MANAGEMENT OF ASCITES

by

Dr Intekhab Alam
Professor of Medicine
Department of Medicine
Postgraduate Medical Institute,
Lady Reading Hospital, Peshawar

Objectives
1.

Understand the basic mechanisms of

portal hypertension (PHT)

2.

Study Ascites as a complication of

PHT

3.

Get an idea on the management of

Ascites and its complications

What is Liver Cirrhosis?

Diffuse

fibrosis of the liver with

nodule formation
Abnormal response of the liver
to any chronic injury

Causes of Cirrhosis
1.
2.
3.
4.
5.
6.

Chronic viral hepatitis

Metabolic: hemochromatosis, Wilson dis,
alfa-1-antitrypsin, NASH
Prolonged cholestasis (primary biliary
cirrhosis, primary sclerosing cholangitis)
Autoimmune diseases (autoimmune
hepatitis)
Drugs and toxins
Alcohol

Anatomy of the portal venous system

The Effect of The Liver Nodule

Mechanism of Portal HTN

Cirrhosis
Resistance portal flow
Mechanical

Dynamic

Nodules

Nitric oxide

Complications of Portal Hypertension

in cirrhosis liver.
Development

of Ascites.

Varices formation.

Hepatic

encephalopathy.

Hepatorenal

syndrome.

Ascites
Definition: presence

of free fluid in the

peritoneal cavity

Nonperitoneal Causes of Ascites

Non-peritoneal causes

Examples

Intrahepatic portal hypertension Cirrhosis

Fulminant hepatic failure
Veno-occlusive disease
Extrahepatic portal
hypertension

Hepatic vein obstruction

(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-Schnlein purpura

Miscellaneous disorders

Eosinophilic gastroenteritis
Whipple disease
Endometriosis

Etiology
Cirrhosis

(75%)

Most common cause of ascites

Most common complication of cirrhosis
Other causes occur more frequently in cirrhotics

Malignancy

(10%)
Cardiac (3%)
TB (2%)
Pancreatic Ascites(1%)
Various others
Hepatology 38:258-66

Pathophysiology of ascites in CLD:

Splanchnic

HTN due to outflow obstruction

Increased vasodilatation (NO)
This sequesters volume in the abdomen
Decreases systemic filling
Decreases systemic BP
Activates antinatriuretic factors
Combination of increased splanchnic BP with
vasodilatation leads to capillary leak
Lymph return can only keep up for sometime
then ascites develops.

Physical Examination

Bulging Flanks
Flank Dullness
Shifting Dullness
Fluid Wave
Puddle sign
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.

JAMA 1992; 267:2645-48

Bulging Flanks

Occur when weight of

ascites is sufficient to
push the flanks
outwards
Difficult to distinguish
from obesity
Sensitivity-72-93%

Pooled data 81%

Specificity-44-70%

Pooled data 59%

JAMA 1992; 267:2645-48

Flank Dullness

Similar to bulging
flanks, although uses
percussion
Typically bowel will float
to the top and ascitic
fluid sinks to the bottom
Sensitivity-80-94%

Most sensitive test

Pooled data 84%

Specificity-29-69%

69% outlying value

Pooled data 59%

JAMA 1992; 267:2645-48

Shifting Dullness

Find the point where

flank dullness occurs
Mark it
Roll the patient away
from the examiner
Repeat percussion and
ensure that the point
moves to the dependent
side
Sensitivity-60-83%

Pooled data 77%

Specificity-56-90%

Pooled data 72%

JAMA 1992; 267:2645-48

Fluid Wave (fluid thrill)

Medial edges of both

hands down midline
Tap flank firmly and feel
for an impulse on the
other side
Sensitivity-50-80%

Pooled data 62%

Specificity-82-92%

Most specific test

Pooled data 90%

JAMA 1992; 267:2645-48

Puddle Sign

Have patient prone 3-5

minutes then rise to crawling
Place the diaphragm of the
stethoscope over the most
dependent area of the
abdomen
Flick a finger until sound
detected
No longer recommended
Formerly used for high
sensitivity
Sensitivity-43-55%
Pooled data 45%
Specificity-51-83%
Pooled data 73%
JAMA 1992; 267:2645-48

International Ascites Club Grading

Grade

Mild, only detectable by U/S

Grade

Moderate, symmetrical distension

Grade

Gross or large with marked distension

Large

typically means painful/uncomfortable

Refractory

Ascites (5-10%)

