1. Abdominal paracentesis is used to diagnose the cause of ascites and detect ascitic fluid infection. It involves inserting a needle through the abdominal wall to drain fluid from the peritoneal cavity. 2. The document provides details on the indications, contraindications, complications, and techniques for performing diagnostic and therapeutic paracentesis. Precautions are taken to minimize risks such as abdominal wall hematoma or puncturing internal organs. 3. Analysis of the drained ascitic fluid can provide information on possible causes of ascites based on characteristics like appearance, cell count, protein level, and triglyceride content. A cloudy or bloody appearance may indicate infection or other conditions.

1. ABDOMINAL PARACENTESIS
PHUNG HUY HOANG, MD
Resident in Internal Medicine
Pham Ngoc Thach University of Medicine
June, 2017

2. Floch M. H. (2009), "Netter's Gastroenterology", Saunders

3. • Most rapid and cost-effective method of diagnosing the
cause of ascites
• The only method of detecting ascitic fluid infection
INDICATIONS
• All inpatients + outpatients with new-onset ascites
• All patients with ascites admitted to the hospital
• Patients (whether hospitalized or not) in whom symptoms, signs, or laboratory abnormalities
suggestive of infection develop
• Therapeutic paracentesis
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Runyon B. A., AASLD (2013), Hepatology, 57 (4), pp. 1651-3

4. Anstee Q. M., Jones D. E. J. (2014), Davidson's Principles and Practice of
Medicines, Brian R. Walker, et al., Editors, Churchill Livingstone, Elsevier, pp.
921-942

5. CONTRAINDICATIONS
• Coagulopathy: clinically evident hyperfibrinolysis (three-dimensional ecchymosis/hematoma)
or DIC
• Mild to moderate coagulopathy: acceptable
• Overall coagulation: usually normal/cirrhosis despite abnormal tests of coagulation 
balanced defciency of procoagulants and anticoagulants
• Cut-off values for coagulation parameters (paracentesis avoided): no data
• Transfusion of blood products routinely before paracentesis in patients with cirrhosis
and coagulopathy: no data
• Local infection overlying the puncture site
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Runyon B. A. (1986), Archives of Internal Medicine, 146 (11), pp. 2259-2261

6. COMPLICATIONS
• Abdominal wall hematoma (2%)
• Breakage of a plastic catheter into the peritoneum  use metal needle
• Complication rates higher: inexperienced operator
• No deaths, infections, hemoperitoneum or entry of the paracentesis needle into the bowel been
report
• Diagnostic paracentesis: safe with a very low incidence of serious complications (particularly
when compared to therapeutic paracentesis)
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Runyon B. A., AASLD (2013), Hepatology, 57 (4), pp. 1651-3
De Gottardi A., Thévenot T., Spahr L., et al. (2009), Clinical Gastroenterology and Hepatology, 7 (8), pp. 906-909

7. “In one series the international normalized ratio (INR) was as high as 8.7 and the platelet count was
as low as 19,000 cells/mm3, yet no one had a bleeding complication and no one received
transfusions of blood products before or after paracentesis”
Grabau C. M., Crago S. F., Hoff L. K., et al. (2004), "Performance standards for therapeutic abdominal paracentesis", Hepatology, 40 (2), pp. 484-488

8. PATIENT’S POSITION
• Volume of fluid in the abdomen, thickness of the abdominal wall
• Large volume, thin abdominal wall: supine position, head of bed elevated slightly
• Less fluid: lateral decubitus position, tapped in the midline or right or left lower quadrant
• Small amounts of fluid: face-down position or with US guidance
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Sakai H., Sheer T. A., Mendler M. H., et al. (2005), Liver Int, 25 (5), pp. 984-6

