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47 Cards in this Set
- Front
- Back
leading causes of TBI |
falls, motor vehicle crashes, blunt impact, assaults |
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leading cause of TBI at extremes of age (<15 and >65) |
falls |
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predominant cause of TBI in teens and young adults |
MVC (motor vehicle collisions) |
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surrogates for cerebral blood flow |
ICP and CPP |
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Poiseuille's laws |
CBF proportional to CPP and radius of vessel raised to fourth power and inversely proportional to blood viscosity |
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primary determinant of cbf |
when autoregulation intact = vessel radius; otherwise, CPP
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additional volume cranial compartment can accommodate before ICP rises |
150 cc
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compensatory mechanisms that allow some volume in cranium before ICP rises |
low pressure veins collapse, cerebral blood volume decreasse, egress of CSF from cranial to spinal subarachnoid space |
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what is cerebral compliance? |
change in cerebral volume per unit change in pressure |
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what is cerebral elastance |
inverse of cerebral compliance |
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TBI and compliance curve |
TBI patients with intracranial HTN operate on steep portion of compliance curve - small changes in volume associated with large changes in ICP |
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contusions
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regions of hemorrhagic necrosis due to acceleration/deceleration |
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where are contusions usually observed? |
gyral crests of orbitofrontal and anterior temporal region |
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what percentage of contusions expand during the first 24 hours of injury? |
1/3 |
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what causes EDH? |
laceration of MMA, injury to middle meningeal vein, diploic veins or venous sinuses |
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describe an EDH |
typically lens shaped and do not cross suture lines |
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What causes SDH? |
rupture of bridging veins |
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describe an SDH |
crescent-shaped and crosses suture lines |
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What causes SAH in trauma? |
tearing of small pial vesssels |
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location of blood in SAH due to trauma |
over cerebral convexities, confined to a few sulci or fissures; may distribute diffusely over cortical surface, basal cisterns, into ventricles |
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regions commonly affected by DAI |
junction between cortex and WM, WM structures close to midline (corpus callosum, internal capsule), brainstem, cerebellum, corona radiata |
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histologic appearance of DAI |
axonal swellings from accumulated material due to interrupted axonal transport --> periodic "axonal varicosities" or single point swelling "axonal bulb / retraction ball" |
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hallmark of penetrating TBI |
cerebral laceration |
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formula for kinetic injury |
1/2 (mass) (velocity)squared = higher velocity more injury |
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distinguishing features of blast TBI |
DAI occurs in dose-dependent fashion; malignant cerebral edema occur rapidly, vasospasm occur in up to 50% and may last as long as 1 month, concomitant eye / ear injuries |
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mechanisms of secondary injury in TBI
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neuronal depolarization, disturbance of ionic homesotasis, glutamate excitotoxicity, generation of NO and O2 free radicals, lipid peroxidation, BBB disruption, secondary hemorrhage, ischemia, cerebral edema, intracranial HTN, mitochondrial dysfunction, axonal disruption, inflammation, apoptosis, necrotic cell death
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appearance of contusions on CT |
hypodense regions without macroscopic hemorrhage or mixed-high density lesions if gross hemorrhage present
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appearance of DAI on CT imaging |
small punctate foci of hemorrhage but usually unremarkable |
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appearance of DAI on MRI |
abnormalities on DWI, GE, diffusion tensor sequences |
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appearance of cerebral swelling on CT |
sulcal effacement, loss of differentiation between gray and WM, compression of ventricles, effacement of basal cisterns |
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vascular injury common in TBI |
disruption of arterial and venous structures: arterial dissection, aneurysms, fistulae, hemorrhage |
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signs of basilar skull fracture |
retraoauricular ecchymosis (Battle sign); periorbital ecchymosis (Raccoon's eyes), hemotympanum, CSF otorrhea, CSF rhinorrhea |
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moderate TBI |
GCS 9-12 |
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two classification schemes to categorize TBI |
Marshall and Rotterdam scores |
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fluid resuscitation in TBI |
hypertonic saline resuscitation has not demonstrated benefit and resuscitation with albumin may be associated with harm |
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primary goals of therapy in prehospital phase of TBI |
avoidance and treatment of hypoxia and hypotension |
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DECRA trial (arms of treatment) |
155 patients, severe diffuse, non penetrating TBI, refractory HTN: decompressive crani vs SOC |
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DECRA trial results |
despite lower ICP, functional outcome worse in crani group |
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DECRA trial criticism |
significant difference in patients with unreactive pupils on admission in surgical group (although post hoc analysis found no difference in outcome) |
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BP recommendations in TBI from BTF
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avoid hypotension (<90mmHg)
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hypotensioin and effects on TBI |
a single episode of hypotension associated with 2-fold increase in mortality |
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O2 recommendations in TBI from BTF |
avoid hypoxia (PaO2<60mmHg or O2sats <90%) |
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BTF recommends when to treat ICP |
if >20mmHg |
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caveat on treatment of ICP in TBI |
despite successfully reducing ICP (crani, hypothermia, pharmacological coma) not shown to improve outcome |
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indications for invasive ICP monitoring |
GCS 8 or less, mass effect on CT; cnosider for normal CT with 2 ormore of: age>40y, posturing, SBP <90mmHg) |
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Ecuador / Bolivia ICP trial |
2012, multicenter RCT 324 patients - targeted therapyto maintain ICP <20 with invasive monitor not superior to therapy based on clinical examination |
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ICP remains >20mm Hg - what to do |
CSF drainage; osmotherapy; surger; metabolic therapy; hypothermia; laparotomy; hyperventilation |