Traumatic Brain

Injury
• 1.6 million head injuries in US
annually
• 250,000 hospital admissions
• 60,000 deaths
• 70,000 - 90,000 permanent
neurologic disabilities
• Causes
- Motor vehicle accidents
- Falls
 Primary
Survey
1. Stabilize the spine
2. Establish adequate airway
3. Ensure adequate ventilation
4. IV access to initiate volume
resuscitation Avoid secondary insults to
brain
Hypoxia Hypotension
Determine level of
.
consciousness examine pupils
 Secondary Survey

• Once relatively stable

• Includes a complete neurologic examination
• Severity of the head injury is classified clinically
by GCS
- 13 to 15 mild
- 9 to 12 moderate
- 8 or less severe
• Assess strength, sensation
 MOTOR LIGHT PIN
SENSORY
TOUCH PRICK
R L KEY MUSCLES
R L R L
KEY SENSORY POINTS
C2 [:::! r::i C2
C3 1··-1
C3
!·-·I0= absent
g•: •• :Ve :;: ,.
,

2 = normal

NT= flOI testsbJe

C7 Elbow einensors
C7 C8 Finger fle,cors (distaf phalanx
of middle finger) C8 T1 Anger abductors ( Ille finger)
T1
T2 i i i ! --------- T2
T13:::::1 r,::1 0 • total pamly,}$
T3
T4 i-••i t-•••i t = pa!ptlb«t or vlslbleconfraction
T4
TS I I ! I 2 = activemo\/8ff'lent.
TS ••
TS j-"i j-"j gravity e(imlnated
TS
T7 1--1 .J,.-. 3=- activemo\/Smenf.

!-····! 1
T7
TS •OO""' gravity
TB
j--! J-··; 4 = adivlt movement.
•
T9 j-.! 1-···l sgo!n,t some ,..,.,._
T9
T10 ;l_jl r' ···•.·, 5 • adMI "'°"""'""'•
TIO
T11 agairt.s.rluN1fflta
T11
I,I
I, I

T12 1-·1 r-..1 NT :t ftOt , s,atM

T12
· ,-! j- j :·:;;;:,.
" "
" "
LS
i
1 . J;-.. Long toe axtenso,s
S2
• • Ankle ,:,&Mtar flexors
LS
s1 '
S3
1
1
·· · H ,--, S3

C=:J
j·
54,.5 :,.._, ...J L J VQlunti,ry anal contraetiOn (Yes/No) S4·5
My snalsensation (Yes/No)
[}(]= c:::JPIN PRICK SCORE (max: 112)
TOTALS □+□= D MOTOR SCORE
 Overall goal with neurologic injury

• Presume injury until proven otherwise

• Identify early
• Allow injured tissue the best chance to repair itself
- Adequate delivery of oxygen and glucose
- Avoid infection
• Preserve residual nervous tissue
• Trauma: concussion, contusion,
diffuse axonal injury
• lschemia: global, regional
• Inflammation
• Direct Injury: hemorrhage,
penetrating injury
• Compression tumor, edema,
Hematoma
• Metabolic insults
• Excitatory toxicity: seizures, illicit
drugs, severe hyperthermia
• Hypoperfusion: hypotension, high intracranial
pressure, vasospasm
- Single episode SBP <90 mm Hg increases morbidity & doubles mortality*

• Hypoxemia* **
- p02< 60 mm Hg increases poor outcome from 28% to 71% *
- Increases mortality
•!• 50% from 14.3% **

• Harmful mediators: reperfusion, inflammation

• Electrolyte changes

"Chestnut RM, et al. JTrauma 1993;34:216-222

"Jones PA, J Neurosurg Anesth 1994:6:4 14
\11-:('II \\IS\I OF CI.OSl·.ll IIE \I> l\.ll In

_,.,.

camoow,1 -- Thl---•-
....,._....ol>jed.... ,_.,.,,_.,.,.,...

