Head Trauma PDF

State of Illinois
Trauma Nurse Specialist Program
HEAD TRAUMA
Connie J. Mattera M.S., R.N., TNS
Time allotment: 2 hours
OBJECTIVES:
Upon completion the participant will
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
state the incidence, morbidity, and mortality often associated with head trauma.
apply knowledge of anatomy and physiology of the CNS to anticipate the pathophysiology
existent in traumatic brain injuries.
predict nervous system trauma based on mechanism of injury.
distinguish between head injury and brain injury.
differentiate primary from secondary injuries.
distinguish between focal and diffuse injuries.
list five immediate complications of head injury that will worsen the prognosis.
explain the dynamics of cerebral blood flow and cerebral perfusion pressure.
sequence the evolution of increased intracranial pressure.
differentiate early from late signs of ICP including herniation syndromes.
explain the primary assessments to be performed on a head injured patient
state the resuscitative priorities based on the BTF guidelines which focus on methods to establish
airway control, provide ventilatory assistance and perfusion support.
sequence the steps in performing a neurological exam on a head injured patient with an
emphasis on the mental status assessment including GCS, cranial nerve exam, motor, sensory
and reflex exams.
interpret assessment data to formulate appropriate nursing diagnoses associated with head and
brain injured patients.
classify head injuries as mild, moderate, or severe according to assessment findings.
describe appropriate nursing interventions for the management of head injured patients.
describe methods by which nurses can appropriately participate in, and assist with, medical
management of head injured patients.
state the radiological and laboratory tests that physicians typically order for head injured patients.
explain the pathophysiology, patient presentation, and management priorities for the following
vault fractures: linear, comminuted, depressed, basilar.
focal injuries: epidural, subdural, and subarachnoid hemorrhages; cerebral contusion; intracranial
hemorrhage.
diffuse injuries: concussion and diffuse axonal injury.
evaluate the effectiveness of emergency interventions and amend the care plan as indicated by
patient responses.
CJM: 6/07
State of Illinois
Trauma Nurse Specialist Program
HEAD TRAUMA
Connie J. Mattera M.S., R.N., TNS
I.
Epidemiology of head trauma

A.
Definitions
1.
A head injury is defined as external influences causing traumatic insult to the head
that may result in injury to soft tissue, bony structures and/or brain.
2.
Traumatic brain injury (TBI), as defined by the National Head Injury Foundation,
is "a traumatic insult to the brain capable of producing physical, intellectual,
emotional, social, and vocational changes." It is classified as direct (primary) or
indirect (secondary) injury to the tissue of the cerebrum, cerebellum, or brainstem.
Brain injury affects who we are, the way we think, act, feel and move. It can change
everything about us in a matter of seconds (Brain Injury Association of America,
2004).
B.
Incidence: Estimated at 200/100,000 population which translates to one every 21 seconds

or 1.6 million/year with 230,000-270,000 hospitalized. Of these, about 50,000 52,000 die
and another 70,000 90,000 survive with disabilities (BTF, 2004, CDC, 2001). TBI is more
than twice as likely in males as in females; with the highest incidence in people 15-24 years
of age and 75 years and older. Children ages 5 and younger are also a high-risk group. An
estimated 5.3 million Americans live with disabilities resulting from traumatic brain injury
(Brain Injury Association (2004), NIH, 2002).
C.
Common etiologies
1.
Motor vehicle crashes (MVCs) are the most common cause of closed head injury
followed by falls, which are seen more frequently in children and the elderly. Other
etiologies: intentional battery, use of firearms, water or recreational or sport-related
injuries, pedestrian impacts, or domestic violence.
2.
Children: 10% of TBI are due to MVCs, falls, recreational (bicycling-related), home
or birth injuries.
3.
Behaviors that increase the risk of sustaining head trauma

a.
b.
c.
d.
e.
D.
Alcohol ingestion
Use of mild-altering drugs
Incorrect use or nonuse of restraint systems
Nonuse of helmets
Participating in team sports without protective equipment
General categories of injury

