AscitesAssociate Professor Dr Meltem Ergun

Yeditepe University

Department of Gastroenterology

Points of this lecture

What is ascites? Etiologies of ascites Clinical presentations Pyhsical examination findings Laboratory tests Prognosis Spontaneous bacterial peritonitis

Pathological accumulation of fluid in abdominal cavity>50 ml

Definition

Pathophysiology of Ascites

From: Robbins Basic Pathology

Causes of Ascites

Cause Frequency

Cirrhosis 81%

Cancer 10%

Heart Failure 3%

Tuberculosis 2%

Dialysis 1%

Pancreatic Disease 1%

Other 2%

Rare Causes of Ascites

Category

Infectious diseases Amebiasis, Ascariasis, Brucellosis, Chlamydia peritonitis, Complications related to HIV infection, Pelvic inflammatory disease, Pseudomembranous colitis, Salmonellosis, Whipple's disease

Hematologic Amyloidosis, Castleman's syndrome, Extramedullary hematopoiesis, Hemophagocytic syndrome, Histiocytosis X, Leukemia, Lymphoma, Mastocytosis, Multiple myeloma

Miscellaneous Crohn's disease, Endometriosis, Gaucher's disease, Lymphangioleiomyomatosis, Myxedema, Nephrotic syndrome, lymphatic tear or ureteral injury. Ovarian hyperstimulation

Imaging

Ultrasound with Dopplers

Easily confirms ascites

May see nodularity of cirrhosis

Evaluate patency of vasculature

No radiation, contrast

CT / MRI

Evaluation for malignancy

Serum to Ascites Albumin Gradient

Is portal hypertension present?

97% accurate

SAAG > 1.1 g/dL Portal HTN

SAAG < 1.1 g/dL Other causes

The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Runyon BA; Montano AA; Akriviadis EA; Antillon MR; Irving MA; McHutchison Ann Intern Med 1992 Aug 1;117(3):215-20.

Serum to Ascites Albumin Gradient

SAAG > 1.1 g/dL SAAG < 1.1 g/dL

Cirrhosis Peritoneal carcinomatosis

Alcoholic hepatitis Peritoneal tuberculosis

Acute liver failure Pancreatitis

Budd Chiari Syndrome Nephrotic syndrome

Congestive heart failure/constrictive pericarditis

Serositis

Tests on Ascitic Fluid

Routine Optional Unusual

Cell count and differential

Glucose concentration

Tuberculosis smear and culture, adenosine deaminase

Albumin concentration

LDH concentration Cytology

Total protein concentration

Gram stain Triglyceride concentration

Culture in blood culture bottles

Amylase concentration

Bilirubin concentration

Cell Count, differential and culture

Is ascites infected?

Greater than 250 PMN = SBP

If ascites is bloody ( > 50,000 RBC/mm3), correct by subtracting 1 PMN / 250 RBC

Is ascites bloody?

5% of pts w/ cirrhosis - spontaneous or s/p traumatic tap.

Non-traumatic associated with malignancy

20% of malignant ascites

10% of peritoneal carcinomatosis

Total Protein

Exudate ( > 2.5 g/dL) or Transudate?

Supplanted by SAAG

Is there gut perforation? (vs SBP)

Total protein >1 g/dL

Glucose <50 mg/dL (2.8 mmol/L)

LDH greater than serum ULN

Glucose and LDH

Consistent with infection or malignancy?

Infection and cancer consume glucoselow

LDH is a larger molecule than glucose, enters ascitic fluid with difficulty.

Ascitis/Serum LDH ratio

~ 0.4 in cirrhotic ascites

Approaches 1.0 in SBP

>1.0, usually infection or tumor

Other tests Amylase

Uncomplicated cirrhotic ascites

About 40 IU/L. The AF/S ratio is about 0.4

Pancreatic ascites

About 2000 IU/L. The AF/S ratio is about 6

Triglycerides — run on milky fluid.

Chylous ascites - TG > 200 mg/dL, usually 1000 mg/dL

Bilirubin — run on brown ascites.

Biliary perforation – AF Bili > serum Bili

Tests for TB

Smear – extremely insensitive

Culture – 62-83% when large volumes cultured

Cell count – mononuclear cell predominance

Adenosine deaminase –

Enzyme involved in lymphoid maturation

Falsely low in pts with both cirrhosis and TB

Cytology

“almost 100%” with peritoneal carcinomatosis have positive cytology

Malignant ascites from massive hepatic mets, HCC, lymphoma are usually negative

Overall sensitivity for detection of malignancy-related ascites is 58 to 75 %

Not helpful

“Some tests of ascitic fluid appear to be useless. These include pH, lactate, and ‘humoral tests of malignancy’ such as fibronectin, cholesterol, and many others”

Biopsy

Cirrhosis Fatty Liver

http://library.med.utah.edu/WebPath/LIVEHTML/LIVERIDX.html#2

Causes of Cirrhosis

Cause Testing

Alcoholic liver disease History, AST / ALT > 2

Chronic hepatitis C Hep C Ab, Viral load

Primary biliary cirrhosis Antimitochondrial antibodies

Primary sclerosing cholangitis Contrast cholangiography , ANA, Anti smooth muscle Ab, ANCA

Autoimmune hepatitis Type 1: ANA, ANCA antismooth muscle Ab Type 2: anti-LKM-1

Chronic hepatitis B Hepatitis B serologies

Hemochromatosis Ferritin, genetic testing

Wilson’s disease Ceruloplasmin

Alpha-1-antitrypsin deficiency Serum AAT

Nonalcoholic fatty liver disease Hx of DM or metabolic syndrome

Malignant Ascites

Definition: abnormal accumulation of fluid in the peritoneal cavity as a consequence of cancer.