tuti19 llllll<IA

...,..,,,,.I_I.
_, -----101..-1M1,lnlbtlln,.galn-Nli<IA
Thltt,,n--ln-001111,­

_,,,,.
Basic Premises: Brai
n
87%

1. Monro-Kellie hypothesis
•!• 3 compartments: brain, blood, & CSF
•!• Increase in one must be compensated
by decrease in others or the ICP will
increase
2. Compliance
•:• volume to pressure relationship
 80 4

I -E 60
E
CJ)

a 40
--

.. 2 1 2
0 0

o lntracranial Volume '

Basic Premises: Brai
n
87%

1. Monro-Kellie hypothesis
2. Compliance
3. Cerebral autoregulation
 Intact autoregulation
A Pressure passive Zone of autoregulation Pressure passive
dilatation • Vasoconstriction dilatation

000000000° 000 0
100
0000
Cerebral blood volume compartment
E
6>
75
0
..s
......
0
....

!
=
-0
0
0
:::0
50
j
(I)
u
25

25 50 75 100 125
(mm150
Hg)
, Arterial blood pressure -----------------
Lang et al JNNP 2003;74:1053-1059
 Intact autoregulation
A Pressure passive Zone of autoregulation Pressure passive
dilatation • Yasoconstriction dilatation
100
0000 000000000° 00 0 0
Cerebral blood volume compartment
c
E
ti, 75
0 Edema,
0
.....
....
- 50
=
E
-u
8
....0 Ischemia
..0
e 25

Q
u
)

25 50 75 100 125 150

Arterial blood pressure (mm Hg)
 Intact autoregulation
A Pre.ssure pauive Zone of outOfegulation Prenure pouive
dilatation • Vo$0C0n,triction
100
0 ooo 0000000000 00 0 0
dilotoiion

Cerebral blood vofu,ne comportmenl

-Ce:
0'c;,,
0

75
......
..
50

=
8
!
..D

.
..e
C 25 -fypertens,on
a..
,

uI
ll
0 25 s 7S 100 12S 150
0
o Arterial blood pr sure (mrn Hg)

Lang et al JNNP 2003;74:1053-1059

 Defective autoregulation

000
A Pressure paS3ive

°0 000
dilatation
100 0 0 0 0 0 0 0 0
Cerebral blood volume
compartment

Ede
ma

8
..n
E
..n
4) 25 Ischem
u
ia

25 50 75 125 150
100pressure {mm
Arterial blood
Hg)
 Basic Premises:

Monro-Kellie hypothesis
2.Compliance
3.Cerebral autoregulation
4.CPP = MAP -ICP
A. Maintaining a mean arterial pressure of
greater than 90 mm Hg.
B. 50-70 mm Hg.
C. greater than 70 mm Hg.
D. determined without an ICP monitor.
E. not important, ICP is the parameter
to follow
 Cerebral perfusion pressure

►
•
CPP = MAP - ICP
!•Normal is 70-100 mm Hg
•!•Adequate 50-60 mm Hg
•!•lschemia 30-40 mm Hg
 High MAP
• WARNING ! i in BP may be a sign of
jlCP DO NOT TREAT/OVERTREAT BP alone

CPP = MAP - ICP 70 = 75 - 5

70 mm Hg = i i
70 = 110 - 40
35 = 75 -
40
►CPP=MAP-ICP
► Current AANS guidelines specify ICP <20
& CPP of 50-70 mmHg
• Lower CPP : poorer outcome (ischemic)
• Higher CPP: more ARDS

J Neurotrauma. 2007; 24:S59-64

 Initial Management - Pre-hospital

• ABC D
• Intubate early if GCS <8
• Systolic BP of< 110 requires fluid resuscitation
• Rapid transport to trauma center
• Avoid sedation if possible to preserve neuro
exam
 Early Hospital Management

• Intubate if GCS <8

• Rapid sequence preferred
- Avoid increased ICP with placement of ETT
• Preferred drugs
- Etomidate - rapid acting, short duration, min BP effect
- Rocuronium- short duration, no BP effect, no increased ICP
• 100% 02 until transferred to ICU
• Initial target PC02 should be 35 to 40 mm Hg
• MAP goal 90
• Use only LR or NS- NO HYPOTONIC FLUID
►Hypoxemia 60
mm
Hg increases poor
outcome from 28°/o
to 71°/o (trauma)
• CT head - non contrast
- All patients at risk
• GCS <15
• Depressed skull or evidence of basilar skull fracture
• Focal neuro deficits

