The Value of Blood Lactate Measurements in ICU: An Evaluation of the Role in the Management of Patients on Haemofiltration.

In response to clinical demand some point-of-care analysers now provide blood lactate measurements in critical care. Recent literature has raised concerns about the value and interpretation of these measurements. Two particular concerns relate to over-interpretation of lactate rises as equating tissue hypoxia and also the failure to recognise the contribution from inotropic support. We undertook this study to evaluate blood lactate measurements in intensive care unit (ICU) patients in the assessment of response to, and requirements for, haemofiltration (HF) with lactate replacement fluid and to evaluate influences from hepatic failure and from inotropic supportive therapy. Haemofiltration is a convenient renal replacement therapy widely used in intensive care management as an alternative to haemodialysis. Mainly used for the treatment of acute renal failure the process involves removal by filtration of fluid, electrolytes, metabolites and other substances and simultaneous replacement of essential fluid and electrolytes as well as a buffer, usually in the form of lactate (sodium salt). There is controversy about whether lactate replacement may be harmful to the patient and, if so, when it would be appropriate to use a lactate-free fluid at greater expense. Serial blood lactate with simultaneous blood gas measurements were recorded in 27 patients requiring HF for acute renal failure. At baseline all patients had base deficits of >5mmol/L and 14 (52%) had blood lactates of >3.5mmol/L. Lactate ‘tolerance’ was monitored by peak changes in these parameters during the procedure. There was a worsening of base deficit in only three of the patients in whom lactate rises exceeded 10 mmol/L at some stage during HF with one survivor. A further twelve patients with rises of blood lactate greater than 5 mmol/L improved their base deficit (+1 to +17) with 8 (67%) survivors. Of the remaining twelve patients with improved base deficit (+2 to +20), 10(83%) survived. The influence on ‘lactate tolerance’ in patients with co-incidental liver disease and those on inotropic support was studied. In these groups lactate tolerance was compromised, particularly those on adrenaline support. Patients with initial blood lactate measurements of >10mmol/l and large base deficits were also lactate intolerant. The data suggest that rises in blood lactate during HF signal harm if accompanied by inadequate improvement in base deficit. Blood lactate and simultaneous acid-base response measurements during HF help to assign correct buffer replacement and should be performed on all patients.