Management of ascites in

cirrhosis
BSG 2006
 Definition
Pathogenesis
Diagnosis- asctitic fluid analysis
Treatment- salt restriction/diuretic
Therapeutic paracentesis
TIPSS
SBP
 Setting the scene
Occurs in 50% of patients over 10yrs
Associated with 50% mortality over two yrs
Indicates the need to consider liver
transplantation
Mortality from cirrhosis is 12.7 per 100,000
population
Approx 4% of population have abnormal
LFT, 10-20% of those develop cirrhosis
over 10-20yrs
 Uncomplicated ascites- not infected and not
associated with HRS
Refractory ascites- cannot be mobilised or early
recurrence of which ( that is after therapeutic
paracentesis) cannot be prevented by medical treatment
Diuretic resistant ascites- refractory to dietary salt
restriction and intensive diuretic treatment
( spironolactone 400mg and frusemide 160mg per day
and salt restricted diet of less than 90mmol/day
( 5.2g/day)
Diuretic intolerant ascites- refractory to therapy due to
the development of diuretic induced complications
 Grading of ascites

1. Grade I: Only detectable by US

2. Grade II: Moderate symmetrical

distension of the abdomen

3. Grade III: Marked abdominal distension

 Pathogensis

Portal hypertension

Sodium and water retention

 Role of portal hypertension
PH increases the hydrostatic pressure
with the hepatic sinusoid and favours
transudation of fluid into the peritoneal
cavity
PH occurs as a consequence of structural
changes within the liver in cirrhosis and
increased splanchnic blood flow
 Progressive collagen deposition and
nodule formation alter vascular
architecture and increases the resistance
to portal flow
Collagen is formed within the space of
Disse and sinusoids become less
distensible
 Increased splanchnic flow because of
vasodilation due to release of NO
 Increased resistance in the hepatic sinusoid
Portal hypertension
Congestion of capillary in intestine
Endotoxaemia
NO release
Arterial vasodilation in both systemic and splanchnic circulation-
systemic ( tachycardia increased stroke volume) and splanchnic
( increased portal flow- and more rise in portal pressure)
Decrease in effective circulatory volume
Activation of RAS system and sympathetic system- ( aldosterone
increase promoting Na retention and secondary fluid retention to
restore blood volume)
Renal vasoconstriction to increase glomerular pressure- ultimately
attempts at homeostasis fails- GFR starts to fall
 Sinusoidal endothelial cells form and extremely
porous membrane almost completely
permeable to macromolecule
Old theory that low albumin is the cause of
ascites is false as there is no oncotic gradient ( it
works for peripheral oedema but not for ascites)
Portal hypertension is critical to development to
ascites and develops when wedged hepatic
portal venous pressure is more than 12mm
TIPSS relieves ascites by reducing portal
hypertension though low albumin and cirrhotic
liver persists
 Presinusoidal portal hypertension does
not produce ascites ( portal vein
thrombosis)
Post sinusoidal portal hypertension does
produce back pressure and cause similar
haemodynamic changes and causes
ascites ( hepatic vein thrombosis)
1. Sinusoidal portal hypertension, in
the presence of severe hepatic
decompensation

2. Leads to splanchnic and systemic

vasodilatation-role of NO

3. Decreased effective arterial blood

volume

4. Activation of systemic vasoactive

factors, such as the renin-
angiotensin system, the
sympathetic nervous system, and
vasopressin aimed at restoring
arterial filling pressure.

5. Renal vasoconstriction increases

concomitantly (leukotrienes and
endothelins), counterbalanced by
the intrarenal hyperproduction of
vasodilating prostaglandins. When
this balance is lost renal
hemodynamics worsens, and
hepatorenal syndrome develops
 Cirrhosis 75%
Malignancy 10%
Heart failure 3%
TB 2%
Pancreatitis 1%
 Blood tests- FBC/U&E/LFT/INR
Ultrasound- liver/spleen/portal vein/LN
Ascitic fluid analysis
 Abdominal paracentesis
15cm lateral to umbilicus
Avoid enlarged spleen and liver
Avoid sp and inf epigastric arteries
No data to support use of FFP
Most clinicians would give pooled platelets if <40
Complication:
Haematoma<1%
Bowel perforation/haemoperitoneum <0.1%
10-20ml of fluid in a syringe with blue/green
needle
 Blood culture bottle- culture
EDTA tube- cell type
Yellow top tube- albumin/amylase
Yellow top tube- blood ( for serum
albumin)
 Ascitic fluid neutrophil count and
culture
SBP is present in 15% patients admitted to
hospital
Ascitic neutrophil count of >250cells/mm3 is
diagnostic of SBP in absence of perforated
viscus or inflammation of intraabdominal organs
RBC count is usually <1000cells/mm3
In 2% of cirrhotic bloody ascites >50,000
In bloody ascites 50% no cause and 30% HCC
 The prevalence of occult ascitic fluid infection in
asymptomatic outpatients undergoing large
volume paracentesis for resistant ascites is low
As a result, the routine culture of fluid during
paracentesis in such patients is probably not
warranted.
Obtain a cell count and differential on all
samples of ascitic fluid while obtaining cultures
only in symptomatic patients.
 Culture in sterile container will identify
onlY 40% of cases of SBP
Whereas culture in blood culture bottle will
identify 72-90 %
Gram stain and AFFB stain inappropriate
Fluid culture for mycobacteria 50%
sensitivity
 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
 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
SAAG is far superior with 97% accuracy
Eg Serum albumin 26 and ascitic albumin 11- so SAAG
is 15- so high SAAG- previously called transudate

