This lecture is for undergraduates and post graduates. It is a case based discussion, taking the audience from definition of ascites and spontaneous bacterial sepsis to its symptomatology, physical findings, diagnostic algorithm and management of ascites and bacterial peritonitis

1. Ascites
SBP
Dr Manoj K Ghoda M.D., M.R.C.P.
Consultant Gastroenterologist
Visiting faculty, GCS Hospital
gujarat gastro group

2. Clinical history
A 42 year old male was referred for ascites.
• He was unwell for some three months
– anorexia,
– abdominal discomfort,
– feverish feeling.
Treated locally

3. • A fortnight later he noticed abdominal
distention for which a sonography was
ordered which showed ..
• inhomogeneous echo texture of liver,
• splenomegaly,
• gross ascites.
• No internal septation were seen

4. Personal history
• Alcohol for last 20 yrs.
• There was no previous illness.

5. Clinical examination
– Conscious, co-operative and oriented.
– Thin built, malnourished
– Few spiders on his back and neck.
• P/A
– Hepato-splenomegaly.
– Moderate ascites.
• Positive fluid thrill
• Horse shoe dullness
– No hernia

6. Investigations
• S. Bilirubin 1.9 mg,
• SGPT 94 IU,
• Albumin 3.0 gm, globulin 3.9 gm.
• Hb 10.4 with microcytic hypo-chromic picture.
• Platelet count: 1.1 lacs
• HBsAg and HCV were non-reactive
• Upper g.i. endoscopy revealed grade - I
esophageal varices.
What would you do now??

7. There is a potential space
between 2 layers of
peritoneum. Collection of
free fluid between these 2
spaces is called ascites.
ASCITES

8. Ascites: Etiology

9. Pathology and Pathogenesis
• Sinusoidal hypertension.
• Na and water retention
• Vasodilatation theory
• Overflow theory

10. International Ascites Club Grading
• Grade 1
– Mild, only detectable by U/S
• Grade 2
– Moderate, symmetrical distension
• Grade 3
– Gross or large with marked distension
• Large typically means painful/uncomfortable
• Refractory Ascites (5-10%)
– Can not be mobilized or early recurrence refractory to
medical management

11. What are the features associated with
ascites irrespective of its etiology?

12. Associated conditions
• Hernias.
– Increased intra-abdominal pressure favors the development
of divarication of recti or hernias in umbilical, femoral or
inguinal areas.
– Develop in about 20% of patients with cirrhosis and ascites
whereas in only 3% with just cirrhosis.
• Hepatic hydrothorax; develops in 5-10%.right sided
85%.due to diaphragmatic seepage.
• Peripheral edema, due to hypoproteinemia. A
functional inferior vana caval block due to pressure of
abdominal fluid is an additional factor.

13. Diagnosing Ascites
• Ultrasound is the
most sensitive test
for ascites (5-10 mL
detection)
– Have to use caution as
small or even moderate
ascites may be difficult to
tap (even when marked)
– Ensure mark is appropriate
• Go with patient to U/S
(ideal)
• If not possible, in order
specify location where you
want to place your needle
Image from www.gastro.org

14. Approach to a case of ascites:

15. Clinical clues in differential diagnosis

16. Cirrhosis
• Stigmata of cirrhosis
– spider angiomata
– palmer erythema
– muscle wasting
– gynecomastia,
– duputreyn’s contracture,
– asterexis
• Jaundice
• Signs of portal HT:
– splenomegaly and abdominal
wall collaterals.

17. Tuberculosis
• Relatively short history of illness
• History of contact
• Evidence of immunosuppression
• Anorexia, evening rise of fever, associated
cough with productive sputum or hemoptysis
• No pedal edema

18. Cardiac ascites
• Past history
• Precordial deformity
• Raised JVP
• Positive HJR
• Pedal edema

19. Pancreatic ascites
• History of acute pain or past history of chronic
pancreatitis.
• There may be blunt trauma to abdomen
• Usually a pseudocyst is responsible.

20. Malignant Ascites
• Comes surreptitiously
• Weight loss may be present
• Commonly caused by cancers of:
– Breast, bronchus, ovary, stomach, pancreas, colon

21. Laboratory in Ascites:

22. Diagnostic Studies
• Recommended
Studies
– Albumin
– Protein
– Cell count
• Looking for PMNs
– Cultures
• If clinically appropriate
– Glucose
– LDH
– Amylase
– RBC count
– TB smear/culture
– Cytology
– Triglycerides
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23. Types of ascites:
Serum to Ascites Albumin Gradient (SAAG)
SAAG > 1.1 g/dL  Portal HTN
SAAG < 1.1 g/dL  Other causes
• 97% accurate
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.