9. ENTRY SITE
• Left lower quadrant (more preferred)
• Right lower quadrant (less preferred  cecum distended with gas from lactulose therapy, more
likely to have a surgical scar  bowel adherent  appendectomy scar precludes)
• Midline site: a vascular (long midline scar precludes, obese patients: abdominal wall usually
thicker in the midline > lower quadrants)
• US guidance: small amount, multiple scars
• Avoid: scars, abdominal wall collaterals, area of the inferior hypogastric artery (midway between
anterior superior iliac spine and pubic tubercle)
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Sakai H., Sheer T. A., Mendler M. H., et al. (2005), Liver Int, 25 (5), pp. 984-6
Runyon B. A., AASLD (2013), Hepatology, 57 (4), pp. 1651-3

10. 2 fngerbreadths (3 cm) cephalad and 2
fngerbreadths medial to the
anterior superior iliac spine
“A laparoscopic study found that collaterals can be present in the midline and thus present a
risk or rupture during paracentesis”
Runyon B. A., AASLD (2013), Hepatology, 57 (4), pp. 1651-3
Oelsner D. H., Caldwell S. H., Coles M., et al. (1998), Gastrointestinal Endoscopy, 47 (5), pp. 388-390

11. CHOICE OF NEEDLE
• Standard metal 22-gauge needle (1.5 inches for not overweight, 3.5 inches for obese)
• Smaller gauge numbers indicate larger outer diameters
• Metal needles:
• preferable to plastic-sheathed cannulas (plastic sheaths may shear off into the peritoneal
cavity, potential to kink and obstruct the flow of fluid after the cannula is removed)
• not puncture the bowel (unless the bowel is adherent to a scar or severe gaseous distention is
present)
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Sakai H., Sheer T. A., Mendler M. H., et al. (2005), Liver Int, 25 (5), pp. 984-6

12. TECHNIQUE
1. Dianostic paracentesis
2. Therapeutic paracentesis
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
BA R. (2012), UpToDate

13. TECHNIQUE
PREPARATION
• Drapes, gown, hat, mask:optional
• Sterile gloves: should be used (ascitic fluid cultures frequently grow skin contaminants)
• Skin disinfection: iodine solution
• Skin and subcutaneous tissue: local anesthetic
• Sterile package (gloves): sterile feld (to place syringes, needles, gauze, and other supplies)
• Ensure the patient has an empty bladder prior to the procedure
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
BA R. (2012), UpToDate
Patel N., Knight D. (2009), Clinical Practical Procedures for Junior Doctors, Mark Palazzo, Editor, Churchill Livingstone Elsevier, pp. 129-140
Diagnosis (1)

14. TECHNIQUE
“Z TRACT” TECHNIQUE
• Prevent leakage of fluid after the needle is withdrawn (If the needle were inserted straight 
fluid would leak out easily because the pathway: straight)
• Not involve manipulating the needle up and down (lead to tissue injury)
• Displacing the skin ~ 2 cm downward  slowly inserting the paracentesis needle mounted on
the syringe held in the other hand (90o to skin)  stabilizes the syringe + retracts its plunger
simultaneously
• If certain that needle tip is inserted far enough but no fluid is apparent  twist syringe + needle
90 degrees (to pierce the peritoneum)
• The skin is released: only after the needle has penetrated the peritoneum and fluid flows
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
BA R. (2012), UpToDate
Diagnosis (2)

15. Patel N., Knight D. (2009), Clinical Practical Procedures for Junior Doctors, Mark Palazzo, Editor, Churchill
Livingstone Elsevier, pp. 129-140

16. Patel N., Knight D. (2009), Clinical Practical Procedures for Junior Doctors, Mark Palazzo, Editor, Churchill Livingstone Elsevier, pp. 129-140

17. Wong C. L., Holroyd-Leduc J., Thorpe K. E., et al. (2008), JAMA, 299 (10), pp. 1166-1178
“Z tract” technique

18. TECHNIQUE
• Slowly inserting the paracentesis needle:
• allows the operator to see blood if a vessel is entered
• allows the bowel to move away from the needle
• allows time for the elastic peritoneum to “tent” over the end of the needle and be pierced
• Syringe should be aspirated intermittently during insertion/5mm (continuous suction 
bowel or omentum may be drawn to the end of the needle  occluding flow  unsuccessful tap)
• Most common cause of unsuccesful:
• continuous aspiration during insertion of the needle
• rapid insertion and withdrawal of the needle before the peritoneum is pierced
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
BA R. (2012), UpToDate
Diagnosis (3)

