1. Ascites refers to the abnormal accumulation of fluid in the peritoneal cavity. It is usually caused by portal hypertension due to liver cirrhosis or diseases affecting the peritoneum. 2. Evaluation of ascites involves history, physical exam, abdominal ultrasound, diagnostic paracentesis and lab tests of ascitic fluid. Management focuses on treating the underlying cause, using diuretics and sodium restriction, and therapeutic paracentesis if needed. 3. Refractory ascites is ascites that does not respond to medical therapy. It requires large volume paracentesis and may necessitate TIPS or liver transplantation. Spontaneous bacterial peritonitis is a complication of ascites requiring antibiotic treatment.

1. APPROACH TO ASCITES

2. Approach To
Ascites
Presenter: NSANZABAGANWA Christian
University of Rwanda medical school

3. Ascites
üThe pathologic accumulation of fluid in the peritoneal cavity
üHealthy men have little or no intraperitoneal fluid
üWomen normally may have up to 20 mL depending on the phase of
the menstrual cycle.

4. Pathophysiology

5. Causes

6. Causes
Normal peritoneum
üPortal hypertension (75%)
üHypoalbuminemia
üMisceraneous
Diseased peritoneum
üInfections
üMalignancy
Ductal disruptions in trauma

7. Causes of ascites in normal peritonium

8. Causes of ascites in diseased peritonium

9. HISTORY

10. HISTORY
History of risk factors for liver disease
üLong term Alcohol consumption
üHistory of viral hepatitis (HBV&HCV) or jaundice
üMultiple sexual partners
üInjection drug use
üTransfusion with non-tested blood for hepatitis
NB: Donated blood screen for HBV began in 1972 in USA
and for HCV in 1992
üTattoos

11. History of long term stable cirrhosis who develop ascites: HCC is likely.
History of cancer or marked weight loss (malignant ascites).
NB: Malignant ascites is frequently painful vs Painless cirrhotic
ascites.

12. History of fevers: Bacterial peritonitis
Behavior and consciousness changes (encephalopathy)
History of Haemorrhoids/ Upper GI bleeding: Portal hypertension
History of TB or TB contact

13. Physical exam aims at diagnosing the cause
General appearance
üJaundice
üCachexia
üAnasarca
Upper limb
üFinger clubbing
üLiver flap
üLeukonikia
üPalmar erythema
Head
üPallor
üKayser-Fleischer ring
üPuffy eye
üLympadenopathies
üOral candidiasis

14. Physical exam
Neck
üVirchow node
üJVP distension
Chest
üGynecomastia
üSpider naevi
üAxillary hair loss
üDisplaced apex beat, Heave
üMurmar, gallop
Abdomen
üSigns of ascites ( distension,
shifting dullness)
üPuddle sign may be there when
fluid is 120 ml
üShifting dullness ≥ 500 ml

15. Abdomen
üDilated collateral veins
üSister Mary Joseph nodule
üHepatomegaly (can be hard,
tender or nodular, liver span)
üSplenomegaly
üTenderness
NB: It may be hard to palpate
the liver in huge ascites or in
cirrhosis

17. Stages
Stage 1+ is detectable only after careful examination.
Stage 2+ is easily detectable but of relatively small volume.
Stage 3+ is obvious ascites but not tense ascites.
Stage 4+ is tense ascites.

18. Investigations
1. Abdominal ultrasound establishes the presence of fluid
2. Diagnostic paracentesis
üTo determine the cause.
üPatient with cirrhosis and ascites or with clinical worsening to exclude
bacterial peritonitis

19. Inspection of ascitic fluid
üMost fluis is transparent and tinged yellow
üCloudy fluid suggests infection.
üMilky fluid in chylous ascites due to high triglyceride
üBloody fluid in traumatic paracentesis (It clots) and 20% of malignant
ascites (Doesn’t clot)
üStraw colored: Cirrhosis
üBile stained: Biliary contamination

20. Paracentesis

21. Routine studies
1. WBCs with differential. Normal <500 leukocytes/mcL &
<250(PMNs)/mcL.
üElevated WBCs in inflammatory condition
üPMN count of >250/mcL and >75% in bacterial peritonitis
üHigher WBCs predominance of lymphocytes in TB or peritoneal
carcinomatosis.
NB: Normal cell count: <500 WBCs/µL and <250 PMNs/ µL

22. 2. Albumin and total protein
Serum ascitic albumin gradient (Serum albumin-ascitic
albumin)
üSAAG for the classification of ascites into portal hypertensive and
nonportal hypertensive causes.
üSAAG ≥ 1.1 g/dL suggests underlying portal hypertension,
üSAAG <1.1 g/dL implicate nonportal hypertensive causes.
üThe accuracy of the SAAG exceeds 95%
NB: 4% of patients have mixed ascites (cirrhosis portal
hypertension + malignancy or tuberculosis).
High SAAG does not exclude concomitant malignancy

