Template:TBI pathophysiology: Difference between revisions

Line 2: Line 2:
====Primary injury====
====Primary injury====
*Contusions
*Contusions
**bruises to brain parenchyma
**Bruises to brain parenchyma
*Hematomas
*Hematomas
**Epidural
**[[Epidural hematoma]]
**Subdural
**[[Subdural hematoma]]
**Intraparenchymal
**Intraparenchymal
**Intraventricular
**Intraventricular
**Subarachnoid
**[[Subarachnoid hemorrhage]]
*Diffuse Axonal Injury
*Diffuse axonal injury
*Direct Cellular Damage
*Direct cellular damage
**neurons
**Neurons
**axons
**Axons
*tearing and shearing of tissues
*Tearing and shearing of tissues


====Secondary injury====
====Secondary injury====

Revision as of 13:55, 23 November 2017

TBI Pathophysiology

Primary injury

Secondary injury

Brain swelling causes increased ICP which compresses the tissue causing ischemia with direct compression of the vasculature causing brain tissue herniation and brain death

  • Leads to expansion of the original injury (predominantly metabolic insult)
    • Calcium and sodium shifts
    • Mitochondrial damage
    • Production of free radicals
  • Ultimately leads to damage to axonal integrity and axonal transport
    • Enzyme activity leads to apoptosis
  • Microscopic structural injury is often unidentifiable on CT or MRI

Cerebral Blood Flow and Autoregulation

  • vasoconstriction
    • HTN, Hypocarbia, alkalosis
  • No good way to measure cerebral blood flow
    • Use CPP as surrogate
      • CPP is amount of pressure needed to perfuse the brain
      • CPP=MAP-ICP
        • When ICP elevates, CPP decreases
        • Normal ICP
          • 15 in adults
          • <10 to 15 in children
          • 1.5 to 6.0 in infants
  • Autoregulation allows the body to control the cerebral blood flow
    • Autoregulatory mechanism is damaged in most TBI patients
  • Cushing Reflex- more common in children than adults
    • Hypertension
    • Bradycardia
    • Respiratory Irregularity