19. TECHNIQUE
• Larger-bore needle (16- to 18-gauge needle) and additional equipment
• Unless the needle is allowed to drift subcutaneously, the needle (or blunt steel cannula) can be
left in the abdomen during a therapeutic paracentesis without injury
• Larger-bore needles or cannulas: permit more rapid removal of fluid but leave larger defects (if
they enter vessels or the bowel inadvertently)
• Ensure when withdrawing the trocar: not withdraw it too quickly (otherwise the drain will kink)
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
BA R. (2012), UpToDate
Patel N., Knight D. (2009), Clinical Practical Procedures for Junior Doctors, Mark Palazzo, Editor, Churchill Livingstone Elsevier, pp. 129-140
Therapeutic (1)

20. Patel N., Knight D. (2009), Clinical Practical Procedures for Junior Doctors, Mark
Palazzo, Editor, Churchill Livingstone Elsevier, pp. 129-140

21. TECHNIQUE
• With respiratory movement  needle may gradually work its way out of the peritoneal cavity
and into the soft tissue  some serosanguineous fluid may appear in the needle hub or tubing
• The pump should be turned off or a clamp placed on the tubing
• The tubing should be removed from the needle and the needle twisted a few degrees
• If flow does not resume  needle should be twisted a bit more If flow still does not resume 
the needle should be inserted in 1- to 2-mm increments until brisk dripping of fluid from the
needle hub is seen
• Excessive manipulation of the needle: avoided (minimize the risk of trauma to the bowel or
blood vessels)
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
BA R. (2012), UpToDate
Therapeutic (2)

22. TECHNIQUE
• As the fluid is removed  bowel and omentum draw closer to the needle  block the flow
of ascitic fluid
• Patient must then be repositioned ( gravity causes the fluid to pool near the needle) 
maximize the amount of fluid removed
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
BA R. (2012), UpToDate
Therapeutic (3)

23. ASCITIC FLUID ANALYSIS
PHUNG HUY HOANG, MD
Resident in Internal Medicine
Pham Ngoc Thach University of Medicine
June, 2017

24. Cesario K. B., Choure A., Carey W. D. Cirrhotic Ascites. 2013 [cited 2017 June]

25. GROSS APPEARANCE (1)
• The opacity of many cloudy ascitic fluid specimens: neutrophils  shimmering effect: glass
tube containing the fluid is rocked back and forth in front of a light
• Transparent and usually slightly yellow: Non-neutrocytic (i.e., ascitic fluid
polymorphonuclear neutrophil [PMN] count < 250/mm3)
• Nearly clear: absolute neutrophil count < 1000/mm3
• Quite cloudy: > 5000/mm3
• Frankly purulent: > 50000/mm3 (gross intraabdominal infection e.g secondary peritonitis or an
abscess)  diferrential milky fluid!  Lack of odor and TG >200 mg/dL: chylous ascites
• No pigment and look like water: very low protein concentration
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Garcia-Tsao G. (2016), Yamada’s Textbook of Gastroenterology, Daniel K. Podolsky, Michael Camilleri, J. Gregory Fitz, Editors, Wiley Blackwell, pp. 2087-2106

26. • Threshold for a pink appearance: RBC count of 10000/mm3
• Distinctly red: > 20000/mm3
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Fuid specimens: bloody
• Traumatic tap (blood-streaked, frequently clot unless the fluid is transferred
immediately to the anticoagulant-containing tube for the cell count)
• Nontraumatic (bloody hepatic lymph/portal hypertension, malignancy, TB/rare) or
remotely traumatic blood-tinged ascitic fluid: homogeneous and not clot (already
clotted and the clot has lysed)
GROSS APPEARANCE (2)

