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