Ascites

Dr Mohammed Hussien

Assistant Lecturer of Hepatology & Gastroentrology

Kafrelsheik University
 ? 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.
Cirrhotic Non cirrhotic
ascites ascites
3

75% 20%

Etiology of
ascites

Mixed ascites
%5
• 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.
Mechanism of ascites
formation
A)Incresased hydrostatic
pressure

• Cirrhosis
• Hepatic vein occlusion (Budd- Chiari
syndrome)
• Inferior vena cava obstruction
• Constrictive pericarditis
• Congestive heart failure
B) Decreased colloid osmotic pressure
7

• End-stage liver disease with poor protein

synthesis

• Nephrotic syndrome with protein loss

• Malnutrition

• Protein-losing enteropathy
2004
C) Increased permeability of peritoneal
capillaries

• Tuberculous peritonitis

• Bacterial peritonitis

• Malignant disease of the peritoneum

D) Leakage of fluid into the
peritoneal
cavity

• Bile ascites

• Pancreatic ascites

• Chylous ascites

• Urine ascites
E) Miscellaneous causes

• Myxedema

• Ovarian disease (Meigs' syndrome)

• Chronic hemodialysis
Pathogenesis of
ascites in cirrhosis
 cirrhosis
Hemodynamic changes.

VC Imbalance VD
substances substances
Favoring VD

Systemic & splanchnic VD

Decrease effective circulating 2004

blood volume
 Decrease in effective circulating
blood volume

Perceived hypovolemia activates

various VC systems

RAAS , SNS , ADH↑

Renal VC

Decrease renal Na &

in GFR oncotic pressure↓ water
reabsorption

Ascites
Renal Dysfunction in Cirrhosis

Ability to Ascites
Ascites
Exc. Sod

SNS R
R perfusion
perfusion
Kidney HRS
HRS
RAS &
& GFR
GFR

ADH Ability to Dilutional

Dilutional
Exc. water Hyponat
Hyponat
““Sod<130
Sod<130””
2004
 Commonest causes
((90% of cases

• Cirrhosis (Cirrhotic Ascites)

• Cancer (Malignant Ascites)
• Congestive Heart Failure
• Mycobacterium tuberculosis
Clinical Manifestations and
Diagnosis
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
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
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
Ultrasonography 20

• 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
• 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
 Analysis of
Ascitic Fluid
 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

to 
beCytology
considered
Lactate
pH
Calculated by subtracting the albumim
concentration of the ascitic fluid from
the albumin concentration of a serum
specimen obtained on the same day.
Serum Ascites Albumin
(Gradient (SAAG
 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% .
• 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).
• 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
 SAAG
30

Helpful diagnostically, as well as

therapeutically in decision making
Low SAAG High SAAG
1.1 > 1.1<

Non –portal Portal hypertensive

hypertensive cases cases

2004
Does not respond to salt Respond to salt
restriction nor Diuretics restriction & Diuretics
 31

2004
 Terms should be replaced
32

Transudative Exudative

high-albumin low-albumin
gradient gradient
> 1.1g/dl 2004
g/dl 1.1<
Types of ascites according to 33

SAAGHigh Gradient Low Gradient

or = 1.1 g/dl)PHT ) < (g/dl 1.1 )>
Portal vein thrombosis Non PHT
Cirrhosis Peritoneal Carcinomatosis
Cardiac Failure Pancreatic ascites
Budd Chiari syndrome Biliary ascites
Alcoholic hepatitis
Peritoneal Tuberculosis
Nephrotic Syndrome
Fulminant hepatic failure Serositis
Massive hepatic metastasis Bowel obstruction or
Fatty liver of pregnancy infarction
Myxedema
Mixed ascites
2016
High gradient
(( SAAG > 1.1 34

• 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.
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 -
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.
2. The amylase concentration
which is elevated in
pancreatic ascites.
3. The triglyceride concentration
which is elevated is chylous
ascites.
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.
5.Red cell count :
• When greater than 50.000/microliter
denotes hemorrhagic ascites, which usually
is due to :
- malignancy
- tuberculosis
- Pancreatitis
- or trauma.
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.
Ascites Fluid: Cell Count with
Differential

RBCs elevated WBC elevated

• Malignant ascites
• Tuberculous peritonitis
>1000
• Neoplasm (>50%
• Pancreatitis Lymphocytes)
• TB peritonitis (>70%
Lymphocytes)
• Bacterial peritonitis
(WBC > 10,000)
• Spontaneous Bacterial
Peritonitis (PMN > 250)
Management
of ascites
 Reversible Causes

43

Refractory ascites
Bed rest

Treatment of
ascites

Diuretics Na+ restriction

Water restriction
2016
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.
 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
 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.
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
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.
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.
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
 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.
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.
 Stepwise treatment of Please
don’t
ascites forget

•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.
• 
• Serum potassium, blood urea nitrogen (BUN), and creatinin
54
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.
 55