27. • Ascitic fluid frequently is lipid-laden, lipid opacifes the fluid
• Most opaque, milky fluid samples (chylous ascite): TG (triglyceride) > 200 mg/dL (2.26
mmol/L) and usually > 1000 mg/dL (11.30 mmol/L)  creamy layer will separate
• Dilute skim milk: TG = 100-200 mg/dL (1.13-2.26 mmol/L)
• Dark-brown fluid (with a bilirubin concentration > serum): biliary perforation (Deeply
jaundiced patients: bile-stained ascitic fluid, but level and the degree of pigmentation < serum)
• Tea-colored to jet black: Pancreatic ascites: may be pigmented (effect of pancreatic enzymes
on RBCs)
• Black ascitic fluid: malignant melanoma
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Runyon B. A. (1987), J Clin Gastroenterol, 9 (5), pp. 543-5
GROSS APPEARANCE (3)

28. Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576

29. Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark
Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-
1576

30. CELL COUNT (1)
• The WBC count in uncomplicated ascites/cirrhosis: usually < 500/mm3
• ULN for absolute PMN count in uncomplicated ascitic fluid/cirrhosis < 250/mm3
• Any inflammatory process can result in an elevated ascitic fluid WBC count:
• Spontaneous bacterial peritonitis (SPB): most common  predominant PMN
• Tuberculous peritonitis and peritoneal carcinomatosis  predominant lymphocytes
• Leakage of blood into the peritoneal cavity (slightly traumatic tap):  ascitic fluid WBC,
PMN count (neutrophils predominate in blood)  corrected PMN/ascite fluid
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
1 PMN is subtracted from the absolute ascitic fluid PMN count for every 250 RBCs

31. • During diuresis/cirrhosis and ascites: WBC count can concentrate to > 1000/mm3  requires
prediuresis count, normal lymphocytes predominate, unexplained clinical symptoms or signs
(e.g., fever or abdominal pain) be absent
• Short survival of PMNs: relative stability of the absolute PMN count during diuresis 
cutoff value remains reliable
• Some laboratories count mesothelial cells in addition to WBCs and label the sum as
“nucleated cells”
• Malignancy-related ascites may also  PMN count (16% of cases in one series) (dying tumor
cells attract neutrophils), predominance of lymphocytes
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Runyon B. A. (2012), Schiff's Diseases of the Liver, Eugene R. Schiff, Willis C. Maddrey, Michael F. Sorrell, Editors, Wiley Blackwell, pp. 393-420.
CELL COUNT (2)

32. SERUM-ASCITES ALBUMIN GRADIENT (SAAG) (1)
• Before the 1980s: total protein to classify ascites as either exudative or transudative (cut-off 2.5
g/dL [25 g/L])  not careful defined and validated.
• The serum-ascites albumin gradient (SAAG): proved to categorize ascites better, reflection
of hepatic sinusoidal pressure
• SAAG: not explain the pathogenesis of ascites formation, nor does it explain where the
albumin came from (liver or bowel)
• Oncotic-hydrostatic balance (Starling forces), difference between the serum and ascitic fluid
albumin concentrations correlates directly with portal pressure.
• The accuracy of the test is excellent (even with ascitic fluid infection, diuresis, therapeutic
paracentesis, IV infusions of albumin, and various causes of liver disease)
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Runyon B. A., Montano A. A., Akriviadis E. A., et al. (1992), Ann Intern Med, 117 (3), pp. 215-20.

33. Runyon B. A. (2012), Schiff's Diseases of the Liver, Eugene R. Schiff, Willis C. Maddrey, Michael F. Sorrell, Editors, Wiley Blackwell, pp. 393-420.