24. Glucose and LDH
• Consistent with infection or malignancy?
– Infection and cancer consume glucoselow
• 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

25. 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 —
– Chylous ascites - TG > 200 mg/dL, usually 1000
mg/dL; Ascitic fluid: S. Triglyceride raion >1.1
• Bilirubin — run on brown ascites.
– Biliary perforation – AF Bili > serum Bili

26. 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

27. Cytology
• “Almost 100%” with
peritoneal carcinomatosis
have positive cytology
• Malignant ascites from
massive hepatic
metastasis, HCC, lymphoma
are usually negative
• Overall sensitivity for
detection of malignancy-
related ascites is 58 to 75 %

28. Imaging in Ascites

29. Hepatic vein congestion in
right sided heart failure

30. Omental cake in a case of malignant ascites

31. Pancreatic ascites

32. Role of diagnostic laparoscopy
in ascites

33. Management principles:
Treatment of the cause:
•Cirrhosis: Diuretics, Albumin, paracentesis
and TIPS
•Tuberculosis: AKT
•Cardiac: Diuretics and removal of cardiac
cause if possible
•Pancreatic: Somatostatin and Pancreatic
stenting
•Malignant: Chemotherapy
•Chylous: Medium chain triglycerides
Therapeutic intervention

34. Therapeutic intervention in ascites
due to liver failure
• Sodium restriction
• Diuretics
• Therapeutic paracentesis
• TIPS
• Liver transplantation

35. Treatment
• Grade 1
– No treatment necessary
– Modify risk factors
– Start low sodium diet
Hepatology 2003; 38: 258-266

36. Treatment
• Grade 2
– Bed rest;increased renal perfusion and portal
venous flow during recumbancy.
• Diuretics work better supine
– studied bemetanide
– GFR lower standing as well
– Sodium and water restriction
– Diuretics
Hepatology 2003; 38: 258-266
Br Med J. 1986;292:1351-3

37. Treatment
• Grade 3
– Paracentesis is the treatment of choice
• Shown to have fewer complications than diuresis
• Faster response
– After this would do Grade 2 treatment options
Hepatology 2003; 38: 258-266

38. Treatment
• Refractory ascites
– Paracentesis with colloid infusion
– TIPS
• Choice between these is controversial
– If repeated paracentesis is contraindicated,TIPS
not an option then consider porto-venous shunt
• PVS shown inferior to repeat paracentesis in NEJM
study
Hepatology 2003; 38: 258-266

39. Diuretics
• Spironolactone
– start with 50-100 per day
– Titrate to max of 400 per day in increments of 100mg/day
if the response is insufficient after 3-4days(weight loss less
than 300mg)
• Can use other potassium sparing diuretics
– Amiloride inferior to canrenoate (anti-mineralocorticoid)
– No other comparison trials, but spironolactone accepted
as first line
– Use second line if spironolactone not possible 2/2
complications (ie gynecomastia)
Hepatology 2003; 38: 258-266

40. Diuretics
• Loop diuretics; added if response with
spironolactone inappropriate or hyperkalemia
as a complication.
– Frusemide: Initial dose 20-40 per day
• Can adjust up to 160mg per day
– Should be used only as an adjunct to
spironolactone
Hepatology 2003; 38: 258-266
Dig Dis 2005; 23:30-38

41. Assessing Diuretic Response
• Weight loss
– Lose 0.5kg a day when no edema
– Lose 1kg a day when edema is present
• Avoid renal failure
• Response rate in up to 90% patients who do
NOT have renal dysfunction
Hepatology 2003; 38: 258-266
Dig Dis 2005; 23:30-38

42. Paracentesis
• Total volume paracentesis is as effective and
as safe as sequential 3L paracentesis
• Hemodynamics
– RA pressure drops immediately
– PCWP takes 6h to decrease
Hepatology 2003; 38: 258-266

43. TIPS
• Transjugular
Intrahepatic
Portosystemic Shunt
• Creates a conduit
from the high
pressure portal system
to the lower pressure
systemic circulation

44. Peritoneovenous Shunts
• Creates a communication between the
peritoneal cavity and the systemic circulation
by a vein
• Used in only in limited cases currently
– Used for palliation if TIPS and paracentesis are not
available or contraindicated
Hepatology 2003; 38: 258-266

45. COMING BACK TO OUR CASE....

46. What do you think ascites is due to
in this case?
• ALCOHOLIC CIRRHOSIS ?
• TUBERCULOSIS ?
• PANCREATITIS ASCITES ?
• MALIGNANT ASCITES ?
• CARDIAC ASCITES ?

