more severe sodium
restriction.

45. Spironolactone
•aldosterone antagonist, acting mainly on the distal tubules
as Potassium-sparing diuretic (inhibit Na+ re-absorption
and K+ excretion).
•It is the drug of choice in the initial treatment.
• There is a lag of 3–5 days between the beginning of
treatment and the onset of the natriuretic effect
•Side effects are those related to its anti-androgenic
activity, such as decreased libido, impotence, and
gynaecomastia in men and menstrual irregularity in women

46. Frusemide
•Frusemide is a loop diuretic that generally used as an
adjunct to spironolactone
• it inhibit re-absorption of Na+/K+/2Cl- in the ascending
limb of the loop of Henle.
•High doses of frusemide are associated with severe
electrolyte disturbance and metabolic alkalosis, and should
be used cautiously.

47. Other diuretics
•Amiloride and triamterene act on the distal
tubule. It blocks Na reabsorption and induces
diuresis in 80% of patients at doses of 15–30
mg/day. It is less effective compared with
spironolactone.
•Bumetanide is similar to frusemide in its action
and efficacy

48. Single or combination therapy
•The initial combination treatment shortens the time to
mobilization of moderate to tense ascites and better for
inpatient treatment.
•So it is preferred approach in achieving rapid natriuresis
and maintaining normokalemia.
•An alternative approach would be to start with
Spironolactone, in particular in the outpatient setting,
then monitoring the patient for adding loop diuretics
after 400mg Spironolactone failure.

49. Dosage
•The doses of both oral diuretics can be
increased simultaneously every 3-5 days
(maintaining the 100 mg:40 mg ratio) if weight
loss and natriuresis are inadequate.
•This ratio maintains normo-kalemia.
•Usual maximum doses are 400 mg/day of
spironolactone and 160 mg/day of furosemide
•Over diuresis is associated with intravascular
volume depletion leading to renal impairment,
hepatic encephalopathy, and hyponatraemia.

50. Therapeutic Paracentesis
•Although initially the recommendation was to
perform daily 5-L paracentesis until the
disappearance of ascites, it was subsequently
determined that total paracentesis (i.e.,
removal of all ascites in a single procedure
accompanied by the concomitant infusion of 6–
8 g albumin per liter of ascites removed) was
as safe as repeated partial paracenteses

51. LVP
•LVP associated with i.v. plasma expander is effective and
associated with a significantly faster resolution and a lower
rate of complications than repeated paracentesis with
intensive diuretics.
•However, it is a local therapy (does not act on the mechanisms
of ascites formation) and ascites recurrence is the rule.
•Additionally, it is more costly and requires more resources than
the administration of diuretics.

52. Use of plasma expanders
•Paracentesis of <5 L of uncomplicated ascites does not
require volume expansion
• Plasma volume expander should always be used whenever
>5 L of ascites are removed.

53. Stepwise treatment of
ascites
•Sodium restriction (88 mmol /d = 2 g)
•Titrate spironolactone (to Na+u / K+u > 1)
•If no success add loop diuretic
•Fluid restriction only if Na+ < 120 mmol/l
•Bed rest is not recommended.
•Aim for weight loss < 1/2 kg/d in non-edematous pts ,
but  should not exceed 1 kg/day when edema is present.
• 
Please
don’t
forget

54. •Serum potassium, blood urea nitrogen (BUN), and creatinin
levels should be serially followed.
• In the event of marked hyponatremia, hyperkalemia or
hypokalemia, renal insufficiency, dehydration, or
encephalopathy , diuretics should be reduced or
discontinued.
•The spot urine Na+ to-K+ ratio might ultimately replace the
cumbersome 24-hour collection:
•A random urine Na+ concentration higher than the K+
concentration has been shown to correlate with a 24-hour
sodium excretion higher than 78 mmol/day with
approximately
90% accuracy.
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56. Avoid NSAIDs & Stop alcohol
Restrict Na = 2g/day
Oral Diuretics
Spironolactone100 mg + Furosemide 40 mg /day
Progressive increase of dose by one /one till maximum 4 tablets of each drug
Frequent large volume paracentesis with albumin
(infusion ( 6-8 gm for each liter ascitic fluid
TIPS
Liver transplantation
Stepwise Management of ascites
Failed Refractory ascites
Failed
Failed

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Effective management of ascitesEffective management of ascites
improves patient well-being & eliminatesimproves patient well-being & eliminates
the patient's risk for these life threateningthe patient's risk for these life threatening
complicationscomplications
HRSSBP
Refractory
ascites

58. Refractory
ascites

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Refractory ascitesRefractory ascites
))10-15%10-15% of cirrhotic ascitesof cirrhotic ascites((
Diuretic-resistant Diuretic-resistant
ascitesascites
Diuretic- intractableDiuretic- intractable
ascitesascites
Ascites fail to respond
to full dose of diuretics
for 2 weeks
Patients who cannot tolerate Patients who cannot tolerate
diuretics because of side diuretics because of side
effectseffects

61. Non-compliance with
sodium restriction is a
major & often
overlooked cause of
refractory ascites.
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Management of Refractory Management of Refractory
AscitesAscites
LiverLiver
transplantationtransplantation
LargeLarge
volumevolume
paracentesisparacentesis
PeritoneovenousPeritoneovenous
shuntshunt
TIPSTIPS

63. Liver transplantation
•It is the most effective &
definitive treatment but

64. Transjugular
intrahepatic Porto
systemic shunt
(TIPS(

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66. 2004
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OV Before TIPS After TIPS

67. TIPS
Advantages of
TIPS

■
High success rate.

