APPROACH TO A

PATIENT WITH
ASCITES
PRESENTED BY - DR MOUNIKA

DR VIKRANTH

DR SUMA

MODERATOR –DR PRIYATAM SIR

DEFINITION

• ASCITES IS DEFINED AS THE ABNORMAL ACCUMULATION OF FLUID IN THE

PERITONEAL CAVITY.
• ASCITES IS THE MOST FREQUENT COMPLICATION IN PATIENTS WITH CIRRHOSIS.
• IT WILL DEVELOP IN APPROXIMATELY 60 PERCENT OF PATIENTS WITHIN 10 YRS OF
DIAGNOSIS OF COMPENSATED CIRRHOSIS.
• THE DEVOLOPMENT OF ASCITES IS ASSOCIATED WITH IMPAIRMENT OF QUALITY OF
LIFE ,AND INCREASED RISK OF DEVELOPING OTHER COMPLICATIONS –SBP ,
HYPONATREMIA ,AKI AND DIMINISHED SURVIVAL.
CAUSES

• CONDITIONS DIRECTLY INVOLVING PERITONEUM -LIKE INFECTIONS,

MALIGNANCY.
• DISEASES REMOTE FROM THE PERITONEUM –LIVER DISEASE ,HEART FAILURE
,HYPOPROTEINEMIA .
CIRRHOSIS IS THE COMMONEST CAUSE OF ASCITES

IN PATIENTS WITH CIRRHOSIS ,

THE DEVELOPMENT OF ASCITES
MARKS THE TRANSITION FROM COMPENSATED
TO DECOMPENSATED CIRRHOSIS.

ASCITES IS THE MOST FREQUENT FIRST

DECOMPENSATING EVENT.
 CAUSES OF ASCITES

 CIRRHOTIC ASCITES : Three most common causes of cirrhosis

• Alcohol, chronic hepatitis C, NASH ( non alcoholic steatohepatitis related to obesity.

 NON CIRRHOTIC ASCITES

• Peritoneal carcinomatosis
• Chylous ascites
• Heart failure
• Nephrotic syndrome
• Infections - Tuberculosis, chlamydia.
• Pancreatic or biliary ascites.
• Budd chiari syndrome.
• Rare causes - Hypo Thyroidism and Familial Mediterranean Fever.
CAUSES OF MALIGNANT ASCITES

• Peritoneal carcinomatosis.
• Massive liver metastasis
• Hepatocellular carcinoma.
• Malignant lymphnode obstruction.
• Malignant Budd-Chiari syndrome ( tumor emboli in hepatic veins )
CT SHOWING PERITONEAL CARCINOMATOSIS(WHITE ARROW) AND ASCITES
(YELLOW ARROW)
REFRACTORY ASCITES

• IT IS DEFINED AS ASCITES THAT CANNOT BE MOBILIZED ,OR THE RECURRENCE

OF WHICH CANNOT BE PREVENTED BY MEDICAL THERAPY BECAUSE OF LACK
OF RESPONSE TO MAXIMUM DIURETIC TREATMENT.
PATHOGENESIS OF
ASCITES
PATHOGENESIS OF
ASCITES IN
CIRRHOSIS
NATURAL HISTORY OF CIRROTIC
ASCITES
DEVELOPMENT OF ASCITES IN CIRRHOSIS IS MAINLY DUE TO:
• PORTAL HYPERTENSION .
• SYSTEMIC CIRCULATORY DYSFUNCTION .
• SODIUM RETENTION AND EXTRACELLULAR FLUID VOLUME EXPANSION .
• SYSTEMIC INFLAMMATION .
PORTAL HYPERTENSION

