Ascietes

by
dr naila masood
Cirrhosis is the late result of any disease that
causes scarring of the liver.

Patients with cirrhosis are susceptible to a

variety of complications that include ascites,
hepatic encephalopathy, and portal
hypertension.

Quality of life and survival are often improved

by the prevention and treatment of these
complications.
Ascites is defined as the accumulation of
free fluid in the peritoneal cavity.

It is a common clinical finding with a variety of

both extraperitoneal and peritoneal etiologies.

It is most often caused by liver cirrhosis which

accounts for over 75% of patients while the
remaining 25 % is due to malignancy (10%),
heart failure (3%), pancreatitis (1%), TB (2%),
or other rare causes.
 Nonperitoneal Causes of
Ascites
Non-peritoneal causes Examples
Intrahepatic portal Cirrhosis
hypertension Fulminant hepatic failure
Veno-occlusive disease
Extrahepatic portal Hepatic vein obstruction
hypertension (ie, Budd-Chiari syndrome)
Congestive heart failure
Hypoalbuminemia Nephrotic syndrome
Protein-losing enteropathy
Malnutrition

Miscellaneous disorders Myxedema

Ovarian tumors
Pancreatic & Biliary ascites

Chylous Secondary to malignancy, trauma

 Peritoneal Causes of Ascites
Peritoneal Causes Examples

Malignant ascites Primary peritoneal mesothelioma

Secondary peritoneal
carcinomatosis

Granulomatous peritonitis Tuberculous peritonitis

Fungal and parasitic infections
Sarcoidosis
Foreign bodies (cotton ,starch,
barium)

Vasculitis Systemic lupus erythematosus

Henoch-Schönlein purpura
Miscellaneous disorders Eosinophilic gastroenteritis
Whipple disease
Endometriosis
Prognosis

The development of ascites is an indication of

deterioration in clinical status and poor prognosis.

Prognosis is worse for those with refractory ascites

and SBP.

Approximately 60% of patients with cirrhosis will

develop ascites requiring therapy and/or liver
transplantation in 10 years duration.

Mortality in cirrhotic patients hospitalized with ascites

is 40% at 2 years.
PATHOPHYSIOLOGY
Ascites is derived from the vascular compartment
subserving the hepatosplanchnic viscera.

Factors important in the formation of ascites:

Increased total body sodium and water
Increased sinusoidal portal pressure.

In cirrhosis
Hepatic dysfunction and sinusoidal portal pressure
send a message to the kidney to retain excess
sodium and fluid.

PH serves to localize excess fluid to the peritoneal

cavity rather than the periphery.
The pathogenesis of ascites formation
remains controversial.

“Underfill" theory
Ascites occurs as a primary event.

Sequestration of fluid into the peritoneal

cavity as a result of changes in Starling's
forces leads to reduction of the circulatory
volume and stimulation of the sympathetic
nervous & RAAS that promote renal sodium
& water retention.
“Overflow theory"

Renal Na retention occurs as a primary

event.

It may be due to increased production of a

sodium retaining factor or reduced synthesis
of a natriuretic factor by the diseased liver.

The circulatory volume is expanded & the

retained fluid is preferentially localized to the
peritoneal cavity as ascites.
The currently accepted theory of ascites
formation which include features of both the
underfill and overflow theories is the

“Peripheral Arterial Vasodilation Hypothesis"

According to this theory, Portal pressure >12

mm Hg is required for the development of
PH which will lead to formation of ascites.
As PH develops, vasodilators are released
affecting the splanchnic arteries resulting in
decrease in effective arterial blood flow and
arterial pressures .

The precise agent (or agents) responsible

for vasodilation is a subject of wide debate;
however, most recent literature has focused
on the role of:

Nitric Oxide
Chronic endotoxemia associated with
cirrhosis may stimulate the synthesis and
release of a potent endothelin-derived
relaxing factor, Nitric oxide.

NO is the likely mediator in cirrhosis:

(1) Increased activity of NO synthase .
(2) High serum nitrite and nitrate levels (an
index of NO synthesis).
(3) Inhibition of NO leads to increased arterial
pressures and systemic vascular resistance.
 Portal hypertension

Vasodilatation, Decrease Splanchnic

Systemic vascular resistance

Reduction in arterial blood volume

Activation of neurohumoral pressor systems

Renal sodium & water retention

When Na reabsorption cannot compensate for
vasodilation, arterial underfilling leads to
further activation of vasoconstrictor &
antinatriuretic mechanisms which leads to
increased Na retention & ultimately ascites is
formed.

