Normal head trauma

  • General
    • See basic specs for brain
    • The brain is 2% of overall weight while accounting for
    • Cerebral metabolic rate of oxygen (CMRO2)
      • Adults
        • Remains relatively constant
        • Approximately 3.5 ml O2/ 100 g/ min
      • Paeds
        • 5.2 ml O2 / 100 g min in children aged 3– 12 years.
    • Glucose is the primary source of ATP in the brain
      • Aerobic metabolism is the primary process in the brain through which glucose is efficiently converted to 36– 38 molecules of ATP by
        • Glycolysis,
        • Citric acid cycle,
        • Aerobic oxidation.
    • Where are the energy used
      • 50%: synaptic activity (i.e. neurotransmitter production, release, and uptake)
      • 25%: maintaining for electrochemical gradients,
      • 25%: molecular transport, biosynthesis, and other processes.
    • Glucose metabolism is disturbed after TBI.
      • There is a significant increase in anaerobic glycolytic turnover and elevated level of extracellular lactate in cerebral circulation as neurons and astrocytes convert glucose to two molecules of ATP and two molecules of lactate.
      • Hyperglycolysis contributes to
        • Prolonged elevated lactate/ glucose ratio,
        • CSF lactic acidosis,
        • Compromised mitochondrial function via calcium mediated interference.
      • The duration of hyperglycolysis and lactate accumulation may reflect the extent of injury and worse prognosis.
    • CMRO2, cerebral metabolic rate of glucose (CMRG), and CBF
      • Are common measurements utilized in neurophysiology.
      • In healthy adults,
        • CMRO2: is 3.3 ml/ 100 g/ min,
        • CMRG is 5.5 mg/ 100 g/ min,
        • CBF is 54 ± 12 ml/ 100 g/ min.
        • See stroke
      • In comatose patients with TBI,
        • CMRO2:1.2 - 2.3 ml/ 100 g/ min
          • Low CMRO2 is associated with
            • Low GCS score
            • Poorer recovery outcome.
          • Storage of glucose and oxygen by neurons and astrocytes is limited, therefore continuous CBF is essential to ensure survival.
            • Arteries and arterioles 30– 300 um in diameter can alter their resistance to control cerebral circulation.
            • There is a linear relationship between CMRO2 and CBF consistent with the notion of diffusion- limited oxygen delivery.
            • Flow metabolism coupling is the process by which blood flow changes in relation to the metabolic demands of cerebral tissue, largely influenced by the changes in tissue CO2
              • PaO2 does not affect CBF except in patients with drastically reduced PaO2 below 50 mmHg.
                • Cerebral metabolism declines after TBI with corresponding decreases in CBF.