Approach to ascites

Supot Nimanong, M.D.

Topics

• Diagnosis of ascites

• Approach to ascitic patient

• Ascitic fluid analysis

• Causes of ascites

- portal hypertension-related

- peritoneal disease

• Treatment of ascites

Introduction

• Askos (Greek) means bag or sack

• The accumulation of excess fluid within the

peritoneal cavity

• Transudate or exudate

• Most frequently encountered in patients with

cirrhosis

Diagnosis of ascites

Sensitivity

• Ultrasound 100 cc

• Puddle sign 150 cc

• Shifting dullness 1-1.5 L

• Fluid thrill > 3-5 L

Cirrhosis Heart failure

Peritoneal tuberculosis

Others

Pancreatic

Budd-Chiari syndrome

Nephrogenic ascites

Peritoneal malignancy

Causes of ascites

Peritoneal pathology

- Malignancy

- Tuberculosis

Sinusoidal

hypertension

-Cirrhosis

-Late Budd-

Chiari

Source of

ascites Hepatic sinusoids

SAAG > 1.1 Peritoneum

SAAG < 1.1

“Capillarized” sinusoid

Ascites protein < 2.5 Peritoneal lymph

Ascites protein > 2.5

Post-sinusoidal

hypertension

- Cardiac ascites

- Early Budd-Chiari

- Veno-occlusive

disease

Normal “leaky” sinusoid

Ascites protein > 2.5

Serum-Ascites Albumin Gradient (SAAG) and Ascites Protein

Portal hypertension Peritoneal disease

Patient evaluation

History • Risk of cirrhosis: alcohol,viral hepatitis B, C,

NASH, etc

• Symptoms of cirrhosis: pedal edema. jaundice, UGIB, HE

• Thrombophilia, pills, spontaneous abortion, DVT

• Heart disease

• Cancer

• TB

• Other: NS, hypothyroidism, CNT disease

Physical examination

• Pedal edema

• Signs of chronic liver disease

• Signs of portal hypertension

• Superficial vein dilatation

• Sister Mary Joseph nodule

• Rectal examination

• Lymphadenopathy

• Neck vein & heart

Patient evaluation

Dilated abdominal vein

Normal Portal hypertension IVC obstruction

Bates' guide to PE and history taking 9th ed, 2007

Peritoneal pathology

- Malignancy

- Tuberculosis

Sinusoidal

hypertension

-Cirrhosis

-Late Budd-

Chiari

Source of

ascites Hepatic sinusoids

SAAG > 1.1 Peritoneum

SAAG < 1.1

“Capillarized” sinusoid

Ascites protein < 2.5 Peritoneal lymph

Ascites protein > 2.5

Post-sinusoidal

hypertension

- Cardiac ascites

- Early Budd-Chiari

- Veno-occlusive

disease

Normal “leaky” sinusoid

Ascites protein > 2.5

Serum-Ascites Albumin Gradient (SAAG) and Ascites Protein

Portal hypertension Peritoneal disease

Signs of PHT

Leg edema

LN, Chest,

PR, Skin

Dilated vein,

Neck vein,

Thrombophilia

Hepatomegaly

Signs of CLD,

Risk factors

Abdominal paracentesis

Indication

-> Diagnostic

• New onset ascites

• At the time of admission

• Rapid accumulation of ascites

• Clinical deterioration

• Suspected infection

-> Therapeutic

Coagulopathy is not a contraindication unless there is primary fibrinolysis or DIC

Procedure

• Site - 4 cm. medial & cephalic to ASIS

- left side: to avoid a distended cecum

• Instrument

- 1.5 inch 22-gauge needles for diagnosis

- 15 gauge needles for therapeutic paracentesis

• "Z-tract" minimizes leakage of fluid

Abdominal paracentesis

Ascitic fluid analysis

Gross appearance

• Clear or turbid

• Color; straw, pink, bloody, milky

• Viscosity; fluid, jelly

Initial Workup of Ascites Diagnostic Paracentesis

Glucose, LDH

Cytology PMN count Culture

Protein/Albumin Amylase

Routine Optional

? secondary infection ?