Commonly caused by cancers of:

Breast, bronchus, ovary, stomach, pancreas, colon

20% of cases have tumors of unknown primary

Survival poor – usually less than 3 months

Becker, G. Malignant ascites: Systematic review and guideline for treatment. European Journal of Cancer 42 (2006) 589 - 597

Malignant Ascites: Pathophysiology

Obstruction of lymphatics by tumor

Prevents absorption of fluid and protein

Alteration in vascular permeability

Hormonal mechanisms (VEGF, IL2, TNF alpha)

Decreased circulating blood volume

Activates RAAS leading to Na retention

Pathophysiology of Malignant Ascites

Management of Malignant Ascites

Therapeutic paracentesis

Removing up to 5L appears safe

No good data on role of volume expanders

Diuretics

Equivocal evidence of efficacy

May be helpful for portal HTN

Less/minimally useful when no portal HTN

Drainage Catheters

Peritoneovenous shunts

Peritoneovenous Shunt

Denver Shunt(Similar to LaVeen Shunt)

Contraindications•Protein > 4.5 g/l (occlusion)•Loculated ascites•Coagulopathy•Advanced renal/cardiac disease•GI malignancy

Complications•Infection•Hematogenous spread of mets•DIC•Pulmonary edema•Pulmonary emboli

Transjugular intrahepatic portosystemic shunt (TIPS)

66 yrs old, man presented with abdominal distension and jaundice , started 3 months ago. He had been diagnosed HBS Ag carrier 20 years ago but had no follow up.

Ascites and peripheral edema

Examination of Abdomen

Percussion liver Spleen

Palpation Liver Spleen

Examination of ascites

Radiological findings Abdominal ultasonography

Irregular and nodular surface of the liver

Splenomegaly

Ascites

Abdominal MRI and CT

Sometimes better than USG

How about liver biopsy

Its highly invasive

%1-2 severe bleeding and

sometimes mortality

Hematologic problems

So when biopsy?

if clinically, radiologically and laboratuary findings do not clearly indicate cirrhosis

If we do not clarify the etiologic factor and suspect of treatable condition

Staging of Cirrhosis

Interpretation:Class A: 5-6Class B: 7-9

Class C: 10-15

Prognosis of Cirrhosis

Points ClassOne year survival

Two year survival

5-6 A 100% 85%

7-9 B 81% 57%

10-15 C 45% 35%

Mortality is usually related with the occurence of complications

Model of End Stage Liver Disease Score (MELD)

Treatment At Early Stage Early treatment may affect prognosis

Stop alcohol drinking

Eradication of viruses

Treatment of the cause

– Autoimmune

– Wilson

– Hemachromatosis

– Sclerozing Cholangitis

Very good followup

Prevention of complications

Low Na Diet

Treatment for Ascites Diuretics (Spironolactone, furosemide)

Low sodium diet

Therapeutic parasentesis

Transplantation

Ascites; usually the first complication !!

Sometimes no symptom Abdominal distension Feeling abdominal

tenderness Treatment

Na restriction Dıuretics Terapeutic parasentesis

•Serum alb – ascites alb >1.1•LDH, protein, glucose

•Cell count•Cytology•Culture

Spontaneous bacterial peritonitis

Spontaneous infection of ascites Any cirrhotic patient with

Fever Abdominal pain Abdominal tenderness Detoriation of clinical situation

Parasentesis Neutrophil count>250/ml Ascites culture: mostly E.coli

Treatment i.v antibiotics: 3th generation cephalosporins (cefotaxim) first

choise, quinalons or penicilins

Spontaneus Bacterial Peritonitis: Mechanism

IntesineAbdominal Cavity

Ascitic Fluid

Portal VeinLIVER

Systemic Circulation

Inte

stin

al P

erm

eab

ility

Bac

teria

l Ove

rgro

wth •Loss of opsanization

•Decreased complemant amount

Kupfher Cell Loss

Dec

reas

ed R

ES

Fun

ctio

n

Collatera

lly pass

Causative microorganisms of spontaneous bacterial peritonitis, bacterascites and secondary peritonitis

Microorganisms SBP BacterascitesSecondary peritonitis

Monomicrobial

Escherichia coli 37 27 20

Klebsiella pneumoniae 17 11 7

Pneumococcus 12 9 0

Streptococcus viridans 9 2 0

Staphylococcus aureus 0 7 11

Miscellaneous Gram-negative

10 14 7

Miscellaneous Gram-positive

14 10 0

Polymicrobial 1 0 53

Liver Transplantation

Each patient who has the complications must be listed for transplantation

Child Score > 9

MELD Score > 10

Urgent Tx

Acute fulminant liver failure

Acute on chronic liver failure

Cadaveric Tx

Living donor Tx

600-700 Tx each year in Turkey

Mostly living donor

Survival % 80 in 2 years, % 70 in 5 yrs

Immunsupressive treatment after Tx

You are free now !!!