Objectives

 Describe the pathophysiology of traumatic

brain injury
 Discuss the scientific rationale for the
therapeutic interventions used in the care of
brain injured
 Provide research based recommendations
for the care of patient with traumatic brain
injury
Rhoads & Pflanzer (1996) Human Physiology p. 211
Layers of the Cranial Vault

Anatomy of the Brain

www.neurosurgery.org/pubpgages/patres/anatofbrain.html#
micro
Definition – Traumatic Brain Injury
Traumatic brain injury (TBI) is a nondegenerative,
noncongenital insult to the brain from an external
mechanical force, possibly leading to permanent or
temporary impairments of cognitive, physical, and
psychosocial functions with an associated diminished
or altered state of consciousness
Annually in the US…
 1.5 million Americans sustain a TBI each year
 80,000 people annually experience the onset of
long-term disability following TBI
 50,000 people die every year as a result of TBI
 Incidents of TBI outnumber Breast Cancer
(175,000), Spinal Cord Injury (11,000), HIV/AIDS
(16,273), Multiple Sclerosis (10,400)
 5.3 million Americans live with TBI-related
disabilities
Head Injury
 Cause of death in 25% of trauma patients
 Cause of death in 50% of MVCs
 Significant long term disability
 Prompt recognition and treatment can improve outcome
 All patients with head or facial trauma have c-spine injury
until proven otherwise!
Cost of TBI
 Survivor typically faces
5-10 years of intensive
services – estimated
cost of $4 million/year
 Economic cost of TBI in
US estimated $48
billion/year
Types of TBIs
Closed Head Injury
 Acceleration/Deceleration  Non-Acceleration
 If a moving object hits a movable head  Much more rare, referred to as a crushing
(e.g., head gets hit with a bat). injury
 If a moving object hits a head that is fixed
 If a moving head hits something
stationary (e.g., if you have a car wreck (e.g., car falls on head while you’re working
and your head hits the dashboard). under it).
 Shaken type of movement (e.g., Shaken
Baby Syndrome when head rocks back
and forth in skull).
 Two types are:
 Linear- brain moves straight along a linear
path.
 Angular- Brain rotates at an angle, twists,
or rolls.
(Ferrand and Bloom, 111-112)
Types of TBIs
Penetrating/Closed Head Injury
 Low Velocity  High Velocity
 Skull is no longer in tact, part of  Skull is no longer in tact, part of
skull or debri gets into the brain skull or debri gets into the brain
(Ferrand and Bloom). (Ferrand and Bloom).
 An example is if you get hit so  An example is if during a gun shot
hard with a baseball that it breaks wound the bullet penetrates the
skull and causes part of it to lay skull and goes into the brain
on the brain. matter.

(Ferrand and Bloom, 111-112)

 Mechanisms of Injury for
TBI
 MVAs are the leading cause of TBI in the
general population, especially among whites in
the United States (~50% of all TBIs)
 Falls are the second leading cause of TBI.
Falls account for (~20-30% of all TBIs)
– In individuals aged 75 years and older, falls are the
most common cause of TBI. The very young also
commonly sustain TBI due to falls.
 Firearms are the third leading cause of TBI
(~12% of all TBIs) and are a leading cause of
TBI among individuals aged 25-34 years
Traumatic Brain Injury (TBI)
Brain injury results from:
 Direct injury to brain tissue

 External forces applied to outside

of skull transmitted to the brain
 Movement of brain inside skull
 Traumatic Head Injury

ALL-NET Pediatric Critical Care Textbook Source: LifeART EM

Pro (1998) Lippincott Williams & Wilkins.
www.med.ub.es/All-Net/english/neuropage/trauma/head-8htm
Traumatic Brain Injury
Primary Brain Injury Secondary Brain Injury
 Results from what has  Physiologic and
occurred to the brain at biochemical events which
the time of the injury follow the primary injury
HEAD INJURIES /
BRAIN INJURIES
Concussion
Diffuse Axonal Injury
Epidural Hematoma
Subdural Hematoma
Coup and Countercoup
Injuries
Concussion
Concussion is caused by deformity of the deep structures
of the brain, leading to widespread neurologic
dysfunction that can result in impaired consciousness
or coma

Concussion is considered a mild form of diffuse axonal

injury
Diffuse Axonal Injury
Diffuse axonal injury is characterized by extensive
generalized damage to the white matter of the brain
Strains during high-speed acceleration/deceleration
produced in lateral motions of the head may cause the
injuries
Diffuse axonal injury also could occur as a result of
ischemia
Epidural Hematoma
 Most often occurs from impact loading to the skull
with associated laceration of the dural arteries or
veins, often by fractured bones and sometimes by
diploic veins in the skull's marrow

