Traumatic brain injury – ICU management

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  1. Intracranial hypertension after severe head injury
    1. develops in 50% of those with Glasgow Coma Scale (GCS) < 8; ICP monitoring should be done in all whose GCS is < 8 AND either abnormal CT, systolic blood pressure of 90 or less, motor posturing or age > 40 years
    2. delayed or postoperative intracranial hematomas occur in 10-15% of patients with severe head injury
    3. treatment goals in TBI : ICP > 20 mmHg, CPP > 60 mmHg, and PbtO2 >15 mmHg
      1. sedation with benzodiazepines causing a coupled reduction in CMRO2 and CBF with no effect on ICP while narcotics have no effect on CMRO2 or CBF but may increase ICP in some patients
      2. elevation of head (although this may decrease cardiac output and lower CPP)
      3. control systemic hypertension provided that there are no intracranial masses or hemorrhages
      4. control hypoxia and hypercarbia (maintain CO2 at 30-40 mm Hg)
      5. control fever and seizures
      6. pharmacologic paralysis, drainage of CSF, mannitol, barbiturate coma
  2. neurochemical mediators of secondary brain injury
    1. glutamate and aspartate appear in very high concentrations in the extracellular space and CSF right after traumatic brain injury
      1. 3 excitatory amino acid receptors mediate the cellular response:
        1. AMPA/KA receptors which open to allow transport of Na and K intracellularly
        2. NMDA
        3. Amino acid receptors that activate phospholipase C
    2. marked increases in the endogenous opioid dynorphin also correlates with regional histopathologic damage and reductions in regional cerebral blood flow
    3. increases also seen in acetylcholine, epinephrine, norepinepherine
    4. cytokines including TNF and IL-1 and IL-6 are elevated after severe head injury
    5. changes in Ca homeostasis are implicated in delayed neuronal death and degeneration after traumatic brain injury; increases in intracellular Ca activate Ca proteases such as calpain cause cytoskeletal degredation and neuronal death
  3. genetic alterations following traumatic brain injury
    1. regional expression of c-fos, c-jun, jun B
  4. heat shock proteins
    1. increased level of heat shock protein 72 is observed in the injured cortex and localized in neurons, glia, and endothelial cells
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