12 Nov 09
By D Noritomi, F Soriano, J Kellum, S Cappi, P Biselli, A Liborio, M Park
Crit Care Med 2009;37:2733-2739
To describe the composition of metabolic acidosis in patients with severe sepsis and septic shock at intensive care unit admission and throughout the first 5 days of intensive care unit stay. Design: Prospective, observational study.
Twelve-bed intensive care unit.
Sixty patients with either severe sepsis or septic shock.
Measurements and main results
Data were collected until 5 days after intensive care unit admission. We studied the contribution of inorganic ion difference, lactate, albumin, phosphate, and strong ion gap to metabolic acidosis. At admission, standard base excess was -6.69 +/- 4.19 mEq/L in survivors vs. -11.63 +/- 4.87 mEq/L in nonsurvivors (p < .05); inorganic ion difference (mainly resulting from hyperchloremia) was responsible for a decrease in standard base excess by 5.64 +/- 4.96 mEq/L in survivors vs. 8.94 +/- 7.06 mEq/L in nonsurvivors (p < .05); strong ion gap was responsible for a decrease in standard base excess by 4.07 +/- 3.57 mEq/L in survivors vs. 4.92 +/- 5.55 mEq/L in nonsurvivors with a nonsignificant probability value; and lactate was responsible for a decrease in standard base excess to 1.34 +/- 2.07 mEq/L in survivors vs. 1.61 +/- 2.25 mEq/L in nonsurvivors with a nonsignificant probability value. Albumin had an important alkalinizing effect in both groups; phosphate had a minimal acid-base effect. Acidosis in survivors was corrected during the study period as a result of a decrease in lactate and strong ion gap levels, whereas nonsurvivors did not correct their metabolic acidosis. In addition to Acute Physiology and Chronic Health Evaluation II score and serum creatinine level, inorganic ion difference acidosis magnitude at intensive care unit admission was independently associated with a worse outcome.
Patients with severe sepsis and septic shock exhibit a complex metabolic acidosis at intensive care unit admission, caused predominantly by hyperchloremic acidosis, which was more pronounced in nonsurvivors. Acidosis resolution in survivors was attributable to a decrease in strong ion gap and lactate levels.
29 Oct 09
By T Jansen J van Bommel, J Bakker
Crit Care Med 2009;37:2827-2839
To decide whether the use of blood lactate monitoring in critical care practice is appropriate. We performed a systematic health technology assessment as blood lactate monitoring has been implemented widely but its clinical value in critically ill patients has never been evaluated properly.
PubMed, other databases, and citation review.
We searched for lactate combined with critically ill patients as the target patient population. Two reviewers independently selected studies based on relevance for the following questions: Does lactate measurement: 1) perform well in a laboratory setting? 2) provide information in a number of clinical situations? 3) relate to metabolic acidosis? 4) increase workers’ confidence? 5) alter therapeutic decisions? 6) result in benefit to patients? 7) result in similar benefits in your own setting? 8) result in benefits which are worth the extra costs?
Data extraction and synthesis
We concluded that blood lactate measurement in critically ill patients: 1) is accurate in terms of measurement technique but adequate understanding of the (an)aerobic etiology is required for its correct interpretation; 2) provides not only diagnostic but also important prognostic information; 3) should be measured directly instead of estimated from other acid-base variables; 4) has an unknown effect on healthcare workers’ confidence; 5) can alter therapeutic decisions; 6) could potentially improve patient outcome when combined with a treatment algorithm to optimize oxygen delivery, but this has only been shown indirectly; 7) is likely to have similar benefits in critical care settings worldwide; and 8) has an unknown cost-effectiveness.
The use of blood lactate monitoring has a place in risk-stratification in critically ill patients, but it is unknown whether the routine use of lactate as a resuscitation end point improves outcome. This warrants randomized controlled studies on the efficacy of lactate-directed therapy
03 Apr 09
By J Powell-Tuck, P Gosling, DN Lobo et al
NHS National Library of Health
From October 2006 the Association of Surgeons of Great Britain and Ireland, SARS, BAPEN Medical, the Intensive Care Society, the Association for Clinical Biochemistry and the Renal Association nominated core members of a steering committee who came together to establish consensus for good perioperative fluid prescribing. Concern arose from a high incidence of postoperative sodium and water overload, and evidence to suggest that preventing or treating this, by more accurate fluid therapy, would improve outcome.
18 Jan 09
By J A Myburgh, A Higgins, A Jovanovska, J Lipman, N Ramakrishnan, J Santamaria and the CAT Study investigators
Intensive Care Med 2008:34;2226-2234
To determine whether there was a difference between epinephrine and norepinephrine in achieving a mean arterial pressure (MAP) goal in intensive care (ICU) patients.
Prospective, double-blind, randomised-controlled trial.
Four Australian university-affiliated multidisciplinary ICUs.
Patients and participants
Patients who required vasopressors for any cause at randomisation. Patients with septic shock and acute circulatory failure were analysed separately.
Blinded infusions of epinephrine or norepinephrine to achieve a MAP =70 mmHg for the duration of ICU admission.
Primary outcome was achievement of MAP goal >24 h without vasopressors. Secondary outcomes were 28 and 90-day mortality. Two hundred and eighty patients were randomised to receive either epinephrine or norepinephrine. Median time to achieve the MAP goal was 35.1 h (interquartile range (IQR) 13.8ñ70.4 h) with epinephrine compared to 40.0 h (IQR 14.5ñ120 h) with norepinephrine (relative risk (RR) 0.88; 95% confidence interval (CI) 0.69ñ1.12; P = 0.26). There was no difference in the time to achieve MAP goals in the subgroups of patients with severe sepsis (n = 158; RR 0.81; 95% CI 0.59ñ1.12; P = 0.18) or those with acute circulatory failure (n = 192; RR 0.89; 95% CI 0.62ñ1.27; P = 0.49) between epinephrine and norepinephrine. Epinephrine was associated with the development of significant but transient metabolic effects that prompted the withdrawal of 18/139 (12.9%) patients from the study by attending clinicians. There was no difference in 28 and 90-day mortality.
Despite the development of potential drug-related effects with epinephrine, there was no difference in the achievement of a MAP goal between epinephrine and norepinephrine in a heterogenous population of ICU patients.