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47 Cards in this Set

  • Front
  • Back

leading causes of TBI

falls, motor vehicle crashes, blunt impact, assaults

leading cause of TBI at extremes of age (<15 and >65)

falls

predominant cause of TBI in teens and young adults

MVC (motor vehicle collisions)

surrogates for cerebral blood flow

ICP and CPP

Poiseuille's laws

CBF proportional to CPP and radius of vessel raised to fourth power and inversely proportional to blood viscosity

primary determinant of cbf

when autoregulation intact = vessel radius; otherwise, CPP

additional volume cranial compartment can accommodate before ICP rises

150 cc

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

what is cerebral compliance?

change in cerebral volume per unit change in pressure

what is cerebral elastance

inverse of cerebral compliance

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

contusions

regions of hemorrhagic necrosis due to acceleration/deceleration

where are contusions usually observed?

gyral crests of orbitofrontal and anterior temporal region

what percentage of contusions expand during the first 24 hours of injury?

1/3

what causes EDH?

laceration of MMA, injury to middle meningeal vein, diploic veins or venous sinuses

describe an EDH

typically lens shaped and do not cross suture lines

What causes SDH?

rupture of bridging veins

describe an SDH

crescent-shaped and crosses suture lines

What causes SAH in trauma?

tearing of small pial vesssels

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

regions commonly affected by DAI

junction between cortex and WM, WM structures close to midline (corpus callosum, internal capsule), brainstem, cerebellum, corona radiata

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"

hallmark of penetrating TBI

cerebral laceration

formula for kinetic injury

1/2 (mass) (velocity)squared = higher velocity more injury

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

mechanisms of secondary injury in TBI

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

appearance of contusions on CT

hypodense regions without macroscopic hemorrhage or mixed-high density lesions if gross hemorrhage present

appearance of DAI on CT imaging

small punctate foci of hemorrhage but usually unremarkable

appearance of DAI on MRI

abnormalities on DWI, GE, diffusion tensor sequences

appearance of cerebral swelling on CT

sulcal effacement, loss of differentiation between gray and WM, compression of ventricles, effacement of basal cisterns

vascular injury common in TBI

disruption of arterial and venous structures: arterial dissection, aneurysms, fistulae, hemorrhage

signs of basilar skull fracture

retraoauricular ecchymosis (Battle sign); periorbital ecchymosis (Raccoon's eyes), hemotympanum, CSF otorrhea, CSF rhinorrhea

moderate TBI

GCS 9-12

two classification schemes to categorize TBI

Marshall and Rotterdam scores

fluid resuscitation in TBI

hypertonic saline resuscitation has not demonstrated benefit and resuscitation with albumin may be associated with harm

primary goals of therapy in prehospital phase of TBI

avoidance and treatment of hypoxia and hypotension

DECRA trial (arms of treatment)

155 patients, severe diffuse, non penetrating TBI, refractory HTN: decompressive crani vs SOC

DECRA trial results

despite lower ICP, functional outcome worse in crani group

DECRA trial criticism

significant difference in patients with unreactive pupils on admission in surgical group (although post hoc analysis found no difference in outcome)

BP recommendations in TBI from BTF

avoid hypotension (<90mmHg)

hypotensioin and effects on TBI

a single episode of hypotension associated with 2-fold increase in mortality

O2 recommendations in TBI from BTF

avoid hypoxia (PaO2<60mmHg or O2sats <90%)

BTF recommends when to treat ICP

if >20mmHg

caveat on treatment of ICP in TBI

despite successfully reducing ICP (crani, hypothermia, pharmacological coma) not shown to improve outcome

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)

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

ICP remains >20mm Hg - what to do

CSF drainage; osmotherapy; surger; metabolic therapy; hypothermia; laparotomy; hyperventilation