- GCS 15, +LOC

• Neurosurgical consultation
- Surgical evacuation
• all acute traumatic extra-axial hematoma >1 cm
• subdural or epidural hematoma > 5 mm with an
equivalent midline shift and GCS<8
• depressed, open, and compound skull fractures
• recommended if hematoma > 20 ml with mass effect
 ICU Management

• Serial neurologic exams

• ICP monitor recommended in patients with a GCS score< 8
- intracranial HTN > 60%
• No RCT's to support improved outcomes with ICP
monitor
• Studies demonstrate outcome is inversely proportional to
max ICP reading and time spent >20
►Different sites Epi Lateral
dura ventricl
1) lntraventricular- l e
Gold standard lntrapare
(anterior
Subara horn)nchym
2) lntraparenchym chnoid
Subara
chnoid
al space

3) Subarachnoid Dura

4) Subdural j mater

5) Epidural
► Different
modalities
1) Fiberoptic F ure 3.Various anatonucal
s,tes to lll0lllt01 ICP
•
 •
I
D
 Jugular Venous
Flberoplfc Oxygen Saturation Catheter
Oximetry
u
Continuous SjV02
Blood Draws for
Cv02

Value Normal lschemia

SjV0 > 60% <50% (10 min.)
2
 • Direct measurement of tissue oxygen
tension (?)
• Local measurement
• Part of ICP-bolt system
• Experimental use in Europe since 1992
• Approved for use in Europe, Canada,
and US

.
\
 HOB up Pain therapy·
If no otthos1at
t 1c fluid
Opt1m1 opioid
ze s s
 Management of lntracranial HTN

• 3 targets
- lntracranial blood volume reduction
- CSF drainage
- Brain parenchyma reduction
 Cerebral blood
volume

• Decrease • Increase
- Elevate head to 30 degrees - lschemia
- Mid line position of head - Acidosis

- Sedation - Hypercapnia

- Muscle relaxation - Increased venous

pressure
- Decrease airway pressure
- Hyperthermia
 Begins almost immediately Peak effect in
30 minutes
Lowers ICP by 25-30°/o in most patients

May decrease cerebral blood flow:

►No lower than pC02 of 30mm Hg
Normalize within hours
 ►PaCO2 of 25-30 mm Hg can
cause
significant vasoconstriction and
reduction in cerebral blood flow

Coles JP, Grit Care Med 2002;30:1950-1959

Diringer MN. J Neurosurg 2002;96:103-108
lmberti R. J Neurosurg 2002;96:97-102
Muizelaar J Neurosurg 1991;75:731-739
Cold. Acta Neurochir 1989;96:100-106
Raichle, et al. Stroke 1972;3:566-575
►raising
Hyperventilation lowers CBF, and therefore ICP, by
the extracellular pH in the CNS
• CO2 is not the direct mediator of this response
►Hyperventilation does not 'stop working;' however,
The choroid plexus exports bicarbonate to lower the pH
•!• 6 hour time course
• The cause of the ICP elevation is usually progressive
• Further attempts at hyperventilation will raise intrathoracic
pressure, decreasing jugular venous return and thereby
raising ICP
 Hemodyna
• mic of MAP between 50-150
CBF is independent
- Autoregulation
- With injury 50% pts lose autoregulation ability
- GOAL - Normal MAP or MAP >90
- Treat hypotension with thoughts of cause
- Treat HTN with B-blockers, nicardipine
- Use vasodilators with caution
 Direct comparison of cerebrovascular effects of norepinephrine and
dopamine in head-injured patients
Luzius A. Steiner, MD, PhD; Andrew J. Johnston, FRCA; Marek Czosnyka, PhD; Doris
A. Chatfield, BSc; Raymond Salvador, PhD; Jonathan P. Coles, FRCA; Arun K. Gupta,
FRCA;
John 0. Pickard, MChir, FRCS, FMedSci; David K. Menon, MD, PhD, FRCP, FRCA,
FMedSci
Objective: To directly compare the cerebrovascular and the drug was exchanged against the other agent. The
effects of norepinephrine and dopamine in patients with protocol was then repeated.
acute traumatic brain injury. Measurements and Main Results: Mean arterial pressure
Design: Prospective randomized crossover trial. and
Setting: Neurosciences critical care w1it of a university intracranial pressure were monitored and cerebral blood
hospital. Patients: Ten acutely head-injured patients flow was estimated with transcranial Doppler.
requiring vas- oactive drugs to maintain a cerebral Norepinephrineled
step increase in cerebral to predictable perfusionand significant
pressure (57.5increases± 19.9
perfusion pressure of 1·- C◄4l
,.,..,..-1velocity "> ..,_ ,..,.,.-1 ..,_.,.f CO t')A O .., ,....,.,.-1 .,...
cc --.J'"• .M' I in flow for"'11"'11
each A

