Lactate is well-known as an important energy substrate for brain tissue and plays a key role in neuroenergetics. Experimental data have shown that exogenous lactate administration may improve metabolism in injured brain cells, and possibly has neuroprotective properties. Till now there has been a paucity of human clinical studies on this subject. Carteron et al recently published a trial in Critical Care Medicine that demonstrates that this effect holds promise also in humans with manifest brain injury. They included 23 patients with acute brain injury (either from TBI or SAH, all with a GCS<9) and took baseline measurements using ICP-monitoring, transcranial doppler (TCD), brain tissue oxygen catheters (Licox) and cerebral microdialysis. They then infused each patient with hypertonic lactate for a three-hour period to evaluate its effect on a variety of parametres. Infusions were initiated 26-49 hours after injury.
Their finding were very interesting. Firstly, it is a chilling reminder to read that as many as 57% of patients had microdialysis values suggestive of reduced substrate delivery to injured tissues, in the absence of any change in ICP. Of greatest interest was that lactate-infusion seemed to significantly improve cellular metabolism and restore glucose availability towards, and above, normal values. TCD evaluations were consistent with increased MCA-flow and reduced pulsatility index during lactate-infusion, as compared with the baseline readings.
This is, of course, a small patient sample, and these findings need validation in a larger trial, with focus on more patient-important outcomes. The results are nonetheless important, firstly because it suggests a beneficial effect from hypertonic lactate administration, but also as a reminder that bioenergetic failure at a cellular level after brain injury is both common (without affecting global parametres such as ICP) and potentially hugely detrimental.