1.
Head injuries can be classified according to

a.
b.
c.
d.
2.
Severity of the injury

Anatomical classification
Pathological classification
Primary and secondary brain injury
Blunt (closed) trauma: The person receives an impact to the head from an
outside force, but the skull and dura remain intact and brain tissue is not exposed
to the environment. More common than penetrating. The structures of the head
and face generally protect well against most blunt trauma. However, when the
magnitude of forces exceeds the tensile strength of the structures, severe injury
can occur. For example, the sinus cavities of the face are frequently injured with
blunt facial trauma. The air-filled spaces collapse upon impact and help to dissipate
energy forces. A person may have a closed head injury with mild to severe
traumatic brain injury.
State of Illinois TNS Program

Head Trauma - page 2
3.
E.
F.
G.
Penetrating (open) trauma: A penetrating injury produces an opening through the

skull into cranial contents exposing them to the environment, creating a risk for
infection and other injuries. Often caused by missiles such as rifles, hand guns, or
shotguns and less commonly by other penetrating implements like knives, ice
picks, exes, etc. While not as common as blunt trauma, they are very disruptive
due to energy forces that can project hair, skin, bone and debris into the brain and
contaminate the region. If the projectile is traveling at a low rate of speed through
the skull, it can ricochet within the skull and widen the area of damage. High
velocity projectiles can produce significant trauma from shock waves. Sharp
projectiles may be superficial because of the protection afforded by the skull, but
may pierce through bone and meninges into the brain. A through and through
injury occurs if an object goes through the skull, brain, and exits the skull. These
will produce the effects of penetration injuries, plus additional shearing, stretching,
and rupture of brain tissue (Brain Injury Assoc. of America, 2004).
Mechanisms of injury: Brain injury is usually due to a combination of forces

1.
Acceleration: Stationary head is hit by a moving object as in car vs. pedestrian,

abuse or sports injury.
2.
Deceleration injury: Moving head hits a stationary object as in falls, abuse, sports
injuries and MVCs. Sudden deceleration may produce bony deformity or cause the
brain to slide back and forth by inch at 38 mph collision. The brain can move in a
straight linear acceleration with no loss of consciousness but can be injured as it
moves across the rough base of the skull. The initial impact and pressure wave
may tear tissue and result in injury on the side of the impact (coup) and the side
opposite the point of impact (contrecoup). When these forces are applied, shearing,
tensile and compressive stresses may lead to fractures, hemorrhage, hematomas,
and contusions.
3.
Acceleration/deceleration injury: Moving head hits a moving object
4.
Distraction injuries: Ex. hanging. If the head is suspended in a drop 18" taller than
the person; it causes a fatal blow to the CNS.
5.
Penetrating trauma
Mortality rates
1.
2.
3.
4.
0%:
Mild head injury
7%:
Moderate head injury
25%: Severe head injury (BTF, 2007)
90%: GSW to head: Nearly 2/3 are classified as suicides. Firearms are the
single largest cause of death from traumatic brain injury, causing 44% of TBI
deaths (CDC, August 22, 2002).
5.
In the last 12 years, more people have died of traumatic brain injury (TBI) than in all
the wars combined. It contributes significantly to the outcome in 40%-50% of all
trauma deaths (Feliciano, 267).
6.
TBI is the leading single-organ cause of death related to trauma. Fifty percent of
deaths due to MVC involve head trauma (Bourg, 2007).
7.
The challenge of improving outcome rests on advances in prehospital

management, critical care and rehabilitation.
Morbidity: Brain injury can result in memory loss, rapid mood swings, fatigue, intellectual
dullness, mental rigidity, personality changes, and physical disabilities. The terms mild
moderate and severe traumatic brain injury are used to describe the level of initial injury in
relation to the neurological severity caused to the brain. There may be no correlation
between the initial Glasgow Coma Score and the initial level of brain injury and a persons
short or long-term recovery or functional abilities (Brain Injury Assoc. of Am, 2003).