• IT IS A MAIN CAUSE FOR DEVELOPMENT OF CIRCULATORY DYSFUNCTION IN

PATIENT WITH ADVANCED CIRHHOSIS .
• CIRRHOSIS IS PROGRESSIVE LIVER INFLAMMATION AND FIBROSIS IN RESPONSE
TO CHRONIC INJURY [ALCOHOL, CHRONIC VIRAL HEPATITIS ……] .
 INCREASE HEPATIC RESISTANCE IN CIRRHOSIS OCCURS DUE TO
VARIOUS MECHANISMS:
• [1] CIRRHOSIS  STRUCTURAL ABNORMALITIES ( DUE TO COLLAGEN
DEPOSITION AND FORMATION OF NODULES IN HEPATIC PARENCHYMA )
DISTURBANCE IN INTRAHEPATIC CIRCULATION -INCREASED RESISTANCE TO
PORTAL FLOW CAUSING PORTAL HYPERTENSON
• [2] CIRRHOSIS. - ACTIVATION OF HEPATIC STELLATE CELLS ----> INCREASE
SMOOTH MUSCLE CONTRACTILITY AND FIBROSIS---INCREASE VASCULAR
TONE AND INTRAHEPATIC RESISTANCE
• [3] CIRROTIC LIVER -DECREASED PRODUCTION OF NITRIC OXIDE(NO) FROM
ENDOTHELIAL NITRIC OXIDE SYNTHASE IN INTRA HEPATIC CIRCULATION
• [4] IN ADVANCED CIRRHOSIS ,KUPFFER CELLS INDUCE PRODUCTION OF PRO
INFLAMMATORY CYTOKINES ,ROS ,VASOACTIVE MEDIATORS-------- CAUSING
HEPATIC AND SYSTEMIC INFLAMMATION ------INCREASED VASCULAR
RESISTANCE .
MEASUREMENT OF PORTAL HYPERTENSION

PORTAL HYPERTENSION IS ASESSED BY MEASUREMENT OF HEPATIC VENOUS

PRESSURE GRADIENT [HVPG------DIFFERENCE BETWEEN WEDGED AND FREE
HEPATIC VENOUS PRESSURE ]
MEASURED BY HEPATIC VEIN CATHETER
• NORMAL HVPG IS ----------5 MM OF HG
• HVPG ---10-12 MM OF HG ---------------------.>. CLINICAL MANIFESTATIONS OF
PORTAL HYPERTENSION [ASCITES]. ARE SEEN .
• HVPG-. >16. MM OF HG -HIGH RISK OF MORTALITY
• HVPG ----- >20 MM OF HG – TREATMENT FAILURE AND MORTALITY
SYSTEMIC CIRCULATORY DYSFUNCTION

• CIRRHOSIS IS ASSOCIATED WITH INCREASED SYSTEMIC CIRCULATORY LEVELS

OF NITRIC OXIDE .
• NO SYSNTHESIS IS ACTIVATED IN PORTAL HYPERTENSION BY ENDOTHELIAL
CELL STIMULI , INCLUDING VEGF , ANGIOTENSIN ,STRESS AND INFLAMMATORY
CYTOKINES -------- SPLANCHNIC ARTERIAL VASODILATION.
 SPLANCHNIC ARTERIAL VASODILATION

↓
DECREASED VASCULAR RESISTANCE AND POOLING OF BLOOD

↓
DECREASED EFFECTIVE ARTERIAL BLOOD VOLUME
AND ARTERIAL PRESSURE

↓
PERCEIVED BY KIDNEY AS HYPOVOLEMIA

↓
COMPENSATORY VASOCONSTRICTION [RELEASE OF ADH,ACTIVATION OF
RAAS AND SYMPATHETIC NERVOUS SYSTEM]
THE RENIN ANGIOTENSIN ALDOSTERONE
SYSTEM
• RENIN IS PRODUCED BY THE KIDNEY IN RESPONSE TO LOW BLOOD VOLUME AND BETA
ADRENERGIC STIMULATION.
• UNDER THE INFLUENCE OF RENIN , ANGIOTENSINOGEN [SYNTHESISED IN LIVER ] IS
CONVERTED TO ANGIOTENSIN 1 WHICH IS CONVERTED TO ANGIOTENSIN 2 BY ACE .
• ANGIOTENSIN 2 IS THE MAIN STIMULANT TO THE SYNTHESIS OF ALDOSTERONE FROM
ADRENAL CORTEX .

