“…40 41 However, Durward et al showed not only that the SIG was a common cause of metabolic acidosis after CPB, but that the SIG was superior to lactate as a predictor of mortality following open cardiac surgery. 29 While there may have been differences in case mix between that patient population and our own, it is interesting to note that hyperchloraemia was also associated with survival in that study. 29 Mortality in this study group was only 1%.…”
Section: Discussionmentioning
confidence: 61%
“…29 While there may have been differences in case mix between that patient population and our own, it is interesting to note that hyperchloraemia was also associated with survival in that study. 29 Mortality in this study group was only 1%. Patients were not pre-selected by diagnosis or surgical procedure at the time of enrolment and we believe the study group is representative of children undergoing open cardiac surgery at this institution, for whom overall mortality was comparable at 2.4%.…”
Section: Discussionmentioning
confidence: 61%
“…28 Durward et al also showed, in children following CPB, that metabolic acidosis was most commonly due to either increase of the SIG or hyperchloraemia. 29 The prognostic significance of acid-base data is difficult to evaluate when cardiac surgical mortality is ,2%. We have used parameters such as predicted mortality and duration of intensive care as surrogate adverse endpoints.…”
Aims: To describe acid-base derangements in children following open cardiac surgery on cardiopulmonary bypass (CPB), using the Fencl-Stewart strong ion approach. Methods: Prospective observational study set in the paediatric intensive care unit (PICU) of a university children's hospital. Arterial blood gas parameters, serum electrolytes, strong ion difference, strong ion gap (SIG), and partitioned base excess (BE) were measured and calculated on admission to PICU. Results: A total of 97 children, median age 57 months (range 0.03-166), median weight 14 kg (range 2.1-50), were studied. Median CPB time was 80 minutes (range 17-232). Predicted mortality was 2% and there was a single non-survivor. These children showed mild metabolic acidosis (median standard bicarbonate 20.1 mmol/l, BE 25.1 mEq/l) characterised by hyperchloraemia (median corrected Cl 113 mmol/l), and hypoalbuminaemia (median albumin 30 g/l), but no significant excess unmeasured anions or cations (median SIG 0.7 mEq/l). The major determinants of the net BE were the chloride and albumin components (chloride effect 24.8 mEq/l, albumin effect +3.4 mEq/l). Metabolic acidosis occurred in 72 children (74%) but was not associated with increased morbidity. Hyperchloraemia was a causative factor in 53 children (74%) with metabolic acidosis. Three (4%) hyperchloraemic children required adrenaline for inotropic support, compared to eight children (28%) without hyperchloraemia. Hypoalbuminaemia was associated with longer duration of inotropic support and PICU stay. Conclusions: In these children with low mortality following open cardiac surgery, hypoalbuminaemia and hyperchloraemia were the predominant acid-base abnormalities. Hyperchloraemia was associated with reduced requirement for adrenaline therapy. It is suggested that hyperchloraemic metabolic acidosis is a benign phenomenon that should not prompt escalation of haemodynamic support. By contrast, hypoalbuminaemia, an alkalinising force, was associated with prolonged requirement for intensive care.
“…40 41 However, Durward et al showed not only that the SIG was a common cause of metabolic acidosis after CPB, but that the SIG was superior to lactate as a predictor of mortality following open cardiac surgery. 29 While there may have been differences in case mix between that patient population and our own, it is interesting to note that hyperchloraemia was also associated with survival in that study. 29 Mortality in this study group was only 1%.…”
Section: Discussionmentioning
confidence: 61%
“…29 While there may have been differences in case mix between that patient population and our own, it is interesting to note that hyperchloraemia was also associated with survival in that study. 29 Mortality in this study group was only 1%. Patients were not pre-selected by diagnosis or surgical procedure at the time of enrolment and we believe the study group is representative of children undergoing open cardiac surgery at this institution, for whom overall mortality was comparable at 2.4%.…”
Section: Discussionmentioning
confidence: 61%
“…28 Durward et al also showed, in children following CPB, that metabolic acidosis was most commonly due to either increase of the SIG or hyperchloraemia. 29 The prognostic significance of acid-base data is difficult to evaluate when cardiac surgical mortality is ,2%. We have used parameters such as predicted mortality and duration of intensive care as surrogate adverse endpoints.…”
Aims: To describe acid-base derangements in children following open cardiac surgery on cardiopulmonary bypass (CPB), using the Fencl-Stewart strong ion approach. Methods: Prospective observational study set in the paediatric intensive care unit (PICU) of a university children's hospital. Arterial blood gas parameters, serum electrolytes, strong ion difference, strong ion gap (SIG), and partitioned base excess (BE) were measured and calculated on admission to PICU. Results: A total of 97 children, median age 57 months (range 0.03-166), median weight 14 kg (range 2.1-50), were studied. Median CPB time was 80 minutes (range 17-232). Predicted mortality was 2% and there was a single non-survivor. These children showed mild metabolic acidosis (median standard bicarbonate 20.1 mmol/l, BE 25.1 mEq/l) characterised by hyperchloraemia (median corrected Cl 113 mmol/l), and hypoalbuminaemia (median albumin 30 g/l), but no significant excess unmeasured anions or cations (median SIG 0.7 mEq/l). The major determinants of the net BE were the chloride and albumin components (chloride effect 24.8 mEq/l, albumin effect +3.4 mEq/l). Metabolic acidosis occurred in 72 children (74%) but was not associated with increased morbidity. Hyperchloraemia was a causative factor in 53 children (74%) with metabolic acidosis. Three (4%) hyperchloraemic children required adrenaline for inotropic support, compared to eight children (28%) without hyperchloraemia. Hypoalbuminaemia was associated with longer duration of inotropic support and PICU stay. Conclusions: In these children with low mortality following open cardiac surgery, hypoalbuminaemia and hyperchloraemia were the predominant acid-base abnormalities. Hyperchloraemia was associated with reduced requirement for adrenaline therapy. It is suggested that hyperchloraemic metabolic acidosis is a benign phenomenon that should not prompt escalation of haemodynamic support. By contrast, hypoalbuminaemia, an alkalinising force, was associated with prolonged requirement for intensive care.
Introduction The base deficit is a useful tool for quantifying total acid-base derangement, but cannot differentiate between various aetiologies. The Stewart-Fencl equations for strong ions and albumin have recently been abbreviated; we hypothesised that the abbreviated equations could be applied to the base deficit, thus partitioning this parameter into three components (the residual being the contribution from unmeasured anions).
“…In a large study of adult intensive care unit (ICU) patients, metabolic acidosis due to hyperlactataemia was the strongest predictor of mortality, compared with hypercholoraemic acidosis and non-lactate acidosis 37. In children, three studies (total n=453) found non-lactate acidosis to be superior to blood lactate in predicting mortality in acutely ill children in PICU,33 38 39 but other researchers found that it compared less favourably 27 37…”
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