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Purpose: To describe the characteristics of patients who die in emergency departments and the decisions to withhold or withdraw life support., Methods: We undertook a 4-month prospective survey in 174 emergency departments in France and Belgium to describe patients who died and the decisions to limit life-support therapies., Results: Of 2,512 patients enrolled, 92 (3.7%) were excluded prior to analysis because of missing data; 1,196 were men and 1,224 were women (mean age 77.3 +/- 15 years). Of patients, 1,970 (81.4%) had chronic underlying diseases, and 1,114 (46%) had a previous functional limitation. Principal acute presenting disorders were cardiovascular, neurological, and respiratory. Life-support therapy was initiated in 1,781 patients (73.6%). Palliative care was undertaken for 1,373 patients (56.7%). A decision to withhold or withdraw life-sustaining treatments was taken for 1,907 patients (78.8%) and mostly concerned patients over 80 years old, with underlying metastatic cancer or previous functional limitation. Decisions were discussed with family or relatives in 58.4% of cases. The decision was made by a single ED physician in 379 cases (19.9%), and by at least two ED physicians in 1,528 cases (80.1%)., Conclusions: Death occurring in emergency departments mainly concerned elderly patients with multiple chronic diseases and was frequently preceded by a decision to withdraw and/or withhold life-support therapies. Training of future ED physicians must be aimed at improving the level of care of dying patients, with particular emphasis on collegial decision-taking and institution of palliative care.

Objective: To evaluate the origin of H+ ions participating in the generation of CO2 coming from sodium bicarbonate infusion during metabolic acidosis. We hypothesized that these H+ ions come from a back-titration of the main non-bicarbonate buffers present in the blood, i. e. the hemoglobin and the albumin, and thus postulated that the rate of CO2 release from a bicarbonate load is dependent on the concentration of these buffers., Design: Prospective clinical and experimental study., Setting: Surgical intensive care unit of a university hospital., Patients and Material: (1) Sixteen stable sedated and artificially ventilated critically ill patients with a mild base deficit. (2) Acidotic human blood (bicarbonate 5 mM, pH 7.0) of hematocrit 5, 10, 20 and 40% regenerated from a mixture of frozen fresh plasma and packed red blood cells., Patients: infusion of 1.5 mmol/kg sodium bicarbonate over 5 min. Regenerated blood: 25 mM sodium bicarbonate load., Patients: continuous measurement of CO2 production (VCO2) on the expired gas using a metabolic monitor and arterial blood gas analysis before (T0), at the end (T5) and at 10, 30 and 60 min after the beginning of the bicarbonate infusion. The increase in VCO2 was 18 +/- 7% leading to a rise in PaCO2 from 39.6 +/- 2.3 at T0 to 46.2 +/- 2.7 mmHg at T5. The increases in VCO2 and in PaCO2 were significantly correlated to the albumin (r = 0.73, p < 0.005 and r = 0.70, p < 0.005, respectively) and to the hemoglobin (r = 0.51, p < 0.05 and r = 0.65, p < 0.01, respectively) concentrations. Regenerated blood: gas analysis 1 min after the bicarbonate load. The increase in PCO2 was closely related to the hematocrit (Ht) of the blood as it was 15.9 +/- 7.5 mmHg for Ht 5%, 29.0 +/- 9.6 for Ht 10%, 44.2 +/- 5.9 for Ht 20% and 71.0 +/- 3.5 for Ht 40% (n = 5 for each, p < 0.001)., Conclusions: The importance of the release of CO2 from a bicarbonate load is dependent on the concentration of the blood non-bicarbonate buffers. It is therefore likely that the adverse effects of bicarbonate therapy linked to the CO2 generation are more important in patients with high blood albumin and hemoglobin concentrations.

Objective: To evaluate the sensitivity, specificity, and predictive values of an elevated anion gap as an indicator of hyperlactatemia and to assess the contribution of blood lactate to the serum anion gap in critically ill patients., Design: Prospective study., Setting: General intensive care unit of a university hospital., Patients: 498 patients, none with ketonuria, severe renal failure or aspirin, glycol, or methanol intoxication., Measurements and Results: The anion gap was calculated as [Na+]-[Cl-]-[TCO2]. Hyperlactatemia was defined as a blood lactate concentration above 2.5 mmol/l. The mean blood lactate concentration was 3.7 +/- 3.2 mmol/l and the mean serum anion gap was 14.3 +/- 4.2 mEq/l. The sensitivity of an elevated anion gap to reveal hyperlactatemia was only 44% [95% confidence interval (CI) 38 to 50], whereas specificity was 91% (CI 87 to 94 and the positive predictive value was 86% (CI 79 to 90). As expected, the poor sensitivity of the anion gap increased with the lactate threshold value, whereas the specificity decreased [for a blood lactate cut-off of 5 mmol/l: sensitivity = 67% (CI 58 to 75) and specificity = 83% (CI 79 to 87)]. The correlation between the serum anion gap and blood lactate was broad (r2 = 0.41, p < 0.001) and the slope of this relationship (0.48 +/- 0.026) was less than 1 (p < 0.001). The serum chloride concentration in patients with a normal anion gap (99.1 +/- 6.9 mmol/l) was comparable to that in patients with an elevated anion gap (98.8 +/- 7.1 mmol/l)., Conclusions: An elevated anion gap is not a sensitive indicator of moderate hyperlactatemia, but it is quite specific, provided the other main causes of the elevated anion gap have been eliminated. Changes in blood lactate only account for about half of the changes in anion gap, and serum chloride does not seem to be an important factor in the determination of the serum anion gap.