• ALDOSTERONE ACTS ON CELLS OF COLLECTING DUCT ,INCREASES BOTH LUMINAL

UPATAKE AND BASOLATERAL PASSAGE OF SODIUM.
NATRIURESIS AFTER SPIRONOLACTONE ,AN ALDOSTERONE ANTAGONIST ,SUPPORTS HYPERALDOSTERONISM
AS A MAJOR CONTRIBUTOR TO SODIUM RETENTION IN CIRRHOSIS .
SODIUM RETENTION

• SODIUM RETENTION IS THE MOST FREQUENT AND EARLIEST RENAL

ABNORMALITY IN PT. WITH CIRRHOSIS
• IT IS THE KEY FACTOR IN EXPANSION OF ECF VOLUME AND DEVELOPMENT OF
ASCITES AND EDEMA
• ASCITES CAN BE RELIEVED BY SODIUM RESTRICTION IN DIET OR ENHANCING
SODIUM EXCRETION BY DIURETICS
• PT. WITH SEVERE OR REFRACTORY ASCITIS HAVE MARKED SODIUM
RETENTION(URINE EXCRETION OF SODIUM <10 MEQ/DAY)
PATHOGENESIS OF ASCITES IN THE
ABSENCE OF CIRRHOSIS
• PERITONEAL CARCINOMATOSIS: TUMOUR CELLS LINING PERITONEUM
PRODUCES PROTEIN RICH FLUID
• TUBERCULOUS ASCITES: TUBERCLES DEPOSITED ON THE PERITONEUM EXCUDE
PROTEINACEOUS FLUID
• PANCREATIC ASCITES:LEAKAGE OF PANCREATIC ENZYMES
• PORTAL VEIN THROMBOSIS
• HYPOALBUMINEMIA SECONDARY TO PROTEINURIA
CHYLOUS ASCITES:MILKY APPEARING PERITONEAL FLUID, RICH IN TRIGLYCERIDES.DEVELOPS
DUE TO DISRUPTION OF LYMPHATIC SYSTEM,TRAUMATIC INJURY OR OBSTRUCTION
 CAUSES-NEOPLASMS:Lymphoma,carcinoid tumor,CIRRHOSIS,CONGENITAL:primary
lymphoid hyperplasia,INFECTIONS:tb,filariasis,INFLAMMATORY:radiation,pancreatitis, etc
BLOODY ASCITES:ASCITIC FLUID WITH RBC >50,000/ MM3
• COMMON CAUSE –TRAUMATIC PARACENTESIS
• NON TRAUMATIC –MALIGNANCY:HEPATOCELLULAR CARCINOMA
ASCITES PRECOX

• ASCITES OCCURS BEFORE LOWER LIMB EDEMA IN CARDIAC PATIENTS

• CAUSES:
 TRICUSPID REGURGITATION
 PERICARDIAL EFFUSION
 CONSTRICTIVE PERICARDITIS
CLINICAL FEATURES

• GRADING OF ASCITES
 GRADE 1:Mild ascites detectable only by ultrasound
 GRADE 2:Moderate ascites manifested by symmetrical distension of abdomen
 GRADE 3:Large or gross ascites with marked abdominal distension
GRADE 2 AND 3 ARE CLINICALLY SYMPTOMATIC AND REQUIRE TREATMENT
SYMPTOMS

• INCREASED ABDOMINAL GIRTH AND RECENT WEIGHT GAIN

• SHORTNESS OF BREATH(ACCUMULATED FLUID ELEVATES THE DIAPHRAGM)
• FEELING OF SATIETY AND GENERALISED PAIN ABDOMEN
TAKE HOME POINTS

