Ascites Pathogenesis and Management

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Ascites Pathogenesis and Management

• Reported by Ri ???

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Pathogenesis

• Chief contributor to ascites is splanchnic
  vasodilatation.
• Portal hypertension either pre hepatic, hepatic
  or post hepatic resulted in local production of
  vasodilators.

NEJM April 2004
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Pathogenesis

• In early cases, arterial vasodilatation could be
  compensated with increased CO.
• In advanced cases, serious vasodilatation
  resulted in activation of vasoconstrictors and
  ANP.
• This resulted in further sodium and water
  retention.

NEJM April 2004 3501646-54
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Complications

• Hepatorenal syndrome
• Spontaneous bacterial peritonitis

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Management of Ascites

• Reduction of sodium intake (1.52.0gm/day)
• Reduction of water intake (1l/day)
• Diuretics
• Paracentesis plasma expanders
• Transjugular intrahepatic portosystemic shunt

NEJM April 2004 3501646-54
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Ascites After Liver Transplantation

• Liver Transplantation
• March 2000 Vol 6 No.2

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Background

• Massive ascites after LT is uncommon but
  represents a serious adverse effect
• Pathogenesis is inadequately studied
• Proposed pathogenesis
• Stenosis of IVC anastomosis
• Acute cellular rejection
• Use of reduced graft

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Patient and Method

• Retrospective study of 378 LT patient who
  survived gt 10 days
• Massive ascites defined as gt500ml/day and lasted
  for more than 10 days

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Hemodynamic Study

• Obtained between 2nd and 3rd week after LT
• Hemodynamic study performed because developed
  massive ascites in a previous study or
  transjugular hepatic biopsy in cases with severe
  coagulopathy that precluded percutaneous liver
  biopsy

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Results

• 100 ascites patients vs 33 non-ascites patients
  have pressure gradient between free hepatic vein
  and right atrial pressure gt6 mmHg
• 100 ascites patients vs 22 non-ascites patients
  have wedge hepatic venous pressure gt12 mmHg in
  patient with ascites.

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Management

• 3 patient underwent side-to-side cavocaval
  anastomosis
• 1 patient under went percutaneous transluminal
  angioplasty
• Ascites in 15 remaining patient who survived
  resolved spontaneously

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Renal Impairment

• Serum creatinine levels were significantly
  greater in patients with ascites
• Serum creatinine levels were the same 1 year
  after LT for both groups.

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Peritonitis

• Patient is associated with a greater rate of
  peritonitis compared to patient without ascites
  (32 vs 6)
• 5/8 peritonitis in patient ascites occurred under
  spontaneous ascites drainage.
• Pathogen in patients with ascites were all
  cutaneous origin in contrast with enteric origin
  in patients without ascites.
• Ascites contamination could be the source of
  peritonitis for patients with open drain.

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Discussion

• Trauma could be the reason for short term ascites
  formation but is insufficient to explain
  prolonged massive ascites.
• From this study, major mechanism of ascites is
  secondary to hepatic vein outflow obstruction.
• Ascites resolved promptly after caval anastomosis
  was reconstructed.
• Hepatic outflow insufficiency could be related to
  kinking of IVC or graft malposition.

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Discussion

• Ascites could also be due to vasodilatation of
  hepatic artery due to denervation of the graft
• Administration of drugs to reduce splanchnic
  blood flow might prove effective.

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Discussion

• Renal impairment could be due to massive ascites
  loss which is aggravated by diuretic use.
• Potential nephrotoxicity drug like
  immunosuppresant might also play a role.
• Removal of drains and control wound leak has been
  recommended to avoid ascites fluid loss.
• Albumin supplement to increase oncotic pressure
  was also suggested
• Renal impairment is reversible after
  normalization of hepatic outflow.

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Conclusion

• Massive ascites is uncommon after LT.
• Present data suggests ascites is due to
  difficulty in hepatic venous outflow
• Measurement of hepatic vein and right atrial
  pressure to detect pressure gradient is the first
  approach in management of these patients.