1Co1t'Glt1sie.11s: Norepinephrine may be mffre

predictable and efficient to augment cerebral perfusion in
patients with traumatic brain injury. (:Crit Care Med 2004;
32:1049-1054,)
KE, Wooos: traumatic brain injury; cerebral perfusion;
cer·ebral
blood flow; norepinephrine; dopamine; transcranial
Cerebral autoregulation in normal subjects and patients with
chronic hypertension

Cerebral blood flow ml/100gm/min

75
Normal
,,,,
,
,
50 ------,, ,/ Chronic
Hypertension
-- -,, -
,,

25 , ,
,, ,

,
40 mm Hg 140
mm Hg
C

-----erebral Perfusion Pressure (mm Hg)

CHEST
Marik, P. E. et al. Chest 2002;122:699-711

lhc- (.:1rtllo11ulmun.;1n .md I l"hl\.d l .tn·Juunw.J

 HOB up Pain therapy·
If no otthos1at
t 1c fluid
Opt1m1 opioid
ze s s
 Osmotic Agents: Mannitol
►Acts within 20-30 minutes
►Dosage: 0.25-1 g/kg bolus
►Filtered needles!
►Actions:
1) osmotic gradient
2) may increase cardiac preload, output
and elevate MAP
3) improves rheology of red blood cells
4) decreases CSF production
5) free radical scavenger
• Serum osmolality <320 mOsm/L vs
osmolar gap <10
• Measured osmoles - (2Na
+glu/18+BUN/2.8)
• Watch for osmotic diuresis: Dehydration
and hypotension
• MAINTAIN EUVOLEMIA
►3°/o saline 250cc bolus (run in as fast
as
possible)
►7°/o saline bolus
►23.4°/o saline 30cc bolus
 Fever

►metabolic
Each increase in 1degree Celsius increases cerebral
rate by 7%
•!• One study w/ exercise: 1.5Q C increased CMR02 by
23%

....
increase in CMR02
Vasodilation CBV ICP
•!• Increases 02 r qarre-
1ents
•!• Increases CO2 production (may need to adjust ventilator
minute ventilation!!!)
..
Nunnely SA et al. J Appl Physiol 2002;92:846-851.
 'he cwEngland Journal of Med1cine

TREATMENT OF TRAUJ\ilATIC BRAIN INJURY WITH MODERATE

HYPOTHERMIA
DONALD W. MARION, M.D. LOUIS E. PENROD, M.D. SHERYLF. KELSEY, PH.D.,
1 1

WALTER D. OBRIST, PH.D., PATRICK M. KOCHANEK, M.D., ALAN M. PALMER,

PH.D., STEPHENR. WISNIEWSKI, PH.D.,
AND STEVENT. DEKOSKY, M.D.