• ASCITES IS THE MOST COMMON DECOMPENSATING EVENT IN CIRRHOSIS

• DEVELOPMENT OF PORTAL HYPERTENSION IS THE FIRST STEP IN FLUID RETENTION
IN CIRRHOSIS
• PORTAL HTN >12MM HG –REQUIRED FOR FLUID RETENTION
• SODIUM RETENTION IS A SENSITIVE MARKER IN PT. WITH CIRRHOSIS
• SPLANCHNIC ARTERIAL VASODILATION IS THE UNDERLYING MECHANISM FOR RENAL
DERANGEMENT
• 5 YR SURVIVAL RATE OF PT. WITH CIRRHOSIS AND ASCITES IS APPROX.30% COMPARED
TO 80% SURVIVAL RATE IN PT. WITH COMPENSATED CIRRHOSIS
THANK YOU
EVALUATION OF ASCITES

PRESENTED BY Dr.VIKRANTH

MODERATOR :Dr.PRIYATHAM SIR

Evaluation of cause of Ascites
IS BY

HISTORY

PHYSICAL EXAMINATION

ACSITIC FLUID ANALYSIS

 • Most of the ascites is due to
cirrhosis(85%)

• RISK FACTORS:

• ALCOHOL

• DRUG USAGE

• BLOOD TRANSFUSION

HISTORY • ACUPUNCTURES

• TATOOS

• EAR PIERCING

• LIFE TIME MAXIMUM BODY WEIGHT

• Ascites in middle age or elderly female-

Viral hepatitis induced cirrhosis
Patient with long history of stable cirrhosis and sudden
development of ascites –s/o of hepatocellular carcinoma

Ascites with history of cancer-s/o of malignancy associated

ascites

Malignant associated ascites is painful where as stable

cirrohis is painless unless bacterial peritonitis or alcoholic
hepatitis is superimposed

h/o of heart failure – s/o of cardiac ascites

Ascites due to tb peritonitis –manifest with fever and abd pain

Ascites occurs in acute pancreatitis with necrosis or ruptured

pancreatic cyst due to chronic panncreatitis or trauma

Ascites in sexually active female –may be due to FITZ HUGH

CURTIS SYNDROME caused by chlamydia or gonorrhea

Diabetic with ascities and anasarca – rule out nephrotic ascites

patients with chylous ascites may have lower extremity edema,

lymphadenopathy, cachexia, abdominal masses, and temporal
wasting
 • Abdominal distension
• Check for Flank dullness, if present
check

shifting (Rule out D/D for distension

of abdomen by percussion)
• d/d- ABD. DISTENSION,OVARIAN
PHYSICAL MASS etc.
• 1500ml approax. Must be
EXAMINATION present before dullness is detected

• Check for the signs of liver cell

failure -palmar erythema ,spider
telangectasias, large collateral veins

• Large veins in the back- s/o of IVC

BLOCKAGE
DIAGNOSIS
• Diagnosis of ascites:
• abdominal paracentesis/USG
 Indications:
• New onset ascites
for evaluation of
ABDOMINAL cause All in-patient
PARACENTESIS with ascites
• Repeat the
paracentesis if signs
of infection appears
CONTR-INDICATIONS:
Coagulopathy: only when clinically evident DIC or
fibrinolysis is present

PATIENT POSITION
Supine or lateral decubitus position

INSERTION SITE

• Left lower quadrant> right lower quadrant

• Careful in the case of surgical scar- risk of
perforation due to adhesion of bowel to scar
tissue
CHOICE OF NEEDLE
1.5 inch, 22 guage needle or 3.5inch ,22 guage
needle (obese)

Steel needles preferred to plastic sheathed canula

TECHNIQUE

DIAGNOSTIC PARACENTESIS:

• Sterile aseptic measures

• local anesthesia infiltrated

• Z technique:it doesn’t involve manipulating needle up

and down

• Technique invloves displacing the skin 2cm downward

and slow insertion of needle and release the skin only
when peritonium is penetrated and fluid flows
ASCITIC fluid Analysis

Routine optional Unusual Unhelpful

Cell count Amylase Bilirubin Cholesterol
Albumin Culture in blood Cytology Fibronectin
culture bottles
Total protein Glucose MTB smear, culture Lactate
and PCR
Gram stain, LDH TG ph

ADA
 GROSS APPEARANCE
Normal Transparent and slightly yellow
Absolute neutrophil count <1000/mm3 Nearly clear
Counts >5000/mm3 Cloudy and shimmering effect
Counts >50,000/mm3 Resembles mayonnaise
RBC count of 10,000/mm3 Pink appearance
RBC count of >20,000/mm3 Distictly red
Traumatic Tap Blood clots
Milky fluid TG >200mg/dl (without shimmering
effect) and layers out if placed in
refrigerator
Dilute Skim milk TG 100-200mg/dl
Jet black or Tea coloured Pancreatic Ascites and Malignant
melanoma
Dark brown fluid Biliary perforation
CELL COUNT
• WBC < 500 cells/mm3
• PMN <250 cells/mm3
• Corrected WBC count in traumatic tap- 1PMN
subtacted for every 250 RBC

• SBP- neutrophilic predominance

• TB peritonitis and peritoneal carcinomatosis-
Lmphocytic predominance
SAAG(serum ascites albumin gradient)
• Based on oncotic-hydrostatic balance
• Calculated by subtracting the albumin values of
both serum and ascitic fluid

• Correlates directly with portal pressure

• SAAG of > 1.1gm/dl considered to have portal HTN
(97% accuracy)
• After diuretics SAAG narrows down in cardiac
ascites ,
never in cirrhosis of liver

• Help ful in management

Draw backs-

• Doesn’t explain pathogenesis of ascites formation

,it only indicates accurate index of portal
pressure

• SAAG falsely low if S.Albumin is less than

1.1gm/dl in cases of cirrhosis is about 1%
• Both serum and acsitic sample should be obtained

simultaneously as levels varies with time

• Lipid interferes in albumin assay->falsely high

SAAG in chylous ascites

• Arterial hypotension ->decrease portal htn.

Further narrows SAAG
• Hyperglobulinaemia (>5gm/dl)-> narrows albumin
gradient by contributing to oncotic forces
• Corrected SAAG in
hyperglobulinaemia=uncorrected
SAAG*0.16*serum globulin +2.5
• Approx 5% cases of ascites have mixed ascites
(TB peritonitis and cirrhosis) and SAAG will be
>1.1gm/dl due to underlying portal htn.
CULTURE

• Done with blood culture bottles with high

sensitivity
• Sensitivity was approx. around 50% in agar
plates and 80% in blood culture bottle
method
TOTAL PROTEIN
• Depends on Serum protein concentration
and
• Almost 20% cases of cirrhosis with relatively
high serum protein will have ascitic fliuid
protein >2.5gm/dl

• Total protein doesn’t increase during SBP

• Cardiac ascites > 2.5gm/dl
• HCC, massive liver metastasis <2.5gm/dl
• SAAG classifies fluid by the presence or
absence of portal htn.
• Old transudate/ exudate classification is
obsolete now
• Combination of total protein , glucose and LDH helps in
• distinguishing SBP from secondary peritonitis
• Pts with neutrocytic ascitic fluid whom the clinical
picture suggests bacterial peritonitis who meet 2/3 of
following criteria
• Total protein> 1gm/dl

• Glucose less than 50mg/dl

• LDH > upper limit of normal for serum(>225u/l)

