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Semi-quantitative Assessment Using [18F]FDG Tracer in Patients with Severe Brain Injury
Published on: November 9, 2018
Correlation of brain flow variables and metabolic crisis: a prospective study in patients with severe traumatic brain
Corrado P Marini1,2, Christy Stoller2, John McNelis1
1Department of Surgery, Jacobi Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA.
Introduction:
Current treatment guidelines for patients with severe TBI (sTBI) are aimed at preventing secondary brain injury targeting specific endpoints of intracranial physiology to avoid the development of metabolic crisis. We sought to identify factors contributing to development of metabolic crisis in the setting of a Multi-modality Monitoring and Goal-Directed Therapy (MM&GDTP) approach to patients with severe TBI.
Methods:
Prospective monitoring of sTBI patients was performed, with retrospective data analysis. MM&GDTP was targeted to intracranial pressure (ICP) ≤ 20 mmHg, cerebral perfusion pressure (CPP) ≥ 60 mmHg, brain tissue oxygen pressure (PbtO2) ≥ 20 mmHg, and cerebral oxygen extraction measured by bi-frontal Near infrared Spectroscopy (NIRS) > 55%. Brain flow abnormality was defined by one of the following combinations: CPP < 60 mmHg with NIRS < 55% (Type 1), CPP < 60 mmHg with PbtO2 < 20 mmHg (Type 2), or PbtO2 < 20 mmHg with NIRS < 55% (Type 3). Cerebral micro-dialysate was analyzed hourly for glucose, lactate, pyruvate, glutamate, glycerol, and lactate/pyruvate ratio (LPR). Statistical analysis was performed with student t-test, chi-square and Pearson's tests as applicable.
Results:
A total of 109,474 consecutive minutes of recorded multimodality monitoring was available for analysis. There was a significant difference in the number of minutes of brain flow abnormalities between survivors and non-survivors: 0.8% (875) versus 7.49% (8,199), respectively (p < 0.05). The duration of Type 1-3 flow abnormality per patient was higher in non-survivors (5.7 ± 2.5 h) compared to survivors (0.7 ± 0.6 h) as well as the duration of metabolic crisis, namely, 5.2 ± 2.2 versus 0.6 ± 1.0 h per patient. The occurrence of severe metabolic crisis was associated with a Type 2 flow abnormality (CPP < 60 mmHg and PbtO2 < 20 mmHg), r = 0.97, p < 0.001, but not with Type 1 and 3.
Conclusions:
Metabolic crisis can occur despite a MM&GDTP approach aimed at optimizing cerebral blood flow. Severe metabolic crisis is associated to failure to maintain CPP and PbtO2 above 60 and 20 mmHg, respectively. The occurrence of severe metabolic crisis portends a poor prognosis in patients with sTBI.
