Traumatic Brain Injury: Difference between revisions
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= Pathophysiology = | = Pathophysiology = | ||
== Anatomy == | |||
* The brain is a viscoelastic organ with different densities and complex geometry that impact how energy is transmitted through tissues to cause injury. | |||
*Areas most susceptible to injury include the frontal and temporal poles, corpus callosum, and brain stem. | |||
* Natural frequency of each tissue type also likely plays a role in which structures are damaged as does the nature of the force applied (blunt force, blast, whiplash, etc.) | |||
* Frontal lobe injury can lead to difficulties with executive functions (sustained and divided attention, planning, problem solving etc.) | |||
* Temporal lobe dysfunction can include difficulty with language and memory | |||
* Both areas are also involved in emotional regulation | |||
* Injury to subcortical white matter impairs intra and interhemispheric signaling and communication | |||
== Edema/ICP Elevation== | == Edema/ICP Elevation== | ||
[[File:The vicious cycle of head injury.jpg|thumb|500x500px|<sub>The vicious cycle of head injury</sub>]] | [[File:The vicious cycle of head injury.jpg|thumb|500x500px|<sub>The vicious cycle of head injury</sub>]] | ||
After severe TBI w/ ↑ [[ICP]] → ⊕ feedback loop can ensue, leading ultimately to brain death. | After severe TBI w/ ↑ [[ICP]] → ⊕ feedback loop can ensue, leading ultimately to brain death. | ||
This situation can be likened to a compartment syndrome w/i the noncompliant skull. | * This situation can be likened to a compartment syndrome w/i the noncompliant skull. | ||
* ↑ of ICP (A) → impedes CBF → ischemia → cytotoxic edema caused in part by ATP–dependent Na+-K+ pump failure. | |||
↑ of ICP (A) → impedes CBF → ischemia → cytotoxic edema caused in part by ATP–dependent Na+-K+ pump failure. | * This in turn further ↑ ICP & ↓ CBF. | ||
* This situation can ultimately progress to brain death if ICP becomes so high that the cerebrum is not perfused.<br clear="all"> | |||
This in turn further ↑ ICP & ↓ CBF. | |||
This situation can ultimately progress to brain death if ICP becomes so high that the cerebrum is not perfused.<br clear="all"> | |||
= Articles = | = Articles = | ||
Line 52: | Line 58: | ||
| style="width: 15%; vertical-align: top;" | [[BEST-TRIP]] | | style="width: 15%; vertical-align: top;" | [[BEST-TRIP]] | ||
| style="width: 85%; vertical-align: top;" | ✓ ICP monitoring in pts /w severe TBI improves o/c ⇒ ICP focused Tx was not better to care based on CT and Px → routine ICP monitoring does not provide additional benefits for pts o/c <i>(N Engl J Med 2012)</i> | | style="width: 85%; vertical-align: top;" | ✓ ICP monitoring in pts /w severe TBI improves o/c ⇒ ICP focused Tx was not better to care based on CT and Px → routine ICP monitoring does not provide additional benefits for pts o/c <i>(N Engl J Med 2012)</i> | ||
|- | |||
| style="width: 15%; vertical-align: top;" | [[Milan Consensus]] | |||
| style="width: 85%; vertical-align: top;" | ICP monitoring in severe adult TBI - <u>not recommended</u> for comatose pts /w <span style="background-color:#fff2cc;">nml initial CT that can be f/u Px</span>; <u>recommended</u> for pts w/ <span style="background-color:#fff2cc;">bifrontal contusions, s/p 2° DC, WUT is c/i</span> <i>(Acta Neurochir 2014)</i> | |||
|} | |} | ||
{{NoteBoxEnd}} | {{NoteBoxEnd}} | ||
[[Category:Neurotrauma]] | [[Category:Neurotrauma]] |
Latest revision as of 07:17, 1 January 2025
Pathophysiology
Anatomy
- The brain is a viscoelastic organ with different densities and complex geometry that impact how energy is transmitted through tissues to cause injury.
- Areas most susceptible to injury include the frontal and temporal poles, corpus callosum, and brain stem.
- Natural frequency of each tissue type also likely plays a role in which structures are damaged as does the nature of the force applied (blunt force, blast, whiplash, etc.)
- Frontal lobe injury can lead to difficulties with executive functions (sustained and divided attention, planning, problem solving etc.)
- Temporal lobe dysfunction can include difficulty with language and memory
- Both areas are also involved in emotional regulation
- Injury to subcortical white matter impairs intra and interhemispheric signaling and communication
Edema/ICP Elevation
After severe TBI w/ ↑ ICP → ⊕ feedback loop can ensue, leading ultimately to brain death.
- This situation can be likened to a compartment syndrome w/i the noncompliant skull.
- ↑ of ICP (A) → impedes CBF → ischemia → cytotoxic edema caused in part by ATP–dependent Na+-K+ pump failure.
- This in turn further ↑ ICP & ↓ CBF.
- This situation can ultimately progress to brain death if ICP becomes so high that the cerebrum is not perfused.
Articles
Key articles
IMPACT Study | ✓ the value of different prognostic factors in TBI ⇒ the most powerful independent prognostic variables identified were age, GCS motor score, pupil response, and CT finding (Marshall classification), labs (PT & glu) (J Neurotrauma. 2007) |
CRASH trial | ✓ effect of early steroids Rx in adults /w TBI ⇒ ↑ death compared to placebo. (Lancet 2004) |
CRASH-2 | ✓ the effects of early TXA Rx in TBI pts /w significant haemorrhage ⇒ ↓ mortality & death d/t bleeding w/o ↑ vascular occlusive events (Lancet 2010) |
DECRA | Efficacy of DC in severe TBI /w refractory ↑ ICP ⇒ DC ↓ ICP & ↓ ICU stay; assoc. /w worse fnx o/c at 6 mn. (N Engl J Med 2011) |
RESCUEicp | ✓ effectiveness of DC in pts /w TBI & refractory ↑ ICP ⇒ DC ↓ mortality; ↑ risk of severe disability & vegetative state compared to medical Tx alone. (N Engl J Med 2016) |
BEST-TRIP | ✓ ICP monitoring in pts /w severe TBI improves o/c ⇒ ICP focused Tx was not better to care based on CT and Px → routine ICP monitoring does not provide additional benefits for pts o/c (N Engl J Med 2012) |
Milan Consensus | ICP monitoring in severe adult TBI - not recommended for comatose pts /w nml initial CT that can be f/u Px; recommended for pts w/ bifrontal contusions, s/p 2° DC, WUT is c/i (Acta Neurochir 2014) |