34. • SAAG = serum albumin - ascitic albumin
• ≥ 1.1 g/dL (11g/L) = high albumin gradient: portal hypertension
• < 1.1 g/dL (11g/L) = low albumin gradient: unlikely to have portal hypertension
• If the frst result is borderline (e.g., 1.0 or 1.1 g/dL [10 or 11 g/L])  repeating the
paracentesis and analysis usually provides a definitive result
• SAAG correlates very well with the hepatic venous pressure gradient (r = 0.72)
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Hoefs J. C. (1983), J Lab Clin Med, 102 (2), pp. 260-73
SERUM-ASCITES ALBUMIN GRADIENT (SAAG) (2)

35. FALSE VALUE (1)
• The accuracy of the SAAG reduced: specimens of serum and ascites are not obtained nearly
simultaneously (should be same day, preferably same hour).
• Both serum and ascitic fluid albumin concentrations change over time; however parallel 
difference is stable.
• Arterial hypotension:  portal pressure and a narrowing of the SAAG.
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
SERUM-ASCITES ALBUMIN GRADIENT (SAAG) (3)

36. FALSE VALUE (2)
• Lipid interferes with the assay for albumin, and chylous ascites may result in a falsely high
SAAG
• The accuracy of the albumin assay at low albumin concentrations (e.g., <1 g/dL [10 g/L])
should be confirmed (If serum albumin < 1.1 g/dL/ascitic cirrhosis, the SAAG will be falsely low)
• Serum hyperglobulinemia (serum globulin level > 5 g/dL [50 g/L])  high ascitic fluid globulin
concentration  narrow the albumin gradient (contributing to the oncotic forces)
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Corrected SAAG = uncorrected SAAG x 0.16 x serum globulin (g/dL) + 2.5
SERUM-ASCITES ALBUMIN GRADIENT (SAAG) (4)

37. ADA, adenosine deaminase; AFB, acid-fast bacilli; Asc prot, ascites total protein levels; CT, computed tomography; CUS, cardiac
echosonography; HVPG, hepatic venous pressure gradient; SAAG, serum–ascites albumin gradient; TJLB, transjugular liver biopsy
Garcia-Tsao G. (2016), Yamada’s Textbook of Gastroenterology,
Daniel K. Podolsky, Michael Camilleri, J. Gregory Fitz, Editors,
Wiley Blackwell, pp. 2087-2106

38. Garcia-Tsao G. (2016), Yamada’s Textbook of Gastroenterology, Daniel K. Podolsky, Michael Camilleri,
J. Gregory Fitz, Editors, Wiley Blackwell, pp. 2087-2106
Anstee Q. M., Jones D. E. J. (2014), Davidson's Principles and Practice of Medicines, Brian R. Walker,
et al., Editors, Churchill Livingstone, Elsevier, pp. 921-942

39. PROTEIN
• Determine susceptibility of developing bacterial infection
• Cirrhotic patients with an ascites protein <1.0 g/dL1 or < 1.5 g/dL2 have a higher risk of
developing infection (SBP)
• Ascites does not become an “exudate” with infection (≠ pleura) = ascitic fluid total protein
concentration does not increase during SBP1,3
•  in peritoneal processes (leakage of high protein mesenteric lymph from obstructed lymphatics
and/or from an inflamed peritoneal surface)
• Exudative ascites is also present in ascites secondary to heart failure
 high or low total ascitic protein level to categorize
1. Garcia-Tsao G. (2016), Yamada’s Textbook of Gastroenterology, Daniel K. Podolsky, Michael Camilleri, J. Gregory Fitz, Editors, Wiley Blackwell, pp. 2087-2106
2. EASL (2010), J Hepatol, 53 (3), pp. 397-417
3. Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576

40. Garcia-Tsao G. (2016), Yamada’s Textbook of Gastroenterology, Daniel K. Podolsky, Michael Camilleri, J. Gregory Fitz, Editors, Wiley Blackwell, pp. 2087-2106

