ABSTRACT
OBJECTIVES: To analyze the mechanism of acid-base disorders in liver transplant recipients and to examine the relationship between these disorders and the fluids administered during surgery. METHODS: This prospective study in a university-affiliated hospital intensive care unit (ICU) included 52 patients admitted to the ICU from December 2009 to January 2011. We examined the contributions of inorganic ion differences, lactate, unmeasured anions, phosphate, and albumin to metabolic acidosis. In addition to laboratory variables, we collected demographic and clinical data. RESULTS: Metabolic acidosis (standard base excess ≤ -2.0 mmol/L) was identified in 37 (71.2%) patients during the immediate postoperative period. The inorganic ion difference was the main determinant of acidosis, accounting for -6.17 mEq/L of acidifying effect. The acidemia was attenuated mainly by the alkalinizing effect of albumin reduction, which contributed +6.03 mEq/L. There was an inverse proportional relationship between the quantity of saline solution used during surgery and the inorganic ion difference during the immediate postoperative period. CONCLUSIONS: Hyperchloremia is the primary contributor to metabolic acidosis in liver transplant recipients. Possibly the use of chloride-rich solutions increases the incidence of this disorder.
Subject(s)
Acid-Base Equilibrium , Acidosis/etiology , Blood Substitutes/adverse effects , Fluid Therapy/adverse effects , Liver Transplantation/adverse effects , Acidosis/blood , Acidosis/physiopathology , Adult , Albumins/adverse effects , Alkalosis/blood , Alkalosis/etiology , Alkalosis/physiopathology , Biomarkers/blood , Chlorides/blood , Female , Gelatin/adverse effects , Hospitals, University , Humans , Hydrogen-Ion Concentration , Hydroxyethyl Starch Derivatives/adverse effects , Intensive Care Units , Isotonic Solutions/adverse effects , Male , Middle Aged , Prospective Studies , Ringer's Lactate , Sodium Chloride/adverse effects , Treatment OutcomeABSTRACT
Distúrbios do equilíbrio ácido-básico são comuns nos pacientes críticos, estando em geral associados à maior morbimortalidade. Métodos que permitam entender a natureza destes distúrbios e auxiliar e consequentemente identificar atidudes que possam evitá-los e/ou corrigi-los são portanto extremamente importantes. A avaliação tradicional
Subject(s)
Water-Electrolyte Imbalance , Critical Care , Critical Care , Intensive Care UnitsABSTRACT
The different potential of initiated and non-initiated urinary bladder mucosa (UBM) to develop neoplasia was quantitatively evaluated in the male Wistar rat. Initiation of carcinogenesis was accomplished with N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN). Stimuli for cell proliferation and apoptosis were obtained by exposure followed by withdrawal of 3% Uracil in the diet. The proliferation index (PI) was estimated in UBM immunostained for the proliferating nuclear cell antigen (PCNA). The apoptotic index (AI) and the density of papillary/nodular hyperplasia (PNH) were estimated in hematoxilin-eosin stained sections. PNH was the main proliferative response to the mechanical irritation by uracil, irrespective of previous initiation with BBN. Uracil exposure induced higher PI and PNH density in the initiated rats. After uracil withdrawal, there was a significant increase of the AI in both uracil-treated groups, which correlated well to the respective PNH density. However, at the end of the experiment, PNH incidence and density were significantly higher in the BBN-initiated mucosa, which also presented 18% incidence of papillomas and 27% of carcinomas. Therefore, under prolonged uracil calculi trauma, the UBM of BBN-initiated Wistar rats gives rise to epithelial proliferative lesions that progress to neoplasia through acquired resistance to apoptosis.