1.
Mild brain injury (MBI) or concussion: Up to 75% of all diagnosed head injuries
(Bazarian et al, 2005) results in brief amnesia or loss of consciousness for a few
seconds up to 30 minutes without major complications such as hematomas. The
person may not lose consciousness, but be dazed and confused. Only 3% should
deteriorate. Five percent with GCS 14-15 and 10% with GCS of 13 will require
surgery (ATLS, 2005). Symptoms include temporary headaches, memory
disturbance, dizziness, irritability, fatigue, mild mental slowing with decreased
concentration and attention span, impaired perception or mood, sleep
disturbances, sensitivity to noise or light, and balance problems. They and almost
always improve over one to three months. Infants and young children may have
observed signs of irritability, lethargy or vomiting following MBI.
2.
Moderate brain injury results in a loss of consciousness usually lasting minutes to

a few hours. It is followed by a few days or weeks of confusion, and may be
accompanied by brain contusions or hematomas. Although people usually have
physical, cognitive and psychosocial or behavioral impairments that may last
several months, treatment will often allow them to recover fully. However, some
symptoms may be permanent.
3.
Severe brain injury is defined as an abbreviated injury score (AIS) for the head of
4, 5, or 6. Severe injury almost always results in prolonged unconsciousness or
coma lasting days, weeks, or longer. Complications include brain contusions,
hematomas, or damage to the nerve fibers, and some may have suffered from
anoxia. It is sometimes possible to make significant improvements in the first year
after injury that can continue to improve slowly for many years with excellent
rehabilitation. However, these patients will often be left with some permanent
physical, behavioral, and/or cognitive impairments (Brain Injury Association, NIH,
2002). Severe brain injury is further categorized into subgroups with separate
features:
a.
b.
c.
d.
e.
f.
4.
Head injury often does not occur alone; 75% are associated with multiple trauma
a.
b.
II.
Coma
Vegetative state
Persistent vegetative state
Minimally responsive state
Akinetic mutism
Locked-in syndrome
30% - injuries limited to one body area
70% - involve two or more body areas
H.
Cost: TBI carries a greater cost than CV disease and stroke combined; $40 billion/year in
U.S.
I.
Three databases provide information about severe head injuries

1.
International Data Bank: (Central and Eastern European Traumatic Brain Injury
program. Established first; population - GCS 8 or less, 6 hours after injury.
Participants: Centers in Glasgow (Scotland), Rotterdam, Groningen (Holland), and
Los Angeles.
2.
NIH Traumatic Coma Data Bank: Population - GCS 8 or less after resuscitation.
Participants: six centers in U.S.
3.
TBI-trac: Interactive database designed as a Q/A program to track prehospital and

in-hospital care and outcome for trauma centers treating patients with severe
traumatic brain injury through the Brain Trauma Foundation.
Patient destination and trauma team composition for optimal outcomes

A.
Need 5 R's for optimal outcomes

1.
Right patient, to the

2.
3.
4.
5.
Right hospital, in the

Right amount of time, to be cared for by the
Right physician (neurosurgeon) and trauma team and receive
good Rehabilitation.
Right hospital note: Patients with severe traumatic brain injury should be transported
directly to a Level I or Level II trauma center that offers CT scanning, neurosurgical care,
ICP monitoring, and treatment capabilities (BTF Prehospital Guidelines for the Management
of Severe Traumatic Brain Injury, 2000) even if this center may not be the closest hospital.
Transport decisions in the field are among the most important decision affecting outcome in
patients with severe TBI. When an integrated EMS and trauma system is in place and EMS
agencies transport a patient directly from the scene of the incident to an appropriate
receiving facility (trauma center) the patient is entered into a system of care that has been
shown to improve overall patient outcome. Hrtl et al (2006) found that indirect transport to
a trauma center (all but two hospitals in their study were Level I) was associated with an
almost 50% increase in mortality. Inter-hospital transfers of these patients are known to
delay the time until neurosurgical consultation and intervention occur at a time of great risk
for secondary insult to the brain (BTF, 2007).
B.
Traumatic brain injury care team should include the following:

1.
2.
3.
4.
5.
6.
III.
EMS providers: ground and/or air transport

Physicians specializing in emergency medicine, trauma, neurosurgery, neurology,
radiology, and anesthesiology
Nursing professionals from the ED, Neuro/Trauma ICU and/or trauma service,
Neuro Med-Surg Units, OR and PACU (some facilities would also include case
management, discharge planners)
Ancillary departments that include CT, radiology, lab, pharmacy, physical medicine
and rehabilitation, speech therapy and dietary
Social services
Pastoral care
How the brain is injured: There are two distinct phases of injury that produce neurological
dysfunction to the tissues of the cerebrum, cerebellum, or brainstem.
A.
Primary (direct) injury: Mechanical injury that occurs at the moment of energy transfer and
is associated with a variety of mechanisms, i.e., acceleration/deceleration, penetration. The
impact or forces may cause bony deformity and injury to cranial contents. Pressure waves
travel across the brain and dissipate causing physical transection, shearing, bruising,
bleeding, or damage of cranial contents that cannot be reversed (Bourg, 2007). Disrupted
blood flow to the injured area may cause ischemia and compromise of the blood/brain
barrier or death of neurons. Irritation of nervous system tissue may create electrical
instability. Treatment is prevention.
B.
Secondary (indirect) injury: All brain damage does not occur at the moment of initial
trauma. Secondary injury occurs as a direct result of the primary injury and evolves over
minutes, hours and days. Patient outcomes improve when these delayed insults are
prevented or respond to treatment (BTF, 2007). Secondary injury is due to a variety of
metabolic and physiologic processes initiated by regional ischemia.
1.
Ischemia: Cerebral ischemia may be the single most important secondary event
affecting outcome following severe traumatic brain injury (BTF, 2003). Cerebral
blood flow during the first day after injury is less than half that of normal individuals
even though levels may subsequently increase to normal or supranormal levels.
The initial hypoperfusion may cause irreversible damage (See section on CPP).
2.
Systemic causes
a.
Hypoxia: Hypoxia, defined as apnea/cyanosis or PaO2 <60 (SpO2 < 90%)

and hypotension are among the five most powerful predictors of poor
outcome, independent of other major predictors such as age, admission
GCS, intracranial diagnosis, and pupillary status (BTF, 2007). There is

intense cerebral vasodilation in the presence of hypoxia that adds to an
increase in ICP. The temporal lobe is particularly sensitive to oxygen
deprivation that results in memory losses due to decreased protein
synthesis. The combination of hypoxia and hypotension increases mortality
to 75% (ATLS, 2005).
IV.
b.
Hypotension: Almost 1/3 of head injured patients present in shock with

hypotension. In the early stages, shock may be more important than
hypoxia to treat due to its threat to cerebral perfusion (Chesnut, 1997). The
injured brain is more susceptible to shock. It has been shown that even
one prehospital BP < 90, doubles the patient's mortality (BTF Field
Guidelines, 2000). This observation was reaffirmed in a recent study by
Henzler et al (2007) that found lower blood pressures in the first four hours
after admission were associated with mortality and may have increased
the rate of secondary brain injury. A MAP <=65 mmHg during the first four
hours after trauma was associated with a four-fold increase in the odds of
non-survival. They also found that intracranial pressure monitoring and
ICU admission tended to be initiated later in non-survivors, possibly
delaying recognition and management of inadequate cerebral perfusion
pressure. In addition, hypothermia did not normalize during the first 24
hours after injury in non-survivors.
c.
d.
e.
Electrolyte imbalances (Na, K, Ca)

Anemia
Hyperthermia
f.
Hypercarbia (respiratory acidosis): also

vasodilation adding to intracranial pressure.
g.
Hypoglycemia
causes
intense
cerebral
3.
Intracranial causes: Intracranial hypertension, delayed intracerebral hematoma

evacuation, edema, hyperemia, carotid dissection, seizures, vasospasm, and
infection. Large mass lesions result in shifts and displacement of IC contents
that result in vascular occlusion, edema, and increased ICP (Feliciano, 268).
4.
Secondary injury causes breakdown of the blood brain barrier, disruption of

cerebral autoregulation, accumulation of toxic extracellular levels of excitatory
amino acids and free radicals, and initiates cellular inflammatory responses and
regional hyperthermia. It diminishes the effectiveness of autoregulatory and
compensatory mechanisms of the brain, thus compromising perfusion and
producing ischemia. The tissue surrounding the initial injury is known as the
ischemia penumbra and is at highest risk.
5.
Secondary injury is often preventable. The "secondary" brain damage opens a

window of opportunity where injury and loss of nerve function may be minimized by
proper medical treatment (Brain Trauma Foundation, 2000).
Pathophysiology of traumatic brain injury