41. GLUCOSE
• Small enough to diffuse readily intobody fluid cavities  concentration of glucose in ascitic
fluid = in serum (unless glucose being consumed by ascitic fluid WBCs or bacteria)
• Ascitic fluid glucose in early detected SBP is similar to that of sterile fluid
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Runyon B. A., Hoefs J. C. (1985), Hepatology, 5 (2), pp. 257-9

42. LACTATE DEHYDROGENASE
• Too large to enter ascitic fluid readily from blood  usually is less than half of the serum level
in uncomplicated ascites/cirrhosis
• In SBP: LDH  because of the release of LDH from neutrophils  ascitic fluid concentration >
serum
• Secondary peritonitis, the LDH level is even > in SBP and may be several-fold higher than
the serum LDH level
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Akriviadis E. A., Runyon B. A. (1990), Gastroenterology, 98 (1), pp. 127-33

43. SECONDARY PERITONITIS
• Measurement of ascitic fluid total protein, glucose, and LDH has been reported to be of value
in distinguishing SBP from secondary peritonitis (gut perforation into ascites)
• Neutrocytic ascitic fluid + 2/3 following criteria = likely to have surgical peritonitis:
1. total protein >1 g/dL,
2. glucose <50 mg/dL,
3. LDH above the upper limit of normal for serum (225 U/L)
• These criteria and/or polymicrobial infection: 96% sensitive/detecting secondary bacterial
peritonitis
Akriviadis E. A., Runyon B. A. (1990), Gastroenterology, 98 (1), pp. 127-33
Soriano G., Castellote J., Alvarez C., et al. (2010), J Hepatol, 52 (1), pp. 39-44

44. Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark
Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-
1576

45. SMEARS AND CULTURE
• Most common bacterial infection of ascitic fluid: SBP (monomicrobial, with a low bacterial
concentration median colony count of only 1 organism/mL)
• SBP: more like bacteremia (number of bacteria present)  culturing ascitic fluid as if it were
blood has a high yield  superiority of the blood culture bottle method + bedside inoculation
• Gene probes: commercially available for the detection of bacteremia
• 50% of the cultures are still negative
• Simultaneous blood cultures should be collected (30%–58% of SBP cases are associated
with bacteremia)
• Gram stain: positive in < a third of the cases of SBP
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Runyon B. A., AASLD (2013), Hepatology, 57 (4), pp. 1651-3
Runyon B. A., Canawati H. N., Akriviadis E. A. (1988), Gastroenterology, 95 (5), pp. 1351-5
Garcia-Tsao G. (2016), Yamada’s Textbook of Gastroenterology, Daniel K. Podolsky, Michael Camilleri, J. Gregory Fitz, Editors, Wiley Blackwell, pp. 2087-2106

46. SMEAR AND CULTURE FOR TB
• A direct smear of ascitic fluid to detect mycobacteria: almost never positive (~3%) (rarity of
tuberculous peritonitis, low concentration of mycobacteria in ascitic fluid in tuberculous peritonitis)
• Conventional culture media: 4–8 weeks to detect AFB
• Cultures: determine susceptibility to antimicrobial agents
• Mycobacterium culture: 50% sensitive
 laparoscopy with histology and culture of peritoneal biopsies has a sensitivity approaching
100%
• DNA probes
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Hillebrand D. J., Runyon B. A., Yasmineh W. G., et al. (1996), Hepatology, 24 (6), pp. 1408-12

47. ADENOSINE DEAMINASE
• Enzyme related to proliferation and differentiation of lymphocytes
• Appears to be a fast and discriminating test for diagnosis PTB
• Recommended in suspected PTB, esp endemic areas
• Cut-off values from 36 to 40 IU/L with an optimal cut-off point of 39 IU/L
Garcia-Tsao G. (2016), Yamada’s Textbook of Gastroenterology, Daniel K. Podolsky, Michael Camilleri, J. Gregory Fitz, Editors, Wiley Blackwell, pp. 2087-2106
Riquelme A., Calvo M., Salech F., et al. (2006), J Clin Gastroenterol, 40 (8), pp. 705-10