2004
 Stepwise Management of ascites

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

Failed Refractory ascites

Frequent large volume paracentesis with albumin
(infusion ( 6-8 gm for each liter ascitic fluid
Failed

TIPS

Failed

Liver transplantation
 Effective management of ascites
improves patient well-being & eliminates 57

the patient's risk for these life threatening

complications

Refractory
ascites
SBP HRS
2004
Refractory
ascites
 59

2004
 Refractory ascites
(of cirrhotic ascites 10-15%) 60

Diuretic-resistant Diuretic- intractable

ascites ascites

Ascites fail to respond Patients who cannot tolerate

2004
to full dose of diuretics diuretics because of side
for 2 weeks effects
Non-compliance with 61

sodium restriction is a
major & often
overlooked cause of
. refractory ascites
 Management of Refractory
Ascites
62

Liver
transplantation TIPS

Large
volume Peritoneovenous
paracentesis shunt
2004
Liver transplantation

• It is the most effective &

definitive treatment but
Transjugular
intrahepatic Porto
systemic shunt
((TIPS
 65

2004
 66

OV Before TIPS After TIPS

2004
 TIPS
Advantages of Disadvantages of TIPS
TIPS ■ Stenosis of the shunt.
■ High success rate.
■ Encephalopathy due to
wide shunt.
■ Low complication
rate.
■ Difficult LTX due to
stent projection into
■ Short hospitalization. I.V.C.
 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.
 69

2004
 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.
 LeVeen Shunt Effect of

Increased effective circulating

volume

Plasma rennin↓ Aldosterone ↓ Norepinephrine ↓

activity

Diuresis and
mobilization of ascites
2004
Sponataneous
Bacterial
Peritonitis
(SBP)
Definition
74

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/mm3 (regardless of
culture results, which may be
(. negative
2004
Symptoms& signs 75

70% 69%
59%
60% 54%
49%
50%
40% 32% 30%
30%
21%
20% 17%
10%
0%
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ar

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in

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ot
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r

ph

er

th
en
ea
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al

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op

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McHutchison JG et al., 1994

2004
Other Clinical Manifestations 76

.Asymptomatic : 30% •
Ascites that does not improve •
following administration of
.diuretics
Worsening or new-onset renal •
.failure
2004
 Secondary vs. SBP
77
Secondary bacterial SBP
peritonitis
Organisms Multiple Single
Ascitic protein >1 g/dL < 1 g/dL
Ascitic glucose conc. < 50 mg/dL ~ serum value
Response to Tx
 PMN cell count Continues to rise Falls
despite treatment exponentially
 Ascitic culture Remains positive Rapidly
becomes sterile
2004
 Management
78

Cefotaxime •Less nephrotoxic

•Broad spectrum
•1 -2 g, 8 hourly

Cefoxitin •Enterococcal coverage

•1 g, 6 to 8 hourly
Aztreonam •0.5 – 1 gm, 8 hourly

Amoxicillin- •1 g amoxicillin & 200 mg

clavulanic acid, 8 hourly
clavulanic acid
2004
 79

Hepatorenal
Syndrome
HRS
2004
Definition of HRS
( Major Criteria (5 80

Chronic
Chronic or
or acute
acute liver
liver disease
disease with
with liver
liver failure
failure-- 11
..and
and portal
portal hypertension
hypertension
:: Low
Low GFR
GFR-- 22
1.5 mg/dL
..Cr>
Cr> mg/dL or
or Cr. clearance <40 mL/min
Cr. clearance mL/min ••

Absence
Absence ofof Shock,
Shock, bacterial
bacterial infection,
infection,-- 33
..nephrotoxic
nephrotoxic drugs
drugs oror excessive
excessive fluid
fluid loss
loss
No
No sustained
sustained improvement
improvement in in renal function ••
renal function
..following
following expansion
expansion with
with 1.5
1.5 LL of
of isotonic
isotonic saline
saline
Proteinuria
Proteinuria << 0.5
0.5 g/d
g/d with
with no ultrasonographic ••
no ultrasonographic
..evidence
evidence ofof renal
renal disease
disease
2004
(Minor Criteria (5 81

..Urine
Urine Volume
Volume <500
<500 mL/d
mL/d-- 11
..Urine
Urine Sodium
Sodium <10
<10 mmol/d
mmol/d-- 22
..Urine
Urine osmolality
osmolality >> plasma
plasma osmolality
osmolality-- 33
..Urine
Urine red
red cell
cell count
count << 50
50 per
per HPF
HPF-- 44
..Serum
Serum sodium
sodium << 130
130 mmol/L
mmol/L-- 55

2004
Type I HRS
82

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 •

2004
Type II HRS
83

Is a more chronic form •

With a slowly progressive increase •
in serum creatinine level >1.5
mg/dL or creatinine clearance <40
.mL/min

2004
 84

Management
Management
of
of
HRS
HRS
2004
Treatment 85

.Liver Transplantation •
MARS “Molecular Adsorbent Recirculating •
” System
.TIPS •
Pharmacological Therapy •
2004
 86

2004