Methods 1!111 a ranicl01nni:z:1ed,00Inttirolll,ed

t1r'iial_,,we 00 r111- 1

pauiedl tti1e, reflects uf

rn1,odle,r,ate, y JJ-
Cth i8 uffl ua ,a rll(
1
f'Ht'llr­
mro,th1er tll il,a 1f'II 8,2 [PatheJ1nts,with :sevefie c[l,osed
heard iITTl­
j\lll fi,es (a iscore of :a to 7
0111 the·1G ,asgow
C,orn1a Seta Ire).
1

Thie peitt:ieflitCS assigr11ed t,0 hy[Poth1errn1ila Wr!E!J!

- 1

F€! COro,ledlto
1
 The New England Journal of Medicine

LACK OF EFFECT OF INDUCTION OF HYPOTHERi\1.IA AFTER ACUTE BRAIN INJURY

GUY L. CLIFTON, M.D., EMMY R. MILLER, PH.D., R.N., SUNG C. CHOI, PH.D., HARVEYS. lEVIN, PH.D., STEPHEN MCCAULEY, PH.D.,
KENNETH R. SMITH, JR., M.D., J. PAUL MUIZELAAR, M.D., PH.D.,
FRANKLIN C. WAGNER, JR., M.D., DONALD W. MARION, M.D., THOMAS G. LUERSSEN, M.D., RANDALL M. CHESNUT, M.D., AND
MICHAEL SCHWARTZ, M.D.

- --•----,
JletlNJ. Th[e sttu drysuhllectbs w[e1t ·392 ptffitie ts 16
1

165
ds y·ear,sof
tt,o age with c01n11.ai aft,er s1U1staiinimi,9
closie( 1hi,ea1d i DILlliries, wh 0 were ran1dEoim
1 1 1

y .ais,signedl tEo be trieate.d w1ith t1ypotthe·r1nili,a

([body te·m1peratijre, 33GiCJ., wh oh was iin irt:iatedl
1

wiiithin 6 h,o,uirs ,arfter u111nu1ry ,a111 d m.ai r1- tah1ed 1

fo1r 48 lh1 u1rs [by m1e•a1mi,isof su1rfa,e[e eoolh1g, 01r 1

normoth1ermia. AU plaitu,ents;otheMuse·rieoeive.d mre·asur,estand­

.arid Tt:1rieat1m1enrt.
rnunctuon1a :s,tatit..i:s,'flhie·
s.irx p.r 11T11ary
mo,nilJns aft' outcome
was ,

•1r the i1t11ju1ty.

Figure 2. Mortality in Therapeutic Hypothermia

Hypothermia, No. Normothermia, No.

Favors I Favors
Study Patients Events Patients Events Hypothermia : Normothermia

Shiozaki et al,47 2001 45 8 46 6

Clifton et al,34 2001 190 53 178 48 +
Yan and Tang,62 2001 24 13 20 16
Jiang et al,48 2000 43 11 44 20
Aibiki et al,w 2000 15 1 11 3
Zhang and Wang,ro 2000 123 41 123 50 _
Shiozaki et al,40 1999 8 0 8 0 ..
Marion et al,11 1997 39 9 42 10
Hirayama et al,61 1994 12 4 10 5 ..
Clifton et al,32 1993 23 8 22 8
Shiozaki et al.331993 16 8 17 14
Clifton et al,12 1992 5 1 5 1
Total 54 15 52 181 ...
3 7 6 .:
I i I I I I llj I I Ii I ilj I III 1111j I I I II ii I
0.01 0.1 1.0 10 100
Relative Risk, 95% Cl

McIntyre Let al JAMA

Figure 4. Poor Neurologic Outcome for Therapeutic Hypothermia*

Hypothermia, No. Normothermia, No.

Favors ' Favors Hypothermia I Normothermia
Study Patients Events Patients Events

Shiozaki et al,47 2001 45 24 46 19 .;....._

Clifton et al.34 2001 190 108 178 102 .