GLUCOSE
• APPROX equal to serum glucose
• In SBP detected late almost drops to 0mg/dl
LDH
• Uncomplicated ascites- half of the serum level
• SBP and secondary peritonitis – concentration is more than
serum
AMYLASE
• Normal-<50u/l
• Acute pancreatitis and intestinal perforation- >2000u/l(5 folds
of serum)
GRAM STAIN of ASCITIC FLUID

• Detects only if >10,000 bacteria/ml

• In SBP concentration usually 1/ml (sensitivity
of 10% for visualisation of bacteria )

• Helpful in diagnosis of secondary peritonitis

Zn STAIN and CULTURE FOR TB
Stain is Rarely positive
Sensitivity of culture is 50% and 100% in laproscopy
with histology and culture of peritoneal biopsy

CYTOLOGICAL EXAMINATION
It wil not detect unless peritoneal in involved
sensitivity is 100% in peritoneal carcinomatosis and 20-30%
in malignancy related ascited

Serum AFP is more sensitive than ascitic fluid cytology in HCC

TRIGLYCERIDES
• Chylous ascites- > 200mg/dl (usually
greater than 1000mg/dl)
• In cirrhosis,

• Sterile but cloudy ascites:60+/- 40mg/dl

• Clear acsites :18+/- 9mg/dl
BILIRUBIN
• >6mg/dl or greater than serum bilirubin(ascitic
fluid/serum bilirubin >1 - s/o biliary or proximal SI
perforation
 Cirrhosis - elevated INR
hypoalbuminemia,
thrombocytopenia,
Anemia
Leukopenia

• Spontaneous leucocytosis
OTHER Bacterial - metabolic acidosis
FINDINGS Peritonitis azotemia

• chylous ascites - hypoalbuminemia,

decreased gamma globulin levels,

lymphopenia.
 patients with SBP, mortality
increases by 3.3 percent/hour of
delay in performing a paracentesis

Ascites in sexually active female –

TAKE may be due to FITZ HUGH CURTIS
SYNDROME caused by chlamydia or
HOME gonorrhea
MESSAGE
• After diuretics SAAG narrows dow
n in cardiac ascites ,never in
cirrhosis of liver
• Paracentesis is preferred
in Left lower quadrant> right
lower quadrant
COMPLICATIONS AND
TREATMENT OF ASCITES
 COMPLICATIONS
1. ASCITIC FLUID INFECTION INCLUDING SBP :
 Classification of ascitic fluid infection :
 Spontaneous bacterial peritonitis
 Culture negative neutrocytic ascites (CNNA)
 Monomicrobial non- neutrocytic bacterial ascites(MNB)
 Polymicrobial bacterial ascites
 Secondary bacterial peritonitis
 CRITERIA
SBP MNB CNNA SEC BACTERIAL POLYMICROBIA
PERITONITIS L
BACTERASCITES
positive ascitic Positive ascitic Negative Positive ascetic Positive
fluid culture ( fluid culture ( culture fluid culture ( ascetic fluid
monomicrobial monomicrobial) polymicrobial) culture(poly