cirrhotic ascites

? pancreatic ascites

? malignant ascites

? SBP

Ascites: cell count

• “Normal" total WBC is up to 500 cells/mm3

• Diuresis: 300 to ~ 1200 cells/ mm3

• PMN: 250 cutoff even end of diuresis

• In traumatic tapping

– 1 PMN per 250 red cells attributed to blood

contamination of ascites

– 1 lymphocyte per 750 red cells

Ascites; secondary peritonitis

Sens Spec • 2/3 of 100% 45%

- total protein > 1g/dL

- LDH > ULN of serum LDH

- glucose <50 mg/dL

• CEA >5 ng/mL or 92% 88%

ALP>240 units/L

Only for free perforation

Ascites; Gram’s stain

Mixed organisms

Ascites: SAAG

High gradient ≥1.1 Low gradient <1.1 cirrhosis peritoneal carcinomatosis

alcoholic hepatitis TB peritonitis

cardiac ascites pancreatic ascites

mixed ascites bowel obstruction/infarct

massive liver metastasis biliary ascites

fulminant hepatic failure nephrotic syndrome

Budd-Chiari syndrome post-op lymphatic leak

Veno-occlusive disease serositis in CNTD

myxedema

acute fatty liver of pregnancy

approximately 97% accuracy.

Cirrhotic ascites Cardiac ascites

Peritoneal malignancy

1.1

4.0

3.0

2.0

1.0

0

Serum –

ascites

albumin

gradient

(g/dL)

(75)

Ascitic fluid

total protein

(g/dL)

7.0

5.0

3.0

2.0

0

2.5

Serum-Ascites Albumin Gradient and Ascites Protein Levels

Runyon, Ann Intern Med 1992; 117:215

Peritoneal pathology

- Malignancy

- Tuberculosis

Sinusoidal

hypertension

-Cirrhosis

-Late Budd-

Chiari

Source of

ascites Hepatic sinusoids

SAAG > 1.1 Peritoneum

SAAG < 1.1

“Capillarized” sinusoid

Ascites protein < 2.5 Peritoneal lymph

Ascites protein > 2.5

Post-sinusoidal

hypertension

- Cardiac ascites

- Early Budd-Chiari

- Veno-occlusive

disease

Normal “leaky” sinusoid

Ascites protein > 2.5

Serum-Ascites Albumin Gradient (SAAG) and Ascites Protein

Mixed ascites

Mixed ascites

• 5% of pts will have "mixed" ascites: underlying portal HT+ secondary cause

• Clue:- high ascitic fluid lymphocyte count

- high total protein

• Chylous ascites may have a falsely high

albumin gradient

Portal hypertension-related

ascites

Systemic arteriolar

resistance

Intrahepatic resistance

Sinusoidal pressure

Ascites

Effective arterial blood volume

Activation of neurohumoral

systems

Cirrhosis

Renal Vasoconstriction

Sodium and water retention

Hepatorenal syndrome

Worsening

liver disease

Refractory ascites

Nitric oxide

Portal systemic collaterals

Distorted sinusoidal

architecture leads to

increased resistance

Portal vein

Cirrhotic Liver

Splenomegaly

Cirrhosis

HEPATIC VEIN OBSTRUCTION LEADS TO ASCITES FORMATION

Hepatic vein outflow block

Hepatic Vein Obstruction Leads to Ascites Formation

Sinusoidal pressure

Splanchnic capillary pressure

Budd-Chiari syndrome

PORTAL VEIN OBSTRUCTION ALMOST NEVER LEADS TO ASCITES

Portal vein obstruction

Portal Vein Obstruction Almost Never Leads to Ascites

Normal sinusoidal

pressure

splanchnic capillary pressure

• Tuberculous peritonitis

• Carcinomatosis peritonii

• Nephrogenic ascites

• Chylous ascites

Noncirrhotic ascites

• Alcoholic cirrhosis, female

• 0.1-0.7% among cases of TB

• Route of transmission

- Reactivation of latent foci in the peritoneum

- Hematogenous spread from 1st infection

• Pleural/pulmonary symptoms 20%-78%

• PPD positive 30-90%

• Subtype

- Exudative (moist type)

- Plastic (dry type) “doughy abdomen”

Gines P et al, Ascites & renal dysfunction in liver diseases 2005;294-304

Manohar A, et al. Gut 1990;31;1130-1132

Tuberculous peritonitis

Manohar A, et al. Gut 1990;31;1130-1132

Symptoms %

Abdominal swelling 73

Fever/night sweats 54

Anorexia 47

Weight loss 44

Abdominal pain 36

Diarrhea 13

Constipation 6

Symptoms

WBC 500-2000 (lymphocytes)

SAAG < 1.1

Total protein > 3 g/dL

AFB stain+ < 5%

Fluid culture 8-83% (> 1L)

PCR 95%/48% (smear +/-)

Peritoneal biopsy 95%

K Poyrazogli et al, Journal of Digestive Diseases 2008;170-174

Gines P et al, Ascites & renal dysfunction in liver diseases 2005;294-304

Ascites profile

Features of TB Peritonitis in the Absence/ Presence of Chronic Liver Disease

TBP TBP+CLD Cirrhosis

Ascites protein (g/L)

