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Abstract Details

Beyond Lactate/Pyruvate Ratios: Patient Characteristics Associated with Metabolic Distress after Traumatic Brain Injury using Cerebral Microdialysis
Neuro Trauma, Critical Care, and Sports Neurology
Neurocritical Care Posters (7:00 AM-5:00 PM)
024

Determine patient characteristics associated with metabolic distress (MDS) following traumatic brain injury (TBI) using cerebral microdialysis (CMD).  

CMD is a promising tool for nearly continuous monitoring of cerebral metabolism in TBI patients, with limited data demonstrating utility for clinical decision-making. MDS is defined as brain lactate/pyruvate ratio (LPR) >40. Low glucose and low pyruvate are indicators of cellular ischemia or mitochondrial dysfunction.

In this retrospective, single institution study, routine admission, discharge, and CMD data were obtained from thirteen consecutive patients with TBI. Samples were collected hourly and glucose, lactate, and pyruvate levels were quantified using a CMA-600 analyzer. Pathological thresholds were defined as: brain glucose <0.8 mmol/L, brain pyruvate <120 μmol/L, brain LPR >40 for at least two consecutive hours. Student’s t-test and Fisher’s exact test were used to determine strength of associations.

Five out of thirteen patients experienced MDS. Mean arrival Glasgow Coma Scale (GCS) was lower in patients who experienced MDS compared to patients who did not (5.6 vs. 10, p=0.028). Mean age (in years) was lower in patients who experienced MDS compared to patients who did not (25.4 vs. 46.2, p= 0.017). All five patients with MDS had brain glucose <0.8 mmol/L and normal serum glucose. Two out of five patients with MDS had pyruvate less than 120 μmol/L, one of whom had brain lactate and pyruvate normalization following blood pressure augmentation. Gender, probe location, presence of cerebral contusion, and unfavorable Glasgow Outcome Scale were not associated with MDS.  

Lower arrival GCS and younger age were associated with MDS after TBI. Low glucose and low pyruvate with LPR>40 represent impending neuronal injury and may inform management. Increased sample size, careful patient selection, and level of concordance with intracranial pressure, cerebral perfusion pressure, electroencephalography, and/or brain tissue oxygenation should be incorporated in future studies investigating MDS after TBI. 

Authors/Disclosures
Ritwik Bhatia, MD (University of California, San Francisco, Dept of Neurology)
PRESENTER
Dr. Bhatia has nothing to disclose.
Joshua Lukas, MD (Riverside Methodist Hospital (Ohio Health)) Dr. Lukas has nothing to disclose.
Jude H. Charles, MD Dr. Charles has nothing to disclose.
Ayham M. Alkhachroum, MD (Columbia University Medical Center) The institution of Dr. Alkhachroum has received research support from Miami CTSI.
Kristine H. O'Phelan, MD (University of Miami) Dr. O'Phelan has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Bard Medical. Dr. O'Phelan has a non-compensated relationship as a DSMB member SIREN network with NIH/NINDS that is relevant to AAN interests or activities.