A.
The initial trauma sets in motion a series of molecular events which activate endogenous
substances, i.e., oxygen free radicals, monoamines, neuropeptides, arachidonic acid
metabolites, and alter calcium metabolism (Wagner, p.2).
B.
Oxygen free radicals: Superoxides and lactic acid are released as a result of
mitochondrial dysfunction in the absence of obvious ischemia. These oxygen radicals
cause lipid peroxidation of polyunsaturated fatty acids disrupting cell membranes and
possibly resulting in the breakdown of the blood-brain barrier and progressive axonal
degeneration (Wagner, p.2).
C.
Either through overt damage or by some other mechanism, voltage gates burst open
releasing bradykinin, kallikrein, excitatory amino acids (particularly glutamate which is the
most excitatory neurotransmitter), and arachidonic acid and its metabolites.

D.
Current research is exploring the causal relationship between these substances and the
development of brain edema and secondary brain damage. Glutamate is stored inside of
cells or is shuttled discretely between them. The temporal lobe is filled with glutamate.
When trauma occurs, this major neurotransmitter spills freely.
E.
There are mechanisms responsible for glutamate uptake by neurons, but these
mechanisms quickly become overwhelmed when there is an excess of glutamate and a
drop in ATP needed to pump it across the membrane.
F.
When the flood of glutamate pours into synaptic clefts, it triggers the opening of key ion
channels in the neuron that receives the glutamate signal and over stimulates the
neurotransmitter's receptors with a subsequent rush of ions across the cell membrane wall,
particularly passage of calcium through N-Methyl-D-Aspartate [NMDA]-receptor mediated
channels. Potassium is flushed out of the cell. Calcium is considered essential in normal
neuronal activity and is normally activated in small amounts. It reshapes parts of the cell
wall membrane under controlled conditions. The drop in energy availability after injury
triggers uncontrolled calcium activity late in the cascade of events.
G.
One of the first effects of this Ca flux is that glycolysis is stepped up to provide more
energy to pump ions across the cell membrane. The Ca blockers used in CV disease are
not very effective in blocking the Ca channels in the brain. Brain ion channels have very
unique properties. Bruce Bean, professor of neurobiology at Harvard Medical School in
Boston and his associates have identified a toxin produced by the funnel web spider of the
Southwestern U.S. Through study of this toxin, they have identified a type of Ca blocker that
appears to occur only in certain kinds of brain cells [Neuron (1992) 9; 85-89]. The spider
venom toxin selectively binds to and blocks a newly recognized Ca channel (P-type),
named after the Purkinje neurons where it was first discovered in rat brains. P-type
channels occur in central and peripheral neurons, but there is no evidence that they occur
in cardiac muscle.
They also appear to be used in synaptic transmission and may play a major role in normal
as well as diseased neuronal activity. If this evidence can be supported, it suggests that the
spider toxin may be a good model for a synthetic compound that could prevent the effects
of stroke, trauma and some epilepsy.
V.
H.
Protein synthesis that is needed for normal membrane permeability is slowed. The
inhibition of protein synthesis (especially in the temporal lobe) may be one cause of postconcussive amnesia.
I.
Glycolysis may initially protect the cell by helping to correct the ion imbalance, but it steadily
increases the amount of lactic acid in the cell through anaerobic metabolism. Studies
have shown that immediately following injury, glucose metabolism increases, but that this
trend is followed by a prolonged decrease that lasts several days. Treating animals with
excitatory amino acid antagonists greatly decreased the brain's demand for glucose.
J.
The resulting acidosis leads to a breakdown of the cell membrane with bloating of the cell.
This causes self-destruction and eventual death. A similar progression can be charted in
both contusion and stroke, although the timing and topography of the events are different.
Within seconds of trauma, the release of fatty acids from the cell membrane is initiated. The
entry of calcium ions into the cell is followed by lipolysis, then proteolysis, and finally protein
phosphorylation, which may ultimately be what kills the cell. Stimulation of lipases and
phospholipases can be prevented by glutamate antagonists like MK-801. It's a receptormediated process.
Dynamics of cerebral blood flow (CBF) and cerebral perfusion pressure (CPP)
A.
Cerebral metabolism: The brain is small but greedy. It is only three pounds of tissue (2%
of body weight), but is the most metabolically active and perfusion-sensitive organ. It
metabolizes 25% of the bodys glucose, burning 60 mg/min. It consumes 20% of the
cardiac output and 20% of the total body oxygen (49 mL/min). It has no storage
mechanism for oxygen or glucose so brain tissue is dependent on an on-going source of
both fuels via a constant source of cerebral blood flow (CBF) via the internal carotid and