 More often, a tear in the middle meningeal artery

causes this type of hematoma.
 When hematoma occurs from laceration of an artery,
blood collection can cause rapid neurologic
deterioration
Clinical Manifestation of Epidural
Hematoma
 Brief loss of consciousness followed by a lucid period.
The lucid period is followed by rapid decrease in level
of consciousness.
 Complaints of severe, localized headache.
 Decreased LOC.
 Fixed and dilated pupil on the same side as the injury.
Subdural Hematoma
 Subdural hematoma tends to occur
in patients with injuries to the
cortical veins or pial artery in severe
TBI

 The associated mortality rate is high,

approximately 60-80%.
 Epidural and Subdural Hematoma

ALL-NET Pediatric Critical Care Textbook - Source: LifeART EM Pro

(1998) Lippincott Williams & Wilkins.
www.med.ub.es/All-Net/english/neuropage/trauma/head-8htm
 Coup and Contrecoup
Contusions
 A combination of vascular and tissue damage
leads to cerebral contusion
 Coup contusions occur at the area of direct
impact to the skull and occur because of the
creation of negative pressure when the skull,
distorted at the site of impact, returns to its
normal shape
 Contrecoup contusions are similar to coup
contusions but are located opposite the site of
direct impact
Coup and Contrecoup
Contusions
 The amount of energy dissipated at the site of
direct impact determines whether the ensuing
contusion is of the coup or contrecoup type
 Most of the energy of impact from a small hard
object tends to dissipate at the impact site,
leading to a coup contusion
 On the contrary, impact from a larger object
causes less injury at the impact site since energy
is dissipated at the beginning or end of the
head motion, leading to a contrecoup contusion
Severity of TBI using the Glasgow
Coma Scale (GCS)
 The severity of TBI according to the GCS score
(within 48 hrs.) is as follows:

 Severe TBI = 1-8

 Moderate TBI = 9-12

 Mild TBI = 13-15

ASSESSMENT
RAPID TRAUMA SURVEY

 Note LOC (AVPU), secure airway and protect c-

spine
 Assess breathing
 Do not allow the patient to become hypoxic
 Assess circulation
 Control major bleeding
 Prevent hypotension
 Transport decision and interventions
 Do brief neuro & GCS if altered LOC
ASSESSMENT DETAILED EXAM
 Vital signs
 SAMPLE history
 Head-to-toe exam, including
neurological and GCS, fluid leak, battle
sign
 Further bandaging and splinting
 Continuous observation
Monroe- Kellie Principle

Rogers (1996) Textbook of Pediatric Intensive Care p.

646
 Cerebral Blood Flow
Regulation of Cerebral Vascular Resistance

CBF

Normal
50 - 100
ml / min

MAP PaCo2
(mmHg) (mmHg)
Normal 60 - 150 mmHg Normal 30 - 50 mmHg
Management of
Traumatic Head Injury
 Maximize oxygenation and ventilation

 Support circulation / maximize cerebral

perfusion pressure

 Decrease intracranial pressure

 Decrease cerebral metabolic rate

Primary vs. Secondary
Brain Injury
 Primary injury is immediate from bruising or
penetrating objects
 Secondary injury is from hypoxia or
 perfusion of the brain
 Caused by swelling, hypoxia, or hypotension
 May be prevented by good patient care
 Hyperventilation decreases perfusion of the brain
tissue
 Protect airway, give oxygen, maintain BP
Hypotension
Kills
the patient with ICP
 Monitoring
 Serial neurologic examinations
 Circulation / Respiration
 Intracranial Pressure
 Radiologic Studies
 Laboratory Studies

Scherer & Spangenberg (1998) Critical Care Medicine, 26(1)

Fibrinogen and platelets are significantly decreased in TBI
patients
 Respiratory Support: Maximize Oxygenation
 Hypoxemia is predictive of morbidity
 Ong et al. (1996) Pediatric Neurosurgery, 24(6)
 Neurogenic pulmonary edema / concurrent lung injury
 Positive End Expiratory Pressure
 May impair cerebral venous return
 Cooper et al. (1985) Journal of Neurosurgery, 63

 Feldman et al. (1997) Journal of Neurosurgical

Anesthesiology, 9(2)
 PEEP > 10 cm H2O increases ICP
 Respiratory Support: Normoventilation
Hyperventilation : Historical management more harm than good?