23. üElevated SAAG with high protein (>2.5 g/dL): Hepatic congestion
üLow SAAG with high Protein: Malignant ascites
ü2/3 of malignant ascites have a total protein level>2.5 g/dL.
Culture and Gram stain
üTo detect bacterial peritonitis in neutrocytic ascites (>250 PMNs/µL)
üCulture detects bacteria with 92% sensitivity
üGram stain has 10% sensitivity
Ascitic fluid cytology: If peritoneal carcinomatosis is suspected:
56-75% Sensitive

24. Other lab studies
üAn elevated amylase: pancreatic ascites or GI perforation
üAscitic bilirubin > serum bilirubin: perforation of the biliary tree.
ü An elevated ascitic creatinine suggests leakage of urine
üAdenosine deaminase may be useful for the diagnosis TB peritonitis.
üGlucose: Low in TB peritonitis
üpH:<7 suggest bacterial infection
üRBCs: more than 50,000/µL suggests TB, malignancy or trauma

25. Imaging
üBoth ultrasound and CT imaging can distinguish between causes of
portal and nonportal hypertensive ascites.
üDoppler ultrasound and CT can detect Budd-Chiari syndrome.
Abdominal ultrasound
üConfirming the presence of ascites in smaller amount as small as 5-10
ml
üGuidance of paracentesis.
üIn patients with nonportal hypertensive ascites
üLymphadenopathy and the masses of liver, ovaries, and pancreas are
seen on U/S

26. CT-ScanUltrasound

27. Laparoscopy
Done in some patients for direct visualization to take biopsies of
üLiver
üPeritoneum (mesothelioma)
üIntra abdominal lymph nodes

28. Management
üAscites is not the diagnosis
üAlleviate symptomes
üManage and Treat the cause

29. Management
Diet: Dietary sodium restriction to 40 mmol (1 g in 24 hours).
Fluid restriction
üNot necessary unless the serum sodium is<120 mmol/L.
Diuretic therapy:
üStart if no response to sodium restriction
üSpironolactone: Starting at 100 mg daily, peak effect at 3days
üIf no response in a week, increase to Spironolactone 400 mg/day and
add Lasix 20-40mg 6-8 hrly to be 160mg/day
NB: Mainstay therapy for ascites is Diuretic therapy with
Spironolactone which helps eliminate sodium, antagonizes
hyperaldosteronism

30. üAmiloride 5–15 mg daily .
Monitoring
üCheck serum electrolytes (sodium levels) & creatinine at the start and
every other day
üMonitor weight of patients, input and output and abdominal girth
On diuretic, weight loss should be 300-500 g/d and 800-1000g/d
(patient with edema) and adjust diuretics as the ascites disappears

31. Electrolyte problems.
üDiuretics must betemporarily discontinued in rise in serum creatinine
level
üStop the diuretics & water restriction if the sodium < 120 mmol/L
üStop the diuretics if hyperkalaemia or encephalopathy occurs
Therapeutic Paracentesis
Done to relieve tense ascites or in refractory ascites
üHypovolemia can occur in fluid removal of ≥ 5L
üIV albumin is infused (8 g per L of ascitic fluid removed).

32. Refractory ascites
Refractory ascites refers to ascites that cannot be resolved by dietary
sodium restriction and diuretic treatment
1. Diuretic-resistant ascites: ascites that cannot be mobilized or its
recurrence cannot be prevented because of a lack of response to dietary
sodium restriction and intensive diuretic treatment.
2. Diuretic-intractable ascites: ascites that cannot be mobilized or its
early recurrence cannot be prevented because of the development of
diuretic-induced complications that preclude the use of an effective
diuretic dosage.

33. Risk factors to Refractory ascites
üWrong diuretics with only loop diuretics when their effect is
prevented by unopposed hyperaldosteronism
üNSAIDs inhibiting the synthesis of vasodilating renal prostaglandins
üACE inhibitors and angiotensin receptor antagonists, which can
impair the renal perfusion and reduce GFR in patients with cirrhosis
and ascites
üNephrotoxic drugs such as aminoglycosides
üComplications precipitating renal failure like vomiting, diarrhoea or
bleeding
üBacterial infections such as SBP

34. The International Ascites Club: Diagnostic
criteria
Treatment duration:
üDiuretic therapy (spironolactone 400 mg/day and furosemide 160
mg/day) for at least 1 week and on a salt-restricted diet of less 5.2 g of
salt/day without a response.
Lack of response:
üMean weight loss of <0.8 kg over 4 days and urinary sodium output
less than the sodium intake.
Early ascites recurrence:
üReappearance of grade 2 or 3 ascites within 4 weeks of initial
mobilization.