Jiang et al,48 2000
Aibiki et al,50 2000
43

15
23
,.
.
44

11
32

7
.
Shiozaki et al.4g 1999
Marion et al,11 1997
8
39
"
2
8
42
1
26
.
1
Hirayama et al,61 1994 12 10 7
5
Clifton et al,32 1993 23 4 22 14

Shiozaki et al,331993 16 17 14
1
Clifton et al.12 1992 5 1 5 2

Total 39 8 383 224 ...;

6 1
I i I I ii "I I I I Ii ii I I ' I I Ii Ii I I I ' II ii I
1 0.01 0.1 1.0 10
9
9
 HOB up Pain therapy·
If no otthos1at
t 1c fluid
Opt1m1 opioid
ze s s
A. hyperthermia.
B. hypertension.
C. increased respiratory drive.
D. unreactive large pupils.
E. increased electrographic activity
 Additional methods to decrease
ICP
for when conventional management fails No
demonstrated benefit
• Barbiturate coma
- Reduce 02 demand
- No cellular toxicity
• Decompressive
- Burst suppression by
continuous EEG Craniectomy
- Last resort
• Hypothermia
- Reduce 02 demand
- Do not actively rewarm
cold patients
 Sedation

• Fentanyl is analgesic of choice

- Min BP effect, depresses cough
• Propofol
easily titratable, rapidly reversible
decreases cerebral metabolic rate Potentiates GABA inhibition
Inhibitions methyl-D-aspartate glutamate receptors Inhibits
voltage-dependent calcium channels Potent antioxidant
Inhibits lipid peroxidation
• Can paralyze if needed, but keep to minimum
 Seizure Prophylaxis

• Anti-seizure medication
- 7 days after severe injury
- Usually phenytoin

• Avoid abnormal electrolytes

• Hyponatremia
- SIADH
- Cerebral salt wasting
• Hypomagnesemia
 types of acute post-traumatic lntracranlal hemoe
Ihage:

Subarachnoid Periventricular
hemorrhage and frontal lobe
contusions with
intraparenchymal
hematoma

Subdura
EPIDURAL
l HEMATOMA
hemato
ma
Th, NEW
ENGLAND
JOURNAL of MEDICINE
EPIDURAL HEMATOMA
EPIDURAL
HEMATOMA Subarachnoid
hemorrhage
 Multiple
intraparenchymal
hematomas with
surrounding edema
 Diffuse Axonal Injury

• May cause immediate and prolonged unconsciousness

• High morality, high morbidity, often persistent vegetative
state
• Identified by diffusion-weighted MRI
• Caused by shearing forces affecting axons leading to
dysfunction of the reticular activating system
• Axons are not torn but sequential, focal changes that
lead to swelling and disconnection over multiple hours
• Apoptosis may play role in axonal injury
 Multiple
lntraparenchymal
hemorrhages

Subarachnoi
d
hemorrhage

Th, NEW
ENGLAND
JOURNAL of MEDICINE
Depressed skul1
fracture
 Poor prognosis

• Advanced age
• Female <50
• Anticoagulation at time of trauma
• Low GCS at arrivaI
• Hypotension
• Abnormal pupillary widening
• Traumatic SAH
 Things to keep in mind...

• Spine injury until proven otherwise

• Many intraparenchymal hematomas may be delayed,
appearing on the CT scan 24 h after the initial insult
• Low threshold to repeat CT scan
- Clinical changes
- Continued uncontrollable intracranial HTN
 Acute Spinal
Injury
• 10,000 new cases annually
• Males 16-30 make up 80%
• Most due to MVA 36%, violence 29%, falls 21%
• Quadriplegia is slightly more common than paraplegia
• Rare to completely transect cord
• 6-8% of head trauma will also have spine injury
• Main goal is early identification
• Insult is associated with an injury response that results in
neuronal destruction
 Secondary injury

• cascade of tissue injury

- vascular compromise
- inflammatory changes
- cellular dysfunction
- free radical generation
• hallmark is spinal cord edema
• peaks 3 to 6 days after injury
• subsides over a period of weeks
 Initial
Resuscitati

• Regular ABC's
• Immobilize neck until cleared or
stabilized
- Head between two sandbags
- Placement of cervical collar
• Immobilize entire spine
- Transportation on a rigid spine board
- Log rolling
• 25-50% of cervical spine injuries also
have head injury
 Neurologic exam

