title: Acid-base balance in combined severe hepatic and renal failure: a quantitative analysis.
abstract: BACKGROUND
  Severe hepatic failure (SHF) commonly leads to major changes in acidbase balance status. However, the direct effects of liver failure per se on acid base balance are poorly understood because this condition is usually associated with acute renal failure (ARF).
  
  
  OBJECTIVE
  To assess the effect of SHF on acid-base balance.
  
  
  METHODS
  Retrospective laboratory investigation.
  
  
  METHODS
  Thirty-seven critically ill patients with SHF complicated by ARF, and 42 patients with severe ARF without liver failure prior to renal replacement therapy.
  
  
  METHODS
  Retrieval of clinical and laboratory data from prospective unit and laboratory databases.
  
  
  METHODS
  Quantitative acid-base assessment using Stewart-Figge methodology. Comparison of findings between the two groups. Comparison of demographic and clinical features.
  
  
  RESULTS
  Patients with combined SHF and ARF were younger and had significantly higher mean bilirubin, ALT and INR levels (p<0.0001). Their mean lactate concentration was higher (6.4 vs. 2.1 mmol/L; p<0.0001) leading to a greater anion gap (25.8 vs. 16.1 mmol/L; p<0.0001). The ionized calcium concentration (1.00 vs. 1.15 mmol/L; p<0.0001) was lower but the strong ion difference apparent (SIDa) was greater (42.0 vs. 38.0 mEq/L; p<0.005) due to hypochloremia. The albumin concentration was low but higher than in control patients (28 vs. 24 g/L; p<0.01) and the calculated strong ion gap (SIG) was greater (12.6 vs. 9.3 mEq/L; p<0.01). The base excess was similar to controls and the pH was preserved in the near normal range by marked hypocapnea.
  
  
  CONCLUSIONS
  Combined SHF and ARF is a syndrome with unique acid-base changes due mostly to lactic metabolic acidosis and, in smaller part, to the accumulation of unmeasured anions. This acidosis, like that of ARF, is attenuated by hypoalbuminemia, by a unique preservation of the SIDa due to hypochloremia, and by marked hypocapnea.
authors.affiliation: Department of Intensive Care, Austin Hospital, Melbourne, Australia.
authors.forename: T
authors.initials: T
authors.lastname: Naka
authors.forename: R
authors.initials: R
authors.lastname: Bellomo
authors.forename: H
authors.initials: H
authors.lastname: Morimatsu
authors.forename: J
authors.initials: J
authors.lastname: Rocktaschel
authors.forename: L
authors.initials: L
authors.lastname: Wan
authors.forename: P
authors.initials: P
authors.lastname: Gow
authors.forename: P
authors.initials: P
authors.lastname: Angus
mesh_terms: D000136:Acid-Base Equilibrium; D000140:Acidosis, Lactic / Q000209:etiology* / Q000503:physiopathology; D058186:Acute Kidney Injury / Q000150:complications* / Q000503:physiopathology; D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000097:blood; D001663:Bilirubin / Q000097:blood; D002245:Carbon Dioxide / Q000097:blood; D002712:Chlorides / Q000097:blood; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006996:Hypocalcemia / Q000209:etiology / Q000503:physiopathology; D019934:International Normalized Ratio; D017093:Liver Failure / Q000150:complications* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012709:Serum Albumin / Q000378:metabolism; D012720:Severity of Illness Index
chemical_list: D002712:Chlorides; D012709:Serum Albumin; D002245:Carbon Dioxide; D000410:Alanine Transaminase; D001663:Bilirubin