Can not be mobilized or early recurrence

refractory to medical management
NEJM 350:1646-54
Hepatology 2003; 38: 258-266

Diagnosing Ascites

Ultrasound is the most

sensitive test for ascites
(100mL detection)

Have to use caution as

small or even moderate
ascites may be difficult to
tap (even when marked)
Ensure mark is
appropriate
Go

with patient to U/S

(ideal)
If not possible, in order
specify location where
you want to place your
needle

Image from www.gastro.org

Paracentesis: General Tips

Do NOT do paracentesis to
see if ascites present, should
know before

If unclear need U/S

Ensure patient has voided

FFP/Platelet transfusion if
indicated

Ensure landmarks

Get Quick-Tap kit, plastic

catheter does not work as
well as the metal one.
Picture from www.kchealthcare.com

Paracentesis:
Site: 5cm cephalic & 5 cm medial to ASIS in the left
lower quadrant of the abdomen has been shown to
be the ideal site with larger pool of fluid.

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

Diagnostic Studies
Recommended

Studies

Albumin
Protein
Cell count
Looking

Cultures

If

clinically
appropriate

for PMNs

Glucose
LDH
Amylase
RBC count
TB smear/culture
Cytology
Triglycerides

www.gastro.org

Diagnostic Studies
1. Check serum
and fluid albumin
2. Check Ascites
Protein
3. Differential
Diagnosis

SAAG
> 1.1
Hepatic Sinusoid source
Ascites Protein <2.5
Capillarized sinusoid

Cirrhosis
Late Budd-Chiari

Ascites Protein >2.5

Peritoneal lymph

SAAG
< 1.1
Peritoneum source
Ascites Protein >2.5
Normal sinusoid

Cardiac ascites
Malignancy
Early Budd-Chiari
Tuberculosis
Veno-occlusive disease

The SAAG does not need to be repeated after the

initial measurement.
Note: Exceptions exist: may have mixed features

Adapted from www.gastro.org

Ascitic fluid analysis:

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.
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.

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.

Prognosis
Poor

outcomes

Refractory

ascites

SBP
HRS
MELD

(Model for end-stage liver disease)

is not specifically validated for patients with
ascites

NEJM 350:1646-54

Prognosis
Any

person with ascites due to cirrhosis

needs transplant evaluation

If MELD is <15 can stop there

Average US wait time 500d
Average wait less in some other countries
120

days in UK
180 days in Spain

If

admitted for ascites 40% chance of dying

within 2 years
Improves to 70-80% 5 year survival after
transplant
Dig Dis 2005; 23:30-38
Hepatology 2003; 38: 258-266

Treatment
Grade

No

treatment necessary
Modify risk factors
Start low sodium diet

Hepatology 2003; 38: 258-266

Treatment
Grade
Bed

rest

Diuretics

work better supine

studied bemetanide
GFR lower standing as well

Sodium

and water restriction

Diuretics

Br Med J. 1986;292:1351-3
Hepatology 2003; 38: 258-266

Treatment
Grade

Paracentesis

is the treatment of choice

Shown

to have fewer complications than

diuresis
Faster response
After

this would do Grade 2 treatment

options

Hepatology 2003; 38: 258-266

Treatment
Refractory

ascites

Paracentesis

with colloid infusion

TIPS
Choice

between these is controversial

If

repeated paracentesis is
contraindicated,TIPS not an option then
consider porto-venous shunt
PVS

shown inferior to repeat paracentesis in

NEJM study

Hepatology 2003; 38: 258-266

Sodium Restriction
No

survival benefit related to ascites

shown, does have benefit in GIB
mortality
50mm restriction is equivalent to
120mm (approx. 2g/day)
Tighter

restriction had faster resolution

Higher incidence of renal dysfunction and
hyponatremia

Hepatology 2003; 38: 258-266

Diuretics
Spironolactone

start 100-200 per day

Titrate to max of 400 per day in severe hyper-aldo

Can

use potassium sparing diuretics

Amiloride inferior to canrenoate (antimineralocorticoid)

No other comparison trials, but spironolactone
accepted as first line
Use second line if spironolactone not possible 2/2
complications (ie gynecomastia)

