Lactate and the lactate-to-pyruvate molar ratio cannot be used as independent biomarkers for monitoring brain energetic metabolism: a microdialysis study in patients with traumatic brain injuries.

BACKGROUND: For decades, lactate has been considered an excellent biomarker for oxygen limitation and therefore of organ ischemia. The aim of the present study was to evaluate the frequency of increased brain lactate levels and the LP ratio (LPR) in a cohort of patients with severe or moderate traumatic brain injury (TBI) subjected to brain microdialysis monitoring to analyze the agreement between these two biomarkers and to indicate brain energy metabolism dysfunction. METHODS: Forty-six patients with an admission Glasgow coma scale score of ≤13 after resuscitation admitted to a dedicated 10-bed Neurotraumatology Intensive Care Unit were included, and 5305 verified samples of good microdialysis data were analyzed. RESULTS: Lactate levels were above 2.5 mmol/L in 56.9% of the samples. The relationships between lactate and the LPR could not be adequately modeled by any linear or non-linear model. Neither Cohen's kappa nor Gwet's statistic showed an acceptable agreement between both biomarkers to classify the samples in regard to normal or abnormal metabolism. The dataset was divided into four patterns defined by the lactate concentrations and the LPR. A potential interpretation for these patterns is suggested and discussed. Pattern 4 (low pyruvate levels) was found in 10.7% of the samples and was characterized by a significantly low concentration of brain glucose compared with the other groups. CONCLUSIONS: Our study shows that metabolic abnormalities are frequent in the macroscopically normal brain in patients with traumatic brain injuries and a very poor agreement between lactate and the LPR when classifying metabolism. The concentration of lactate in the dialysates must be interpreted while taking into consideration the LPR to distinguish between anaerobic metabolism and aerobic hyperglycolysis.

Normobaric hyperoxia in traumatic brain injury: does brain metabolic state influence the response to hyperoxic challenge?

This study sought to investigate whether normobaric hyperoxia (NH) improves brain oxygenation and brain metabolism in the early phase of severe and moderate traumatic brain injury (TBI) and whether this effect occurs uniformly in all TBI patients. Thirty patients (9 women and 21 men) with a median initial Glasgow Coma Score (GCS) of 6 (range, 3-12) were monitored using a brain microdialysis (MD) catheter with a brain tissue oxygen sensor (PtiO(2)) placed in the least-injured hemisphere. The inspired oxygen fraction was increased to 100% for 2 h. Patients were divided into two groups: Group 1: patients with baseline brain lactate ≤3 mmol/L and Group 2: patients with baseline brain lactate >3 mmol/L, and therefore increased anaerobic metabolism in the brain. In Group 1, no significant changes in brain metabolic parameters were found after hyperoxic challenge, whereas a significant increase in glucose and a decrease in the lactate-pyruvate ratio (LPR) were found in Group 2. In this latter group of patients, brain glucose increased on average by 17.9% (95% CI, +9.2% to +26.6%, p<0.001) and LPR decreased by 11.6% (95% CI, -16.2% to -6.9%, p<0.001). The results of our study show that moderate and severe TBI may induce metabolic alterations in the brain, even in macroscopically normal brain tissue. We observed that NH increased PaO(2) and PtiO(2) and significantly decreased LPR in patients in whom baseline brain lactate levels were increased, suggesting that NH improved the brain redox state. In patients with normal baseline brain lactate levels, we did not find any significant changes in the metabolic variables after NH. This suggests that the baseline metabolic state should be taken into account when applying NH to patients with TBI. This maneuver may only be effective in a specific group of patients.

Monitoring intracranial pressure in patients with malignant middle cerebral artery infarction: is it useful?

OBJECT: Intracranial pressure (ICP) monitoring is increasingly used in the treatment of patients with malignant middle cerebral artery (MCA) infarction. However, neurological deterioration may exist independent from intracranial hypertension. This study aimed to present the findings of continuous ICP monitoring in a cohort of patients with malignant MCA infarction and to correlate these findings with clinical and radiological features. METHODS: The authors studied a prospective cohort of 25 patients with malignant MCA infarction consecutively admitted to the neurotrauma intensive care unit of the Vall d'Hebron University Hospital between March 2002 and September 2006. The patients were treated using a combined protocol of initial moderate hypothermia and hemicraniectomy. The latter was performed when patients showed a midline shift (MLS) > or = 5 mm or ICP > 20 mm Hg. Six patients had an MLS > or = 5 mm on the first CT scan and underwent surgery without prior ICP monitoring. This study focuses on the subgroup of 19 patients who underwent intraparenchymatous ICP monitoring before surgery. RESULTS: Intracranial pressure readings were evaluated and correlated with pupillary abnormalities, MLS, and ischemic tissue volume. In 12 of the 19 patients, ICP values were always < or = 20 mm Hg, despite a mean (+/- SD) MLS of 6.7 +/- 2 mm and a mean ischemic tissue volume of 241.3 +/- 83 cm(3). In 2 patients with anisocoria, ICP values were also normal. CONCLUSIONS: In patients with a malignant MCA infarction, pupillary abnormalities and severe brainstem compression may be present despite normal ICP values. Therefore, continuous ICP monitoring cannot substitute for close clinical and radiological follow-up in the management of these patients.