53+15 30+11 8+6

Ascites albumin (g/L)

21+7 10+5 3+2

SAAG 6+3 14+7 20+5

Shakil et al, Am J Med 1996:179-185

Adenosine Deaminase (ADA) in Tuberculous Peritonitis A Meta-analysis

ADA value 39 IU/L sensitivity 100%, specificity 97%

Riquelme A et al, J Clin Gastroenterol 2006;40:705-710

Imaging in TB peritonitis

Findings US % CT %

Ascites 100 100

Septation in ascites 68 14

Peritoneal thickening (2-8 mm)

74 93

Mesenteric involvement

52 100

Omental involvement 52 93

Bowel involvement 37 50

Enlarged lymph node 10 21

Vardareli et al, Digestive and Liver Disease 2004;36;199-204

TB Peritonitis

Malignancy-related ascites

• Peritoneal carcinomatosis 2/3

• Massive liver metastases 1/3

• Others - Budd Chiari syndrome

- hypoalbuminemia

- ruptured HCC

Pathogenesis of Malignant Ascites

● Cachexia

Reduced

oncotic pressure

Increased extravasation

? VEGF, VPF, IL-6, TNF

Intraperitoneal

fluid

Secretion by tumor cells

Change in permeability

Lymph drainage

Mechanical obstruction

Venous drainage

Gines P et al, Ascites & renal dysfunction in liver diseases 2005;294-304

Chung M et al, Treatment of malignant ascites, Curr Treat Opinion Onc 2008;215-233

●

●

●

Malignant ascites

• Female:male 67%:33%

• Ovarian, pancreaticobiliary, gastric, esophageal,

colorectal, breast

• Median survival ~ 5.7 mo

• Ovarian cancer has better prognosis than GI cancer

• Bloody 10-20%

• HCC ascites: bloody 50%

Becker G et al, EJC 2006:589-597

Chung M et al, Curr Treat Opinion Onc 2008;215-233

Diagnosis

• Total protein > 3 g/dL

• SAAG <1.1

• Cytology is positive 96.7%

- 3 samples

- 50 mL of fresh warm ascites

- immediate processing

Becker G et al, EJC 2006:589-597

Chung M et al, Curr Treat Opinion Onc 2008;215-233

Carcinomatosis peritonei

Carcinomatosis peritonei

Pseudomyxoma peritonei

Treatment

• Treatment of primary tumor

• Diuretics: spironolactone, loop diuretics

(may avoid in patients with SAAG <1.1)

• Therapeutic paracentesis (no consensus in volume replacement fluid)

• Peritoneovenous shunt (ovarian, breast)

-> Contraindications of PV shunt:

- hemorrhagic ascites

- ascitic protein >4.5 g/L

- coagulation disorders

- advanced cardiac or renal failure

Malignant ascites

Becker G et al, EJC 2006:589-597

Chung M et al, Curr Treat Opinion Onc 2008;215-233

Chylous Ascites

• Milky and creamy ascitic fluid

• Triglyceride content > 200 mg/dL

Cardenas A et al, AJG 2002:1896-1900

Etiology of Chylous Ascites

Neoplastic (common in adult) Lymphoma

Ovarian, breast, pancreatic, colon, carcinoid

Lymphangiomyomatosis

Cirrhosis

Congenital (pediatric) Primary lymphatic hypoplasia

Intestinal lymphangiectasia

Infectious

Tuberculosis, filariasis, M Avium intacellulare

Inflammatory Radiation

Pancreatitis

Retroperitoneal fibrosis

Postoperative Abdominal aneurysm repair

Inferior vena cava resection

Traumatic Blunt abdominal trauma

• Minimal extremity edema

• Moderate to massive ascites

• History of dialysis-associated hypotension

• Ascites profile

- Straw color

- WBC 80-1900/mm3

- Ascitic protein > 3 g/dL (2.6-5.9)

- SAAG 0.99 (0.5-2.0)

- Negative culture and cytology

Nephrogenic Ascites

Hammond T et al, J Am Soc Nephrol 1994;5;1173-77

Han S et al, Medicine 1998;77:233-45

Conclusion • SAAG is a useful tool to differentiate etiology of ascites

• SAAG > 1.1 does not always mean CIRRHOSIS

• Non-cirrhotic ascites: Therapy aim to correct primary disease

WBC SAAG Ascitic

protein

g/dL

Other tests

TB 500-2000+ <1.1 >3.0 ADA, fluid PCR

Malignant <1.1 (peritoneal carcinomatosis)

>3.0 Cytology

Chylous 500 <1.1 2.5-7.0 Triglyceride >200 mg/dL

Nephrogenic 80-1900 <1.1 > 3

Thank you