In the late stages of cirrhosis, free water

accumulation is more pronounced than the Na
retention leading to dilutional hyponatremia.
DIAGNOSIS
I) History

Approximately 85% of patients with ascites

have cirrhosis.

Patients who don’t have cirrhosis should be

questioned about lifetime body weight as
NASH may be the cause.

Past history of cancer, heart failure, or TB.

II) Physical Examination

Approximately 1.5 L must be present before

flank dullness is detected.
If no flank dullness is present, the patient has
less than 10% chance of having ascites.

Shifting dullness & fluid thrill mean that more

fluid is present.

Abdominal ultrasound to determine with

certainty if fluid is present and in obese.
Two grading systems for ascites have been
used in the literature.

An old system which grades ascites from 1+

to 4+, depending on the detectability of fluid
on physical examination.

More recently, the International Ascites Club

has proposed a system of grading from 1 to 3.
The older system
1+ is minimal and barely detectable.
2+ is moderate.
3+ is massive but not tense.
4+ is massive and tense.

The International Ascites Club grading (2003)

Grade 1: mild ascites detectable only by US.
Grade 2: moderate ascites manifested by
moderate symmetrical abdominal distension.
Grade 3: large or gross ascites with marked
abdominal distension.
III) Diagnostic Paracentesis
Indications
(1)Evaluation for a non-cirrhotic patient developing
clinically apparent ascites of recent onset.
(2)New development of ascites in a cirrhotic patient
does not routinely require paracentesis only if :
(a) General condition deteriorates.
(b) In presence of unexplained fever, abdominal
pain, encephalopathy.
(c) Admission to hospital for any cause (SBP).
(3)Laboratory investigations indicating infection:
Leucocytosis Acidosis
Worsening of renal functions
Site
Midline was usually chosen.
Abdominal wall in the left lower quadrant, 2
finger breadths cephalic & 2 finger breadths
medial to ASIS, has been shown to be
thinner with larger pool of fluid than midline.

Complications (1% of patients)

Abdominal wall hematomas.
Hemoperitoneum or bowel entry.

Contraindications
Clinically evident fibrinolysis or DIC.
 Gross Appearance of Ascitic Fluid

Color Appearance

Translucent or yellow Normal/sterile

Brown Hyperbilirubinemia
GB or biliary perforation
Cloudy or turbid Infection
Pink or blood tinged Mild Trauma
Grossly bloody Malignancy
Abdominal trauma
Milky ("chylous") Cirrhosis
Thoracic duct injury
Lymphoma
 Ascitic Fluid Testing

Routine Sometimes useful Rarely helpful

Cell count & Total protein pH
differential
Albumin LDH Lactate
Culture Glucose Gram stain
Amylase
Triglycerides
Bilirubin
Cytology
TB smear and
culture
Ascitic fluid analysis (Routine)
I) Cell count with differential
Abnormal results are an indication for further non
routine tests.

If the PMN count is >250 cells/mm3, another

specimen is injected into blood culture bottles at
bedside.

Bacterial growth occurs in about 80% of specimens

with count of >250 cells/mm3.

The PMN count is calculated by multiplying the white

cells/mm3 by the percentage of neutrophils in the
differential.
In a "bloody" sample that contains a high
concentration of RBC, the PMN count must be
corrected:
one PMN is subtracted from the absolute PMN
count for every 250 red cells/mm3 in the
sample.

The results must be available within 1 hour, so

that important diagnostic and therapeutic
decisions can be made.

A Gram stain is of particular low yield unless

free gut perforation, is suspected.
II)Total protein ,albumin & serum albumin .
Serum-ascites albumin gradient
(SAAG) = serum albumin - ascitic fluid
albumin.

If > 1.1 g/dL, the patient has PH-related

ascites.

If < 1.1 g/dL (about 97% accurate), the

patient does not have PH-related ascites.