PMN>250/mm3 PMN<250/mm3 PMN>250/mm3 PMN > 250/mm3 PMN<250/mm3

No evidence of No evidence of No antibiotic Evidence of Previous

intraabdominal intraabdominal given intraabdominal traumatic tap
surgically surgically surgically treatable
treatable source treatable source source of infection
of infection of infection.
PATHOGENS COMMONLY INVOLVED
PATHOGENESIS
SIGNS AND SYMPTOMS
RISK FACTORS :
 Bacterial infection occurred in 34% of hospitalized patients
due to low ascitic fluid protein and phagocytic destruction.
 Ascites associated with cirrhosis
 Paracentesis
 Iatrogenic peritonitis when paracentesis needle enters the
bowel during paracentesis
 Gastrointestinal hemorrhage and UTI.
 Ascitic fluid conc <1gm /dl is a risk factor for SBP .
DIAGNOSIS :
 Clinical deterioration , especially fever , abdominal pain
 An elevated absolute ascitic fluid PMN with predominance
of neutrophils in a clinical setting should prompt empirical
antibiotic therapy.
 SBP is 6 times as common as surgical peritonitis , but
secondary peritonitis should be considered in a pt with
neutrocytic ascites.
 Perforation should be suspected if the specimen is
neutrocytic and total protein >1g/dl , glucose<50mg , LDH >
 Ascitic fluid amylase - >5 times serum level – intestinal rupture
 Brown ascetic fluid – bilirubin conc.>6 times serum – biliary /
small bowel perforation.
TREATMENT OF INFECTION
 Oral antibiotics : oral ofloxacin is as effective as IV
cefotaxime 400mg/BD .
 Duration – 10-14 days
 IV albumin – 1.5g/kg of body wt. at the time the infection
Is detected and 1g/kg body wt. on day 3 can increase
intravascular volume and in combination with cefotaxime has
been shown to reduce the risk of renal failure and improve
the pt condition.
PROGNOSIS :
 48-95% with spontaneous ascetic fluid infection died during
hospitalization despite antibiotic treatment.
 The trial in which cefotaxime and albumin was studied –
lowest mortality rates.
 To maximize survival, it is important that paracentesis is
performed in all patients with ascites at the time of
hospitalization , so that infection can be detected and
treated.
 Paracentesis should be repeated if any manifestation of
clinical deterioration develops including abdominal pain,
fever, change in mental status , renal failure.
PREVENTION
 2. TENSE ASCITES:
 Tense ascites can be drained without untoward
hemodynamic effects .
 Total paracentesis even more than 22L has been safe .
 It improves venous return and hemodynamics .
 3. PLEURAL EFFUSION :
 a large effusion in patient with cirrhotic ascites is designated
hepatic hydrothorax.
 Most common symptom – SOB
 Infection (SBP) – transmission across diaphragm .
 Sodium restriction and use of diuretics with intermittent
thoracocentesis - safest and most effective first line therapy.
 4.HYPONATREMIA :
 Serum sodium conc.- <130meq/l (dilutional) in 22% of pts.
 Normal inhibition of vasopressins by water load is blunted or
absent .
 May contribute to encephalopathy.
 Treated by short term use of vaptans( lixivaptan / satavaptan)
 IV albumin
 5. HEPATO- RENAL SYNDROME : severe complication in
cirrhosis with ascites .
 2 types : rapidly progressive reduction of renal function
progressive but slow deterioration in renal function
 main predictors : hyponatremia , refractory ascites ,
increase in plasma renin activity .
 General measures : diuretics should be stopped ,
intravascular volume expanded by IV albumin – 1g/kg body
wt . Upto 100g .this can be repeated in 12 hrs .
 Search for sepsis and ascetic tap done for WBCs , grams
stain , culture .
 Liver transplant is the definitive treatment for HRS
 Pharma therapy : vasoconstrictors + IV albumin
ALGORITHM FOR TREATMENT OF ASCITES
TREATMENT OF ASCITES:
 Accurate determination of the etiology of ascites is crucial
.the SAAG is helpful diagnostically and for therapeutic
decision making .
 Low SAAG – no portal HTN , does not respond to salt
restriction and diuretics .
 High SAAG – respond to salt restriction and diuretics .
 Low gradient ascites –
 TB peritonitis – ATT
 Pancreatic ascites – spontaneous resolution or stenting
 Chlamydia – doxycycline