47. However obvious is the cause..
Always do the diagnostic tap.
(Sheila Sherlock)

48. Ascitic fluid
• Protein 6.4 gms, (Albumin 3.4 Vs S.Albumin
3.0)
• Sugar 67 mg,
• Cells 900 mainly lymphocytes,
• no malignant cells were seen.
• Ascitic fluid amylase and lipase were normal
• AFB culture was sent.
• ADA 70

49. How will you proceed now?
What are the options available
with us?

50. Follow up in our case..
• Treated with 4 drug AKT
• IV Albumin
• Diuretics

51. Spontaneous Bacterial Peritonitis
•It is an acute bacterial infection of ascitic fluid.
•It occurs in both children and adults and is a well-known
and ominous complication in patients with cirrhosis.
•Of patients with cirrhosis who have SBP, 70% are Child-
Pugh class C. In these patients, the development of SBP is
associated with a poor long-term prognosis.
•.

52. Epidemiology:
•Adults with SBP typically have ascites, but most children
with SBP do not have ascites.
•Nearly one in six patients with ascites could develop
SBP.
•Mortality could be low if the underlying etiology is
nephrotic syndrome but in cirrhotics mortality could be as
high as 40-70%.
•Any comorbid condition like renal failure could add to the
mortality and morbidity.
•Early diagnosis and aggressive treatment may result in
dramatic decrease in mortality and morbidity.

53. Pathophysiology:
•Intestinal bacterial overgrowth, impaired
phagocytic function, low serum and ascites
complement levels, and decreased activity of the
reticuloendothelial system, are possible
underlying factors

54. Microbiology:
•Enteric organisms from GI tract are isolated from
more than 90% of infected ascites fluid in SBP.
•There may be a hematogenous spread also.
•With wide spread use of fluoroquinolones for
prophylaxis in cirrhotic patients, recently there is a
higher predominance of gram-positive pathogens
in ascitic fluid cultures.

55. Clinical presentation:
•Fever and chills followed by abdominal pain or discomfort is
the most common presentation. Pain could be very severe
and diffuse and may be confused with acute abdomen.
•Diffuse abdominal tenderness, which could be severe and
sometimes with rebound tenderness and even guarding, is
found in more than 50% of patients with SBP.
•In cirrhotics, there may be decompensation
•Diarrhea
•Completely asymptomatic cases are also seen in as many
as 30% of patients.

56. Investigations and diagnosis:
Diagnostic ascitic tapping is the gold standard. Peritoneal fluid should be
analyzed for protein, glucose, albumin, cell count, gram stain, and
anerobic, aerobic and fungal culture.
Combination of an ascites fluid pH of <7.35 and polymorphonuclear
neutrophil (PMN) count of >500 cells/µL is virtually diagnostic of SBP.
If PMN count is >250 cells, but less than 500 cells/µL, a positive bacterial
culture is required for the diagnosis.
SBP could still exist if the culture is negative and the PMN count is
between 250-500 cells. This is seen in monomicrobial SBP.
Sometimes blood culture is positive with cell count of less than250. This
is taken as positive evidence for SBP.
Lactate level: An ascites lactate level of >25 mg/dL is suggestive of SBP.

57. Treatment:
•IV fluid is started to maintain peripheral perfusion.
•Pending culture, IV cefotaxime (or similar 3rd generation cephalosporins)
is started at the dose of 2 gm IV every 8 hourly.
•Metronidazole is started at the dose of 400 mg. IV every 8 hourly.
•Aminoglycosides like gentamycin at the dose of 3 mg./Kg in divided
doses is useful for Pseudomonas aeruginosa, E coli, Proteus, Klebsiella,
and Staphylococcus species. Amikacin may also be used instead at the
dose of 15mg./Kg as a single dose. These drugs are nephrotoxic and their
levels must be monitored closely as well as renal functions.
•Sometimes Ampicillin 1-2 gms. every 6 hourly together with one of the
aminoglycosides is also used effectively.
•IV albumin, especially when serum albumin is low is very useful in
reducing ascites and increase phagocytosis by monophages.

58. Prophylaxis:
Outpatient prophylaxis, with norfloxacin 400 mg
daily or ciprofloxacin 750 mg weekly is useful in
patients with,
•Ascites and acute GI bleeding
•Ascitic fluid protein levels of less than 1 g/dL
•A history of SBP

59. Thank you..! Any questions??
Dr Manoj K Ghoda M.D., M.R.C.P.
Consultant Gastroenterologist
Visiting faculty, GCS Hospital
Gujarat gastro group