• Early
• Sequential
• Include
- Strength
- Sensation - pain, position
• Neurologic level: most caudal segment of the spinal cord with normal
bilateral motor (strength >3/5) and sensory (light touch and pinprick) function
Table J... The NEXUS Low-Risk Cri ria.*

Cervical-spine ..-adiography is indicated £or patients withtrauma unless they

mec:t- all of"thc: -f'ollovving criteria:
No poste-rior mid line cervical-spine tenderness.i­No evidence oFintox:ic:ation.
A normal level of°alertness.§
No f"ocal neur-ologic deficit:. and No painful distracting injuries.II

Criteria are frorn Hoffman and colleagues..20

i ... M idline postel""ior bony ce-r"'Vica.1-spine tenderness is pr-esent iFthe patient.reports
pain on palpa"ti<:>n o thc posterior midi inc ncc:k -From the:: nuc:hal ridge t-othe prominence o-Fthe first thoracic verte,bra. or if'the patient
evinces pain with direct palpation oFany cervical spinous pr-ocess..
Patients should be considered in·t.oxicated i -they ha-ve cit.her o-f' he-FollCll\ooVing: a recent history provided bythe patient or an observer oFintoxication or intox­
icating ingestionp or evidence o-Fintoxication on physical examination such as an odor of'alcohol., slu,.-re-dspeech_. at.-a.xia.,dysrnetr-ia_. or ot:her cerebellar find­ings ..
or any behavior consistent wi-t;h intoxication_ Patients may also be c;:;:on­sid ered to be intoxicated if"tests of"bodily secretions are
positive Toralcohol or

drugs that affect the level of"a.lertness.

§, An altc:rc:d lcvd o-Falc:rtness c:.an inc:.ludc:: any of"t-hc:: f"oll<>V"Ving: a Glasgow Coma Sc.alescore of14 or less; disorientation to person.,
place..tirne: .. or even-ts; an in­ability to remer-nber three objects at five rninuLes; a delayed or inappropriate response to external stin,uli; or ot-he-r findings_
A Focal nc::urologic defic.it is any Toc::;al ncurologic finding on motor or sensory

II No precise definition OTa painf"ul distracting injury ispossible. This category includes any c:e>ndition thought- bythe clinician te>be producing
examination ... to dfstract: the patientf°rorn a second (neck) injury. Such injuries may include. but are not limited to., any long-bone Fr.-ac.ture; a visceral injury
pain sufFic:.icnt
requiring sur-gi­c:::al consuhation; a large laceration., degloving in.Jury., or crush injury; large. burns; or any other injury causing acute -Functional impairment.
Physicians may also classify any injury as distracting if°ft ts thought to have the potential t:oir-npai..- the pa- ienr"'s ability o appreciate other injuries_

Th, NEW
ENGLAND
JOURNAL of MEDICINE
 Any hlgh-.-isk factor th.at mandates radiography/'
Age :a:,65 y-r or dangerous rnechc,inism
or pa resthes,as ,n e:xtre..nilties

No
Yes

Any k>w rislc factor that allows safe

a.sses:s:me.nt of"ra.ns-e of' tT1otio-n?
Simple f"Cilr-cnd motor vch,c(,c cx:>flision Of" sitting
position in the ernc,ycncy dopa rtrnc-nt or ambub o,y

/ --
No--- R ad,og,..phy )
.it anyt>rT"e or dof.lyed (not imrncdia le)
ons t orneck pain or .absence of
m:rdltne- cc-rvical--spinc tenderness

Unbak,
Yes
+
Able to rotate nectc: actively?
-45• left and nght
I
Yes
+
r:=- '