SAAG>11g/L SAAG<11g/L
Cirrhosis Malignancy
Cardiac failure Pancreatitis
Nephrotic syndrome Tuberculosis
 Amylase in pancreatic ascites
Triglyceride in chylous ascites
Bilirubin in post op ascites
 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
 Treatment- salt restriction
Typical UK diet has 150mmol/day- 15% added
salt and 70% is manufactured salt
Suggestion is no added salt diet and avoidance
of prepared food
So that patient gets 90mmol/day ( 5.2gm)
Lowers diuretic requirement, faster resolution of
ascites and shorter hospital stay
Avoid high salt content of fluid and medicine
except in HRS
 Treatment- water restriction
No role in uncomplicated ascites
Most hepatologists restrict fluid in ascites associated with
hyponatraemia- but is illogical
The downside is water restriction causes increase in the central
effective hypovolaemia- more ADH- more water retension 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
To be effective the intake should be less than urine output rather
than arbitrary 1.5L/day
If the serum sodium concentration does not increase within the first
24 to 48 hours, the degree of fluid restriction has been insufficient.
 Treatment- diuretic
Spironolactone is drug of choice
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- gynaecomazia- tamoxifen
20mg bd
Hyperkalaemia frequently limits the use
 Treatment- diuretic
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
 Treatment- diuretic
Stepped care approach
Till oedema is present no need to slow down the daily
weight loss
Once oedema is resolved daily weight loss should be
less than 0.5kg per day
Over diuresis is associated with intravascular volume
depletion, leading to renal impairment, hepatic
encephalopathy and hyponatraemia
10% will have refractory ascites
Dietary history to exclude salt ingestion- 24hr urinary Na
excretion should be less than recommended intake
Drug history - NSAID
 Problem with hyponatraemia
Na 126-135 and normal Continue diuretic
creatinine Do not water restrict

Na 121-125 and normal Continue/? discontinue

creatinine

Na 121-125 and high Stop diuretic and give

Creatinine volume expansion

Na <120 Stop diuretic

 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
 Therapeutic paracentesis
Total paracentesis is associated with
significant haemodynamic changes
Large volume paracentesis causes
marked reduction of IAP and IVC
pressure- decrease in right heart pressure
and
This changes are maximal at 3hrs
 International ascites club recommend if <5L is removed synthetic
plasma expander can be used and as good as albumin ( some
hepatologist suggests no albumin/plasma expander if <5L)
Compared to albumin, artificial plasma expander cause more
activation of RAS , causes more hyponatraemia and results in
longer hospital stay
20% albumin should be infused after paracentesis of >5L at dose of
8g/L of ascites drained ( 100ml of 20% albumin= 20gm, so 3L of
ascites fluid removal needs 3x8=24 gm of albumin replacement =
125ml but we tend to round it to 100ml)
So if >10L remember to give an extra 100ml of albumin
25% albumin can be given if the patient is hypervolemic while 5
percent albumin can be given if dehydration is suspected.
 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
 10% of patients will have refractory ascites
and will need paracentesis
Following paracentesis ascites will recur in
93% if diuretic is not reinstituted and only
18% if treated with spironolactone
Reintroduction of diuretics after 1-2 days
does not appear to increase the risk of
post paracentesis circulatory dysfunction
 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
 Prognosis
Mortality of 50% within 2yr of diagnosis
Once refractory to medical therapy 50%
die within 6 months
Time for referral to transplant centre as
paracentesis and TIPSS does not improve
long term survival except improving quality
of life