48. CYTOLOGY
• Only 58–75% sensitive in detecting “malignant ascites” (when tumor cells line the peritoneal
cavity)
• Patients with peritoneal carcinomatosis have viable malignant cells exfoliating into ascitic fluid
 these cells detected in their ascitic fluid cytologies
• DNA cytometry  improve the sensitivity of effusion cell analysis to 95%
Runyon B. A. (2016), Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576
Runyon B. A. (2012), Schiff's Diseases of the Liver, Eugene R. Schiff, Willis C. Maddrey, Michael F. Sorrell, Editors, Wiley Blackwell, pp. 393-420.

49. BILIRUBIN
• The bilirubin concentration should be measured in ascitic fluid that is dark brown
• Ascitic fluid bilirubin > 6 mg/dL (102 µmol/L) and > serum level  suggests biliary or proximal
small intestinal perforation into ascitic fluid
Runyon B. A. (1987), J Clin Gastroenterol, 9 (5), pp. 543-5
Akriviadis E. A., Runyon B. A. (1990), Gastroenterology, 98 (1), pp. 127-33

50. TRIGLYCERIDE (1)
• Should be measured in opalescent or frankly milky ascitic fluid
• Accumulation of peritoneal fluid rich in triglycerides  presence of lymph in the abdominal
cavity
• Chylous ascites = TG > 200 mg/dL (2.26 mmol/L) and > serum level; usually, the level is
greater than 1000 mg/dL (11.30 mmol/L)
Runyon B. A. (2012), Schiff's Diseases of the Liver, Eugene R. Schiff, Willis C. Maddrey, Michael F. Sorrell, Editors, Wiley Blackwell, pp. 393-420.

51. • Pathogenesis
• Disruption of the lymphatic system/obstruction (malignant infltration or inflammatory)
• Traumatic injury (surgery, trauma)
• Altered hemodynamics   caval (constrictive pericarditis) and hepatic venous pressures
(cirrhosis)  increased formation of hepatic duct lymph.
• SAAG may be falsely elevated in chylous ascites
• Lymphangiography and lymphoscintigraphy
Runyon B. A. (2012), Schiff's Diseases of the Liver, Eugene R. Schiff, Willis C. Maddrey, Michael F. Sorrell, Editors, Wiley Blackwell, pp. 393-420.
TRIGLYCERIDE (2)

52. UNUSEFUL TESTS
• pH
• Lactate
• Fibronectin
• Cholesterol
• CEA
• α1-antitrypsin
• Cyclic adenosine monophosphate
• (cAMP)
• Glycosaminoglycans
Runyon B. A. (2012), Schiff's Diseases of the Liver, Eugene R. Schiff, Willis C. Maddrey, Michael F. Sorrell, Editors, Wiley Blackwell, pp. 393-420.
Runyon B. A., AASLD (2013), Hepatology, 57 (4), pp. 1651-3

53. ABDOMINAL PARACENTESIS
PHUNG HUY HOANG, MD
Resident in Internal Medicine
Pham Ngoc Thach University of Medicine
June, 2017