Th, NEW
ENGLAND
JOURNAL of MEDICINE
 Imaging
• Cervical spine films
AP, lateral, and odontoid Additional laterals
• If entire c-spine or C7-Tl space not seen
• Abnormal vertebral alignment, bony structure,
intervertebral space, and soft tissue thickening
• Flexion and extension films
• SCIWORA {spinal cord injury without radiologic abnormality)
• CT scan - best for bones
- If not adequate visualization by X-ray
• MRI
Modality of choice for characterizing acute cord injury Best for
edema, hemorrhage, ligamentous injury
 Neuroresuscitative Agents

• High dose steroids

- 30mg/kg bolus
- 5.4mg/kg/hr x 23H
- Give for 48H if not given
within 3H

• Effective if given in first 8 hours

Injury classification
- Stable
- Unstable
- Soft tissue or fracture

Surgery
• Decompress neural tissue
• Prevent cord injury by ensuring stability
• Options include
- bed rest in traction (rarely done)
- external immobilization
- open reduction with internal fixation
 Order of injury Repair

• Any open fractures first

• Then any closed fracture
- Tibia
- Femur - within 24h
- Pelvis
- Spine
- Upper extremity
Ligamentous injury
 Odontoid Fracture

Atlas fracture
C2 Hangman's Fracture
CG Fracture with retropulsion to
cord
 subluxation of C4-CS with
spinal cord compression

Soft tissue swelling

 Lumbar
Burst
fracture

- - - -

Compression fracture
 Cord Injury Syndromes

• Complete cord lesion - all sensory and motor function below the
lesion is abolished
• Central cord lesion - motor function lost upper>lower
suspended sensory loss in cervicothoracic dermatomes
• Posterior Cord syndrome - diminished proprioception and
fine touch
• Brown-Sequard syndrome - cord hemisection ipsilateral loss of
pain and proprioception, contralateral pain and temp loss, suspended
ipsilateral loss of all sensation

• Spinal shock - lack of neurologic function after trauma that can

last until 4 weeks
 Systemic Effects of SCI
• Cardiovascular
Almost solely related to interruption of
sympathetic pathway at Tl-L2
Bradycardia
• Resolves with stimulation
• Resolves after 2 months
• Rare to need pacemaker
Hypotension
• Give volume
• Low dose pressors
• Respiratory
Related to level of injury
Thoracic levels eliminates intercostaIs
Diaphragm alone to inspire - phrenic
nerve (C3-5)
Cervical lesions decreases cough and
secretion clearance
Decreased tidal volumes Minimal
expiratory help Status improves with
time
 Autonomic
hyperreflexia
• Loss of central inhibition
• hyper-reactive sympathetic
reflexes to cord below level of
lesion
• Bladder or bowel distention
usual causes
,,._.
_.
fi - - - ... -
• - )( -
- HTN • W..-

- Arrythmias
- Headaches
- Vasodilation above lesion
level
InSummary

•Appropriate pre-hospital
care is essential
•Assume injury until
proven otherwise
•Evaluate as early as
possible to prevent
unnecessary
immobilization
•Earlier steroids with
spinal injury
 References

• Czosnyka M. Pickard JD. Monitoring and interpretation of intracranial pressure. Journal

of Neurology, Neurosurgery & Psychiatry. 75(6):813-21, 2004 Jun.
• Gunnarsson T. Fehlings MG. Acute neurosurgical management of traumatic brain injury
and spinal cord injury. Current Opinion in Neurology. 16(6):717-23, 2003 Dec.
• Hutchinson PJ. Kirkpatrick PJ. Decompressive craniectomy in head injury. Current
Opinion in Critical Care. 10(2):101-4, 2004 Apr
• Longhi L. Stocchetti N. Hyperoxia in head injury: therapeutic tool?. Current Opinion in
Critical Care. 10(2):105-9, 2004 Apr
• Marik, PE. Varon, J. and Trask, T Managament of Head Trauma*Chest. 2002; 122: 699
- 711.
• Marshall LF. Head injury: recent past, present, and future. Neurosurgery. 47(3):546- 61,
2000 Sep
• Patel RV. Delong W Jr. Vresilovic EJ. Evaluation and treatment of spinal injuries in the
patient with polytrauma.Clinical Orthopaedics & Related Research. (422):43-54, 2004
May.