Originally
adapted
from
Skippen et
al. (1997)
Critical
Care
Medicine,
25

ALL-NET Pediatric Critical Care Textbook

www.med.ub.es/All-Net/english/neuropage/\protect/vent-5htm
Iperventilazione
HYPERVENTILATION IS NO
LONGER RECOMMENDED
FOR TREATING HEAD
INJURY EXCEPT IN THE
CASE OF HERNIATION
SYNDROME
 Evidence Supporting Normoventilation
 Forbes et al. (1998) Journal of Neurosurgery, 88(3)

 Marion et al. (1995) New Horizons, 3(3)

 McLaughlin & Marion (1996) Journal of Neurosurgery, 85(5)

 Muizelaar et al. (1991) Journal of Neurosurgery, 75(5)

 Newell et al. (1996) Neurosurgery, 39(1)

 Skippen et al. (1997) Critical Care Medicine, 25(8)

 Yundt & Diringer (1997) Critical Care Clinics, 13(1)

Use of Hyperventilation ...

 Management of very acute elevation of intracranial

pressure
 Preemptive for activities known to increase intracranial
pressure
 No lower than 32-35 cmH20

--- Moderate and transient

Circulatory Support:
Maintain Cerebral Perfusion Pressure
6

5
Number of 4 Good
Hypotensive Moderate
Episodes 3
Severe
2 Vegetative
1 Dead

0
Outcome
Kokoska et al. (1998), Journal of Pediatric Surgery,
33(2)
Circulatory Support:
Maintain Cerebral Perfusion Pressure
CPP = MAP - ICP
 Adelson et al. (1997) Pediatric Neurosurgery, 26(4)
 Children (particularly < 24 months old) are at
increased risk of cerebral hypoperfusion after TBI
 Low CBF is predictive of morbidity

 Rosner et al. (1995) Journal of Neurosurgery, 83(6)

 Management aimed at maintaining CPP (70
mmHg) improves outcomes
Altered Cerebral Autoregulation
Intracranial Pressure (ICP)
 ICP is usually low (<15mmHg)
 Cerebral perfusion pressure (CPP)
depends upon BP and ICP
 CPP = MAP - ICP
 If the ICP goes up the BP must go up to
maintain the CPP

Bottom line, need BP between 80-90

mmHg systolic to perfuse the brain
 Lowering ICP

Brain Blood

CSF Mass
 Evacuate hematoma Bone
 Drain CSF
 Intraventricular catheters use is limited by degree of
edema and ventricular effacement
 Craniotomy
 Permanence, risk of infection, questionable benefit
 Reduce edema
 Promote venous return
 Reduce cerebral metabolic rate
 Reduce activity associated with elevated ICP
Hyperosmolar Therapy: Increase Blood Osmolarity

Brain Blood
cell vessel
Fluid

Movement of
fluid out of
cell reduces
edema
Osmosis: Fluid will move from area of lower osmolarity
to an area of higher osmolarity
 Diuretic Therapy
Osmotic Diuretic Loop Diuretic
 Mannitol (0.25-1 gm / kg)  Furosemide
 Increases osmolarity  Decreased CSF formation
 Vasoconstriction (adenosine) /  Decreased systemic and
less effect if autoregulation is cerebral blood volume
impaired and if CPP is < 70 (impairs sodium and water
 Initial increase in blood volume, movement across blood
BP and ICP followed by decrease brain barrier)
 Questionable mechanism of
 May have best affect in
lowering ICP
conjunction with mannitol
 Rosner et al. (1987) Neurosurgery,
21(2)  Pollay et al. (1983) Journal of
Neurosurgery, 59 ; Wilkinson
(1983) Neurosurgery,12(4)
 Hypertonic Fluid Administration
 Fisher et al. (1992) Journal of Neurosurgical Anesthesiology, 4
 Reduction in mean ICP in children 2 hours after bolus
administration of 3% saline

 Taylor et al. (1996) Journal of Pediatric Surgery,31(1)

 ICP is lowered by resuscitation with hypertonic saline vs.
lactated ringers solution in an animal model

 Qureshi et al. (1998) Critical Care Medicine, 26(3)

 Reduction in mean ICP within 12 hours of continuous
infusion of 3% saline acetate solution
 Little continued benefit after 72 hours of treatment
 Hyperosmolar Therapy

Goal:
Sodium
145-
155

Sodium:
square
ICP:
circle

Qureshi et al. (1998) Critical Care Medicine,

26(3)
 Promote Venous Drainage
Keep neck mid-line and elevate head of bed …. To what degree?

