Journal List > Korean J Gastroenterol > v.56(3) > 1006709

Kim: Ascites, Hepatorenal Syndrome and Spontaneous Bacterial Peritonitis in Patients with Portal Hypertension

Abstract

Ascites, hepatic encephalopathy and variceal hemorrhage are three major complications of portal hypertension. The diagnostic evaluation of ascites involves an assessment of its etiology by determining the serum-ascites albumin gradient and the exclusion of spontaneous bacterial peritonitis. Ascites is primarily related to an inability to ex-crete an adequate amount of sodium into urine, leading to a positive sodium balance. Sodium restriction and diuretic therapy are keys of ascites control. But, with the case of refractory ascites, large volume paracentesis and transjugular portosystemic shunts are required. In hepatorenal syndrome, splanchnic vasodilatation with reduction in effective arterial volume causes intense renal vasoconstriction. Splanchnic and/or peripheral vasoconstrictors with albumin infusion, and renal replacement therapy are only bridging therapy. Liver transplantation is the only definitive modality of improving the long term prognosis.

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Table 1.
Ascitic Fluid Laboratory Data
Routine Optional Unusual Unhelpful
Cell count & differential Culture in blood culture bottle Acid-fast bacteria smear/culture pH
Albumin Glucose Cytology Lactate
Total protein Lactate dehydrogenase Triglyceride Cholesterol
Amylase Bilirubin Fibrinonectin
Gram's stain Adenosine deaminase Glycosaminoglucans
Table 2.
Criteria for Diagnosis of Hepatorenal Syndrome in Cirrhosis
Cirrhosis with ascites
Serum creatinine >1.5 mg/dL
Absence of shock
Absence of hypovolemia as defined by no sustained improvement of renal function (creatinine decreasing to <133 mmol/L) following at least 2 days of diuretic withdrawal (if on diuretics), and volume expansion with albumin at 1 g/kg/day up to a maximum of 100 g/day
No current or recent treatment with nephrotoxic drugs
Absence of parenchymal renal disease as defined by proteinuria <0.5 g/day, no microhaematuria (<50 red cells/high powered field), and normal renal ultrasonography
Table 3.
Types of Response to Treatment Using Vasoconstrictors
Complete response (Reversal of HRS) Decrease of serum creatinine to below 1.5 mg/dL
Relapse of HRS Recurrence of renal failure (creatinine >1.5 mg/dL)) after discontinuation of therapy
Partial response Decrease in serum creatinine to ≥50% of its pre-treatment value, without reaching a level below 1.5 mg/dL
No response No decrease of serum creatinine or decrease to <50% of its pre-treatment value, with a final level above 1.5 mg/dL

  HRS, hepatorenal syndrome.

Table 4.
Classification of Infected Ascites
Type of infection PMN/mm3 Culture
Spontaneous bacterial peritonitis ≥250 Positive (usually monomicrobial)
Monomicrobial non-neutrocytic bacterascites <250 Positive
Culture-negative neutrocytic ascites ≥250 Negative
Secondary bacterial peritonitis ≥250 Positive (polymicrobial)
Polymicrobial bacterascites <250 Positive
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