Traumatic Brain Injury: Difference between revisions
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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 = | ||
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) |