Template:TBI pathophysiology: Difference between revisions
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*Production of free radicals | *Production of free radicals | ||
*Enzyme activity that lead to apoptosis | *Enzyme activity that lead to apoptosis | ||
====Causes==== | |||
*Predominantly metabolic insult | |||
**Mitochondrial dysfunction | |||
**shifts in calcium and sodium balances | |||
*Ultimately leads to damage to axonal integrity and axonal transport | |||
*Microscopic structural injury is often unidentifiable on CT or MRI | |||
Revision as of 23:16, 21 November 2017
TBI Pathophysiology
- 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
- Use CPP as surrogate
- 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
Primary injury
- contusions
- bruises to brain parenchyma
- Hematomas
- Epidural
- Subdural
- Intraparenchymal
- Intraventricular
- Subarachnoid
- Diffuse Axonal Injury
- Direct Cellular Damage
- neurons
- axons
- tearing and shearing of tissues
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
- Calcium and ion shifts
- Mitochondrial damage
- Production of free radicals
- Enzyme activity that lead to apoptosis
Causes
- Predominantly metabolic insult
- Mitochondrial dysfunction
- shifts in calcium and sodium balances
- Ultimately leads to damage to axonal integrity and axonal transport
- Microscopic structural injury is often unidentifiable on CT or MRI