The SAAG does not need to be repeated

after the initial measurement.
III)Based on clinical judgment, additional
testing can be performed :

a) Cytology ,smear & culture for mycobacteria.

b) Cytology : in peritoneal carcinomatosis

(sensitivity increased by centrifuging large
volume).

c) Elevated bilirubin level suggest biliary or gut

perforation.
d) LDH >225mU/L, glucose <50mg/dL, total
protein >1g/dL and multiple organisms on
gram stain suggest secondary bacterial
peritonitis.

e) High level of TG's confirms chylous

ascites.

f) Elevated amylase level suggest

pancreatitis or gut perforation.
AASLD Recommendations
1.Paracentesis should be performed ,ascitic fluid
should be obtained from inpatients & outpatients with
clinically apparent new-onset ascites
2. Since bleeding is uncommon ,prophylactic use of
FFP or platelets is not recommended.
3. Initial evaluation of ascitic fluid should include cell
count ,differential, total protein & SAAG.
4. If infection is suspected, ascitic fluid should be
cultured at the bedside in blood culture bottles.
5. Other studies can be ordered based on pretest
probability of disease.
 Management of Ascites -
Guideline
• Treat the Underlying Cause
• Childs C – 75% 3-year survival Vs. 0%
• Non-Alcoholic less reversible therefore
consider referral for transplant earlier
 Treatment Options
• Bed rest
• Diet
• Diuretics
• Fluid Restriction
• Paracentesis
• TIPSS
• Shunts
• Transplant
 Management of ascites -
Bed Rest
• Bed rest : No clinical trials
• Upright posture activates sodium retaining
mechanisms , impairs renal perfusion and
sodium excretion.
 Management of ascites-
Sodium Restriction
Sodium restriction :
Water will follow Sodium
Educate the Patient
Aim for 2000mg (88 mmol) per day
Studies show severe restriction (22mmol/day)
compared with less restricted is associated with
longer duration of evolution of ascites, but higher
incidence of diuretic induced renal impairment
and hyponatraemia
 MANAGEMENT OF ASCITES-
Salt restriction (cont)
• One controlled study, showed slightly reduced
salt diet (120mmol/day) was equally effective
when compared to a low salt diet ( 50mmol/day).
• No significant survival difference, although low
salt diet (50mmol/day ) improved survival in
those with previous GI bleed
 MANAGEMENT OF ASCITES-
WATER RESTRICTION
• Central hypovolaemia - > stimulates ADH receptors
• - > decreases free water clearance - > dilutional
hyponatraemia.
•
• Therefore, treat by water restriction – no trials to
assess effect of water restriction in patients with
cirrhosis and dilutional hyponatraemia. Restriction
may worsen central hypovolaemia.

• Water restriction not first option, sodium restriction

appropriate first line, water restrict if Na
<125mmol/L
 MANAGEMENT OF ASCITES-
DIURETICS
• Antimineralocorticoids –
• Secondary hyperaldosteronism promotes sodium
retention in distal tubules and collecting ducts
• Controlled and uncontrolled trials - >
Spironolactone effective antimineralocorticoid
• S.E gynaecomastia, renal impairment,
hyperkalaemia
• Other K sparing diuretics: amiloride, triamterene
• Loop Diuretics : Frusemide – S.E : hyponatraemia,
hypokalaemia, hypovolemia, renal impairment of
prerenal origin
 ASCITES-
Assess response to diuretics :
• Weight loss of 0.5kg/day in absence of
oedema and 1kg/day when oedema
present
• Use Spironolactone & Frusemide
100mg/40mg ratio
• Medical treatment based on sodium
restricted diet, diuretics – response in 90
% without renal failure.
 ASCITES-
Assess response to diuretics :
• Weight loss of 0.5kg/day in absence of
oedema and 1kg/day when oedema
present
• Use Spironolactone & Frusemide
100mg/40mg ratio
• Medical treatment based on sodium
restricted diet, diuretics – response in 90
% without renal failure.
 Ascites-
Refractory Ascites
• Unresponsive to Salt restriction & high dose diuretics
(400mg Spironolactone & 160mg Frusemide)

• Recurs rapidly after Paracentesis (< 4/52)

• Diuretic induced complication – encephalopathy,

renal impairment, hyponatraemia (<125mmol/L),
hypo (3mmol/L) or hyperkalaemia (6mmol/L)
 Ascites-
Paracentesis
• Repeated daily paracentesis ( 5L/day )
• Single total paracentesis- reduced hospital
stay
 Refractory Ascites -
Treatment Options
• Serial Paracentesis
• Liver Transplantation
• TIPSS
• Peritoneovenous Shunts
 Refractory Ascites -
Treatment Options
• Liver Transplantation
THANK YOU