54. 1. Akriviadis E. A., Runyon B. A. (1990), "Utility of an algorithm in differentiating spontaneous from secondary bacterial
peritonitis", Gastroenterology, 98 (1), pp. 127-33.
2. Anstee Q. M., Jones D. E. J. (2014), "Liver and biliary tract disease", Davidson's Principles and Practice of Medicines, Brian R.
Walker, et al., Editors, Churchill Livingstone, Elsevier, pp. 921-942.
3. BA R. (2012), "Technique of diagnostic and therapeutic abdominal paracentesis", UpToDate.
4. Cesario K. B., Choure A., Carey W. D. Cirrhotic Ascites. 2013 [cited 2017 June].
5. De Gottardi A., Thévenot T., Spahr L., et al. (2009), "Risk of Complications After Abdominal Paracentesis in Cirrhotic Patients: A
Prospective Study", Clinical Gastroenterology and Hepatology, 7 (8), pp. 906-909.
6. EASL (2010), "EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal
syndrome in cirrhosis", J Hepatol, 53 (3), pp. 397-417.
7. Garcia-Tsao G. (2016), "Ascites and its complications", Yamada’s Textbook of Gastroenterology, Daniel K. Podolsky, Michael
Camilleri, J. Gregory Fitz, Editors, Wiley Blackwell, pp. 2087-2106.
8. Grabau C. M., Crago S. F., Hoff L. K., et al. (2004), "Performance standards for therapeutic abdominal paracentesis",
Hepatology, 40 (2), pp. 484-488.
9. Hillebrand D. J., Runyon B. A., Yasmineh W. G., et al. (1996), "Ascitic fluid adenosine deaminase insensitivity in detecting
tuberculous peritonitis in the United States", Hepatology, 24 (6), pp. 1408-12.
10. Hoefs J. C. (1983), "Serum protein concentration and portal pressure determine the ascitic fluid protein concentration in patients
with chronic liver disease", J Lab Clin Med, 102 (2), pp. 260-73.
11. Oelsner D. H., Caldwell S. H., Coles M., et al. (1998), "Subumbilical midline vascularity of the abdominal wall in portal
hypertension observed at laparoscopy", Gastrointestinal Endoscopy, 47 (5), pp. 388-390.
12. Patel N., Knight D. (2009), "Abdominal Paracentesis and Ascitic Drain Insertion", Clinical Practical Procedures for Junior Doctors,
Mark Palazzo, Editor, Churchill Livingstone Elsevier, pp. 129-140.
REFERENCES

55. 13. Runyon B. A. (2016), "Ascites and Spontaneous Bacterial Peritonitis", Sleisenger and Fordtran’s Gastrointestinal and Liver Disease,
Mark Feldman, Lawrence S. Friedman, Lawrence J. Brandt, Editors, Elsevier Saunders, pp. 1553-1576.
14. Runyon B. A. (2012), "Ascites and Spontaneous Bacterial Peritonitis", Schiff's Diseases of the Liver, Eugene R. Schiff, Willis C.
Maddrey, Michael F. Sorrell, Editors, Wiley Blackwell, pp. 393-420.
15. Runyon B. A. (1987), "Ascitic fluid bilirubin concentration as a key to choleperitoneum", J Clin Gastroenterol, 9 (5), pp. 543-5.
16. Runyon B. A. (1986), "Paracentesis of ascitic fluid: A safe procedure", Archives of Internal Medicine, 146 (11), pp. 2259-2261.
17. Runyon B. A., AASLD (2013), "Introduction to the revised American Association for the Study of Liver Diseases Practice Guideline
management of adult patients with ascites due to cirrhosis 2012", Hepatology, 57 (4), pp. 1651-3.
18. Runyon B. A., Canawati H. N., Akriviadis E. A. (1988), "Optimization of ascitic fluid culture technique", Gastroenterology, 95
(5), pp. 1351-5.
19. Runyon B. A., Hoefs J. C. (1985), "Ascitic fluid chemical analysis before, during and after spontaneous bacterial peritonitis",
Hepatology, 5 (2), pp. 257-9.
20. Runyon B. A., Montano A. A., Akriviadis E. A., et al. (1992), "The serum-ascites albumin gradient is superior to the exudate-
transudate concept in the differential diagnosis of ascites", Ann Intern Med, 117 (3), pp. 215-20.
21. Sakai H., Sheer T. A., Mendler M. H., et al. (2005), "Choosing the location for non-image guided abdominal paracentesis", Liver
Int, 25 (5), pp. 984-6.
22. Soriano G., Castellote J., Alvarez C., et al. (2010), "Secondary bacterial peritonitis in cirrhosis: a retrospective study of clinical
and analytical characteristics, diagnosis and management", J Hepatol, 52 (1), pp. 39-44.
REFERENCES