 Peritoneal carcinomatosis(MC) – repeated paracentesis
 High gradient ascites:
 Cirrhosis – most common cause
 Abstinence from alcohol is the most important step.
 Diet education – dietary sodium restriction (upto 2g/day) is
essential for fluid loss and weight change .
 Fluid restriction – severe hyponatremia does warrant fluid
restriction . Sodium restriction not fluid restriction results in wt
loss.
 Avoid bladder catheterization.
 diuretics :
 Start spironolactone and furosemide together on 1st day
with 100mg and 40mg once in the morning orally.
 Amiloride 10 mg /eplirenone are new drugs
 Half life of spironolactone is 24 hrs , multiple doses not
needed.
 If these doses are ineffective , both drugs should be
increased simultaneously .
 100:40 ration to maintain normokalemia .
 If hypokalemia – spironolactone alone until k+ normalizes .
 IV diuretics - decrease gfr in cirrhosis and ascites . IV
furosemide leads to azotemia and hepatorenal synd .
 Discontinue diuretics – encephalopathy , sr.sodium conc;
<120mol/L , sr.creatinine ;> 2mg/dl
 NSAIDS – should be avoided as they inhibit diuresis
 No data exists that supports withheld of diuretics if BP is low
,baseline bp is usually low .
 Patients can be discharged after they are responding to
medical regimen and are normokalemic and with normal
or slightly low sodium level .
 Revisit to OP after 1 week and monitor body wt ,
sr.electrolytes , urea , creatinine levels.
 Lactulose, rifaximin ( 550mg BD ) , zinc – encephalopathy
 Refractory ascites:
 Ascites unresponsive to a sodium restricted diet , and high
dose diuretic therapy .
 Minimal or no wt loss despite diuretics or development of
complications of diuretics .
 Viable options include liver transplantation, serial
therapeutic paracentesis , TIPS , peritoneovenous shunts .
 Abdominal paracentesis :
 Indication - new onset ascites for evaluation of cause
all in-patient with ascites
repeat if signs of infection appears
Contraindications – coagulopathy ( clinical DIC or fibrinolysis)
 patient in supine or lateral decubitus position
 Insertion site – left lower quadrant > rt lower quadrant , 2
finger breadth cephalad and 2 finger breadth medial
 Choice of needle – 1.5 inch , 22 guage or 3.5 inch 22 guage
 Technique –
 for diagnostic : sterile aseptic measures
local anasethetia , Z technique
slow insertions with intermittent aspirations
approx. . 30 ml of fluid
discard the needle and attach another
inoculate into 2 blood culture bottles
For therapeutic : 1.5 inch 18 guage
use of vaccum bottles or pump
2 to 4 litres of fluid is removed in diuretic
sensitive . Total tap is done for diuretic resistant .
 Indications :
 Tense acites
 Diuretic resistant ascites ( second line management )
 Childs score grade B
 Selection of patients :
 serum bilirubin - < 10 mg/dl
 Plt >40,000
 Sr.creatinine ,3mg/dl
 Complictions : persistant leak from the site, wound infection ,
abdominal wall hematoma , spontaneous hemoperitoneum ,
hollow viscus perforation
 Colloid replacement : avoid serial large volume paracentesis in
pts with diuretic sensitive ascites.
 IV infusion of albumin – LVP decreases the risk of “post
paracentesis circulatory dysfunction” – 6 – 8 g/l of fluid removed
 With hold albumin after taps of 5 L or less
 Consider albumin infusion after taps of large volume of
paracentesis in diuretic resistant ascites.
 TIPS : it is a side to side portocaval shunt ., it was first used iin
refractory variceal bleeding . Now in diuretic resistant ascites ,
varices, hepatic hydrothorax
 Peritoneo venous shunt. : contraindicated in coagulopathy ,
loculated ascites , advanced renal or cardiac disease .
 Take home message : pearls
 It is important to recognize SBP early in course of infection – to
ensure a good outcome
 E.Coli is the commonest causative organism of infection.
 Delayed paracentesis in patients with SBP leads to 2.7
increase risk of death .
 First line treatment of patient with cirrhosis and ascites:
sodium restriction , and diuretics.
 Use of ACEIs and ARBS may be harmful
 Oral midodrine has been shown to improve clinical outcomes
in refractory
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