Hepatology 2003; 38: 258-266

Diuretics
Loop

diuretics

Lasix
Initial

dose 20-40 per day

Can adjust up to 160mg per day
Should

be used only as an adjunct to

spironolactone
Risks of K depletion, hyperchloremic
alkalosis, hyponatremia and hypovolemia
with subsequent renal dysfunction
Dig Dis 2005; 23:30-38
Hepatology 2003; 38: 258-266

Assessing Diuretic Response

Weight

loss

Lose

0.5kg a day when no edema

Lose 1kg a day when edema is present
Avoid

renal failure
Response rate in up to 90% patients
who do NOT have renal dysfunction

Dig Dis 2005; 23:30-38

Hepatology 2003; 38: 258-266

Paracentesis

Paracentesis
First

used by the Ancient Greeks

Decreased in the 1950s when diuretics
were discovered
Resurgence in 1980s after 1987 article
found paracentesis with lower
complications than diuretics
More effective than diuresis
Shorter

hospital stay

Dig Dis 2005; 23:30-38

Paracentesis
Total

volume paracentesis is as
effective and as safe as sequential 3L
paracentesis
Hemodynamics
RA pressure

drops immediately
PCWP takes 6h to decrease

Hepatology 2003; 38: 258-266

Paracentesis
Post

paracentesis volume expansion

Side

effects and albumin

without

30%
with 16%
Albumin

prevents increased renin/aldo

better than synthetic agents
HRS decreases
Less Hyponatremia

NEJM 350:1646-54
Hepatology 2003; 38: 258-266

Paracentesis-Complications
Bleeding

- can be

fatal
Ascitic fluid leak

Purse string suture

Lie with puncture site
up

Bowel

perforation
Renal impairment
Hypotension/Cardio
vascular collapse

TIPS
Transjugular

Intrahepatic
Portosystemic Shunt
Creates a conduit
from the high
pressure portal
system to the lower
pressure systemic
circulation

TIPS
Ascites

can only form when portal

pressure is >12
Response rates 51-79% in RCT

Dig Dis 2005; 23:30-38

TIPS - Benefits
May

improve nitrogen balance

Will decrease portal pressure reducing
GIB risk
Improves hemodynamics
Increased

CO, RA pressure, PCWP and

decreased SVR with increased Na
excretion

Improves

response to diuresis
NEJM 350:1646-54
Hepatology 2003; 38: 258-266

TIPS - Risks
Encephalopathy
30%

those treated
Typically can improve with shunt revision
or medical management
Increased risk if
Age

>60
History of Encephalopathy
100%

mortality if refractory to TIPS

occlusion

CHF

- this is due to increased preload

NEJM 350:1646-54
Am J Gastro 2003;98:2521-27

TIPS - Complications
Capsule

perforation

Stenosis
75%

in 6-12 months
Decreased risk with stents coated in
polytetrafluoroethylene (PTFE)
Increased

cost relative to paracentesis

NEJM 350:1646-54
Radiology 1999;231:759-766

TIPS v. Paracentesis
Several

studies (2 examples)

Lebrec 1996
No

ascites recurrence benefit in CP class C patients with

worsened survival
CP class B showed decreased recurrence
Small study (25 patients)

Salerno - 2004
Shown

to have survival improvement with multivariate

analysis (only trend to improved survival without this)
Non-blinded 3 center study
Had to have 4 taps in the last month
Decreased ascites recurrence HR 0.37 (0.18-0.76)
66 patients
J Hepatol 1996;25:135-44
Hepatology 2004;40:629-635

Cochrane Database
No

difference in mortality
Decreased re-accumulation at 3 and 12
months
Increased PSE OR 2.11(1.22-3.66)
Surprisingly no difference:

GIB, ARF, Infection or DIC

Some

issues in differences between the

studies, not all paracentesis had postparacentesis albumin, differences in
MELD/CP between studies
Hepatology 2003; 38: 258-266

Reasons for TIPS over Paracentesis

TIPS

better if

Loculated

ascites
Patient unwilling to have repeat taps
Frequent recurrences

Am J Gastro 2003;98:2521-27

Peritoneovenous Shunts

Peritoneovenous Shunts
Creates

a communication between the

peritoneal cavity and the systemic
circulation by a vein
Used in only in limited cases currently
Used

for palliation if TIPS and paracentesis

are not available or contraindicated

Hepatology 2003; 38: 258-266

Spontaneous Bacterial Peritonitis

H/O Chronic Liver Disease.
Fever and abdominal pain (66%)
Signs of peritonitis uncommon (<50%)
Neutrocytic ascites on diagnostic

paracentesis.
20-30% of pts with CLD develop SBP.
Almost always monomicrobial.
Anaerobes are not associated with SBP
20% are asymptomatic.
Typically due to translocation