■
Low complication
rate.

■
Short hospitalization.
Disadvantages of TIPS

■
Stenosis of the shunt.

■
Encephalopathy due to
wide shunt.

■
Difficult LTX due to
stent projection into
I.V.C.

68. Large volume paracentesis
•Repeated LVP is a safe and effective mean of controlling
refractory ascites.

•Single LVP can be safely performed without the infusion of
plasma expanders such as albumin.
•However, patients who require frequent repeated LVP or a
single total paracentesis should receive albumin infusion.

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70. Peritoneovenous shunt
Le Veen Shunt
•It is a device that returns ascitic fluid from the peritoneal
cavity to the systemic circulation.
•Its use is restricted to patients with well preserved hepatic
function since survival following it falls off dramatically in
patients with severe liver dysfunction.
•The associated complications, including technical problems,
makes this an option for only selected patients.

71. 2004
LeVeen Shunt Effect of
Increased effective circulating Increased effective circulating
volumevolume
↓ ↓ Plasma rennin Plasma rennin
activityactivity
↓↓ AldosteroneAldosterone ↓↓ NorepinephrineNorepinephrine
Diuresis and Diuresis and
mobilization of ascitesmobilization of ascites

73. Sponataneous
Bacterial
Peritonitis
(SBP)

74. Definition
•It is an acute bacterial infection of
ascitic fluid without an evident intra-
abdominal, surgically treatable
cause.
•SBP is defined as an ascites fluid
polymorph nuclear leukocyte (PMN)
count > 250/mm
3
(regardless of
culture results, which may be
negative(.
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75. Symptoms& signs
69%
59%
54%
49%
32%
30%
21%
17%
0%
10%
20%
30%
40%
50%
60%
70%
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McHutchison JG et al., 1994McHutchison JG et al., 1994

76. Other Clinical Manifestations
•Asymptomatic : 30%.
•Ascites that does not improve
following administration of
diuretics.
•Worsening or new-onset renal
failure.
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77. Secondary vs. SBP
Secondary bacterial Secondary bacterial
peritonitis peritonitis
SBPSBP
OrganismsOrganisms MultipleMultiple SingleSingle
Ascitic protein Ascitic protein >1 g/dL>1 g/dL < 1 g/dL< 1 g/dL
Ascitic glucose conc.Ascitic glucose conc.< 50 mg/dL< 50 mg/dL ~ serum value~ serum value
Response to TxResponse to Tx
PMN cell countPMN cell count Continues to rise Continues to rise
despite treatmentdespite treatment
Falls Falls
exponentiallyexponentially
Ascitic cultureAscitic cultureRemains positiveRemains positive Rapidly Rapidly
becomes sterilebecomes sterile
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78. Management
Cefotaxime Cefotaxime
•Less nephrotoxicLess nephrotoxic
•Broad spectrumBroad spectrum
•1 -2 g, 8 hourly1 -2 g, 8 hourly
CefoxitinCefoxitin
•Enterococcal coverageEnterococcal coverage
•1 g, 6 to 8 hourly1 g, 6 to 8 hourly
AztreonamAztreonam •0.5 0.5 –– 1 gm, 8 hourly 1 gm, 8 hourly
Amoxicillin-Amoxicillin-
clavulanic acid clavulanic acid
•1 g amoxicillin & 200 mg 1 g amoxicillin & 200 mg
clavulanic acid, 8 hourly clavulanic acid, 8 hourly
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79. Hepatorenal
Syndrome
HRS
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80. Definition of HRS
Major Criteria (5(
1- Chronic or acute liver disease with liver failure
and portal hypertension.
2- Low GFR:
•
Cr>1.5 mg/dL or Cr. clearance <40 mL/min.
3- Absence of Shock, bacterial infection,
nephrotoxic drugs or excessive fluid loss.
•No sustained improvement in renal function
following expansion with 1.5 L of isotonic saline.
•Proteinuria < 0.5 g/d with no ultrasonographic
evidence of renal disease .
1- Chronic or acute liver disease with liver failure
and portal hypertension.
2- Low GFR:
•
Cr>1.5 mg/dL or Cr. clearance <40 mL/min.
3- Absence of Shock, bacterial infection,
nephrotoxic drugs or excessive fluid loss.
•No sustained improvement in renal function
following expansion with 1.5 L of isotonic saline.
•Proteinuria < 0.5 g/d with no ultrasonographic
evidence of renal disease .
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81. Minor Criteria (5(
1- Urine Volume <500 mL/d.
2- Urine Sodium <10 mmol/d.
3- Urine osmolality > plasma osmolality.
4- Urine red cell count < 50 per HPF.
5- Serum sodium < 130 mmol/L.
1- Urine Volume <500 mL/d.
2- Urine Sodium <10 mmol/d.
3- Urine osmolality > plasma osmolality.
4- Urine red cell count < 50 per HPF.
5- Serum sodium < 130 mmol/L.
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82. Type I HRSType I HRS
•Rapidly progressive renal failure
•With a doubling of serum creatinine
to a level > 2.5 mg/dL or creatinine
clearance < 20 mL/min.
•In less than 2 weeks.
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83. Type II HRSType II HRS
•Is a more chronic form
•With a slowly progressive increase
in serum creatinine level >1.5
mg/dL or creatinine clearance <40
mL/min.
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84. 2004
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Management Management
of of
HRSHRS
Management Management
of of
HRSHRS

85. Treatment
•Liver Transplantation.
•MARS “Molecular Adsorbent Recirculating
System ”
•TIPS.
•Pharmacological Therapy
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