35. The International Ascites Club: Diagnostic
criteria
Diuretic-induced complications:
ü Diuretic-induced hepatic encephalopathy in the absence of any other
precipitating factor.
ü Diuretic-induced renal impairment: increase of serum creatinine by
>100% to a value >2 mg/dl in patients with ascites responding to
treatment.
ü Diuretic-induced hyponatraemia: decrease of serum sodium by >10
mmol/L to a serum sodium of <125 mmol/L.
ü Diuretic induced hypo or hyperkalaemia:to <3 mmol/L or >6 mmol/L
despite appropriate measures.

36. Prevention of refractory ascites
To restore responsiveness to the standard treatment.
üWithdrawal of the offending drug
üResolution of the complication
üAppropriate plasma volume expander if hypovolemic

37. Treatment of Refractory ascites
üRepeated large-volume paracentesis but it does not correct sodium
retention and ascites usually recurs
NB:
1. The first-line therapy of refractory ascites is large-volume
paracentesis adding albumin if >5 L of fluid are removed.
2. Routine ascitic PMNC count is recommended with each
paracentesis to detect SBP

38. Surgery for Refractory ascites
Implantation of the LeVeen shunt may offer better long-term control of
ascites but occlusion can occur
Transjugular intrahepatic portosystemic shunt (TIPS) is better than
large-volume paracentesis in the control of ascites
TIPS is done when
üLarge-volume paracentesis > 2/ month
üWhen ascites is loculated and cannot be
easily removed with a paracentesis
üThe patient becomes intolerant of repeated taps.
NB: Liver transplantation is the only improve the survival of
cirrhotic patients with refractory ascites

39. Surgery for Refractory ascites
LeVeen Shunt TIPS

40. SBP ( Spontaneous Bacterial Peritonitis)
Most common bacteria is E. Coli.
Bacteria are believed to gain access to peritoneum by hematogenous route.
Low ascitic fluid albumin (<1g/dl) predisposes to SBP
Clinical Presentation
üAbrupt onset of Fever,
üChills,
üGeneralized Abdominal Pain,
üRebound tenderness.

41. Labs
üAscitic Fluid analysis shows WBCs >500/mm3 and
neutrophil>250/mm3
Treat with
üCefotaxime 2 g every 8 h or ceftriaxone 2 g/day or
amoxicillin/clavulanate (1 g tid) for for at least 5 days
üWhen feasible, paracentesis should be repeated after 48 h to document
>25% decrease in PMNC count.
üIf not decreased, antibiotic should be changed according to the
bacterial susceptibility if cultures positive.

42. In Patients with elevated bilirubin (>4 mg/dl) and evidence of acute
renal dysfunction (defined as a BUN>30 mg/dl and
creatinine>1.0 mg/dl)
üGive albumin at days 1 and 3 of acute SBP therapy to prevent further
renal deterioration and improve survival
üAlbumin given is 1.5 g/kg on day 1 and 1 g/kg at day 3 up to a
maximum of 100 g/day.

43. Long-term antibiotic prophylaxis with oral norfloxacin (400 mg/day) for a
week is indicated in:
1. Patients with a prior history of SBP
2. Patients without a prior history of SBP but who:
ü have a low ascites protein (<1 g/dl) plus renal failure (creatinine
>1.2 mg/dl or BUN>25 mg/dl)
ü A serum sodium ≤130 mEq/L
ü Severe liver disease with serum bilirubin ≥3 mg/dl
Ciprofloxacin 750 mg once weekly can also be given prophylactically

44. Take home message
üAscites is not the diagnosis
üAlleviate symptoms
üManage and Treat the cause
üDetect SBP early and refractoriness and manage them
üEducate patients & relatives about risk factors of the causes ( eg:
Hepatitis treatment and prevention, early consult, less alcohol
consumption, etc…)

45. References
üUptodate
üCurrent medical diagnosis and treatment-2015
üDavidsons Principles and Practice of Medicine 22ed by Dr. Mahin
üOxford Handbook of Clinical Medicine (Oxford Handbook Series) by
Murray Longmore, Ian Wilkinson, Andrew Baldwin and Elizabeth
Wallin (Mar 9, 2014)
üUSMLE Step 2 CK Internal Medicine,2017
üHarrison's Principles of Internal Medicine, 18th ed.
üKumar & Clarks Medical Management and Therapeutics, Sep 21,
2011

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