This is why E. Coli is the most common

SBP: Diagnosis.
Diagnosed

with >250 polys or > 50-70%

of the total cell count.
Ascitic protein >1gm/dl against SBP.
10-30% are ascitic fluid culture negative.
3% have secondary Bacterial Peritonitis.
Ascitic fluid Glucose, LDH and total
proteins may be helpful in DDx.
Erect Abd X-ray in suspicious cases.
NEJM 350:1646-54
Hepatology 2003; 38: 258-266

SBP: Treatment and Prophylaxis

Treat with 3rd generation Cephalosporins.

Repeat PMN count after 48 hrs.
40% develop HRS during the course of illness.
Human Albumin 1.5gm/Kg o day one and 1 gm/Kg on day three
has shown improvement in both morbidity and mortality.

Prophylaxis:
70% recur within one year.

Norfloxacin 400mg qd
Ciprofloxacin 750mg q week
Tri-Sulpha: Has never been tested in a trial with mortality.
Ultimate treatment:
Liver transplant.

References
Moore K, Wong F, Gines P, Bernardi M et al. The Management of Ascites in Cirrhosis: Report on the Consensus Conference of the International
Ascites Club. Hepatology 2003;38: 258-266
Gines P, Cardenas A, Arroyo V, Rodes J. Management of Cirrhosis and Asictes. NEJM. 2004;350:1646-1654
Haskal Z. Improved Patency of TIPS in Humans: Creation and Revision with PTFE Stent-Grafts. Radiology. 1999; 213: 759-766
Cardenas A, Arroyo V. Refractory Ascites. Dig Dis. 2005; 23:30-38
Russo M, Sood A, Jacobson I, Brown R. TIPS for Refractory Ascites: An Analysis of the Literature on Efficacy, Morbidity and Mortality. Am J
Gastroenterol. 2003; 98:2521-2527
Heuman D, Abou-assi S, Habib A et al. Persistent Ascites and Low Serum Sodium Identify Patients with Cirrhosis and Low MELD Scores who are at
High Risk for Early Death. Hepatology. 2004; 40: 802-810
Salerno F, Merli M, Riggio O, Cazzangia M, et al. Randomized Controlled Study of TIPS v. Paracentesis Plus Albumin in Cirrhosis with Severe
Ascites. Hepatology 2004;40: 629-635.
Ring-Larsen H, Henriksen J, Wilken C, Clausen J, et al. Diuretic treatment in decompensated cirrhosis and congestive heart failure: effect of posture.
Br Med J 1986; 292: 1351-1353
Lebrec D, Giuily N, Hadengue A, Vilgrain V, et al. TIPS: comparison with paracentesis in patients with cirrhosis and refractory ascites: a randomized
trial. French Group of Clinicians and a Group of Biologists.
Saabs, Nieto JM, Ly D, Runyon BA. TIPS versus paracentesis for cirrhotic patients with refractory ascites. The Cochrane database of Systematic
Reviews 2004, Issue 3 Art. No.: CD004889
Cattau EL, Stanley BB, Knuff TE, et al. The Accuracy of the Physical Examination in the Diagnosis of Suspected Ascites. JAMA. 1982; 247: 11641166.
Williams JW, Simel DL. Does This Patient Have Ascites?. JAMA. 1992; 267: 2645-2648.
Mallory A, Schaefer JW. Complications of Diagnositc Paracentesis in Patients with Liver Disease. JAMA. 1978; 239: 628-630
Runyon BA. Paracentesis of Ascitic Fluid a Safe Procedure. Arch Intern Med. 1986; 146: 2259-2261
Simel DL, Halvorsen RA, Feussner JR. Quantitating bedside diagnosis: clinical evaluation of ascites. J Gen Intern Med. 1988; 3:423-428.
www.uptodate.com
Images:
www.lf2.cuni.cz/Projekty/interna/foto/001/
www.scielo.br/img/revistas/rb/v38n1/
www.krauth-medical.de/onlinekatalog/grafiken/bilder_mm/

Shukriya
smed-ialam@cpsp.edu.pk
intekhab07@yahoo.com