Feldman et al.
(1992) Journal of
Neurosurgery, 76
March et al.
(1990) Journal of
Neuroscience
Nursing, 22(6)
Parsons & Wilson
(1984) Nursing
Research, 33(2)

Dicarlo in ALL-NET Pediatric Critical Care Textbook

www.med.ub.es/All-Net/english/neuropage/\protect/icp-tx-
3.htm
Reduction of Cerebral Metabolic Rate
 Reduction in cerebral oxygen requirement
 Anticonvulsants - Prevent seizure activity
 Pentobarbital
 Adverse effects include hypotension and bone
marrow dysfunction
 Used only after unsuccessful attempts to control
ICP and maximize CPP with other therapies
 Improved outcome not fully supported by research

Traeger et al. (1983) Critical Care Medicine, 11

Ward et al. (1985) Journal of Neurosurgery, 62(3)
 ICP management continued...

Management of Pain & Agitation

Difficult to assess
 Opiods neurologic exam
 Benzodiazepines
Monitor for
Management of hypotension
Movement Short acting
agents beneficial
• Neuromuscular blockade
Do opiods increase CBF?
Increased ICP with concurrent decreased MAP and CPP has
been documented. Elevation in ICP is transient and there is no
resulting ischemia from decreased MAP / CPP.

Albanese et al. (1999) Critical Care Medicine, 27(2)

 Nursing Activities and ICP
20
18
16
14
12
ICP Turning
10
8
Suctioning
6 Bathing
4
2
0
Before During After

Rising (1993) Journal of Neuroscience Nursing,

25(5)
 Family Contact and ICP

Presence, touch and voice of family / significant

others...
• Does not significantly increase ICP
• Has been demonstrated to decrease ICP
Bruya (1981) Journal of Neuroscience Nursing, 13
Hendrickson (1987) Journal of Neuroscience Nursing,
19(1)
Mitchell (1985) Nursing Administration Quarterly, 9(4)
Treolar (1991) Journal of Neuroscience Nursing, 23(5)
Traumatic Brain Injury
Factors that Effect Secondary Brain Injuries
 Blood Pressure
 Oxygenation
 Temperature
 Control of Blood Glucose
 Fluid Volume Status
 Increased Intracranial Pressure
 Treatment of Severe Head Injury

Refractory intracranial hypertension

Second tier therapies

Surgical Barbituates
decompression

Hypothermia Hyperventilation

Corticosteroids
Blood Glucose
 Stress response
 Hypoglycemia
 Cochran (2003)
Hypothermia
 Prevention and aggressive treatment of fever
 Significant beneficial effect on neurologic outcome
with transient, mild hypothermia (32  – 34 C for 24 –
48 hours)
 Seizure incidence and ICP reduced
 Hyperthermia produces deleterious effects on
neuronal recovery and BBB integrity
Glucocorticoids
 Standards - not recommended
 Guidelines - none
Anti-seizure prophylaxis
 Standard - not rec for the prevention of late PTS
 Guidelines - none
 Options - may be used to treat early PTS in high risk
patients
Hyperventilation
 Moderate hyperventilation (PaCO2 < 30 mmHg) may
be associated with worse outcome

 Avoid even prophylactic hyperventilation in first 24 h

post TBI to prevent ischemia
Summary of Recommended Practices

 Maximize oxygenation (PEEP < 10)

 Normoventilate
 Suction only as needed, limit passes, pre-
oxygenate, +/- pre-hyperventilate (not < 30), use
lidocaine when possible
 Maintain blood pressure and maintain CPP > 60
 Evacuate intracranial blood
 Drain CSF with ventriculostomy when possible
Summary of Recommended Practices
 Hyperosmolar therapy
 Avoid hyperthermia, +/- hypothermia
 Prevent seizures
 Reserve pentobarbital for refractory conditions
 Mid-line neck, elevated head of bead, ? not > 30 degrees
 Treat pain and agitation - consider pre-medication for
nursing activities
 Avoid hyperglycemia
 Allow family contact
 Monitoring Brain Metabolism
Jugular Venous Catheter
Jugular Venous Oxygen Saturation (SJVO2)
Arteriojugular Venous Oxygen Difference (AJVO2)
Cerebral Metabolic Rate For Oxygen (CMRO2)
Possible better outcome in adults
Cruz (1998) Critical Care Medicine, 26(2)
Brain Sensors
Brain tissue pH, PaO2, PcO2, lactate
Kiening (1997) Neurology Research, 19(3)
HERNIATION SYNDROME
 Increased ICP
 Coma
 Dilatation of ipsilateral or both
pupils
 Contralateral hemiparesis
 Decreasing respiration
 Cushing’s Reflex
 Hypertension
 Bradycardia