vertebral arteries and will demonstrate altered mental status within moments of a reduction
in either.
B.
Cerebral blood flow is a function of cerebral perfusion pressure and the brains ability to
autoregulate cerebral blood vessels. Any injury that affects CBF (perfusion) has a rapid and
devastating effect on the brain and its control of body systems (Bledsoe, 2006). Cerebral
blood flow (CBF) following injury may be disrupted by compression of cerebral blood
vessels from mass lesions, reduced cerebral metabolism, or to posttraumatic vasospasm
as has been documented in as many as 40% of these patients (BTF, 2003). It can also be
reduced due to increased ICP or low systemic BP (hypotension).
C.
Autoregulation
1.
The capacity of the brain to regulate its own cerebral blood flow to meet the needes
of the brain despite variations in systemic arterial pressures.
2.
The fluctuating tone of cerebral arterioles depending on the brains changing

metabolic needs, normally maintains a constant blood flow to the brain over a wide
range of perfusion pressures. Normal cerebral blood flow is 50 mL/100 Gm/min.
Autoregulation functions maximally at a MAP of 60 - 180 mmHg.
3.
Metabolic or chemical influences: A change in metabolic rate will lead to a change

in CBF.
a.
pO2
(1)
(2)
(3)
(4)
b.
4.
Little effect on CBF when in physiologic ranges

Hyperbaric levels result in vasoconstriction
Hypoxia increases the severity of any head injury. A pO2 < 50
mmHg (SpO2 < 90) causes cerebral vasodilation, increased CBF,
and increased cerebral blood volume. This contributes to
increased ICP.
PaO2 < 30 doubles the CBF
pCO2
(1)
1 mmHg change = 2%-3% change in CBF between 20-80 mmHg
(2)
A pCO2 > 45 (hypercarbia) causes cerebral blood vessels to dilate

with corresponding increases in CBF and cerebral blood volume.
In the presence of an already high ICP, this extra dilation can have
devastating effects.
(3)
Conversely, low levels of CO2 cause pronounced vasoconstriction

that can almost stop perfusion through the brain. This effect will
decrease after 6 to 10 hours.
(4)
Impaired CO2 reactivity impairs O2 reactivity.
Impaired autoregulation in TBI

a.
Autoregulation is often compromised in the TBI patient. There is a

flow/metabolism uncoupling. Stimulation of the brain (increased metabolic
demand) does not increase cerebral blood flow.
b.
Increased ICP with pressure on the brain stem leads to increased MAP
(Cushings response) with no compensatory cerebral blood flow control,
which further increases ICP.
c.
The brain now becomes dependent on BP for perfusion. If arterial pressure

is 160 torr, cerebral blood volume increases.
d.
Low flow states may lead to blood brain barrier breakdown, an increase in
cerebral edema, and predisposes patients to secondary brain injury from
ischemia (ATLS, 2005). In states of ischemia, CBF drops to 18-20 mL/100
Gm/min. At 8-10 mL/100 Gm/min, the brain will infarct.

D.
Intracranial pressure: The intracranial volume is fixed in an adult (1200-1500 mL) and
does not vary
1.
Three intracranial components

a.
b.
c.
80%: Cerebral tissue: Brain is 75% H2O; constant blood brain barrier
from intact cell wall membranes
12%: Cerebral blood volume: Result of cerebral blood flow 750 mL
constant. 80% of brain blood is venous. Head position is critical to maintain
venous outflow and to prevent venous congestion.
8%:
Cerebral spinal fluid (CSF): 125-150 mL is constant.
2.
Any increase in volume in one compartment must be matched by a similar

reduction in another compartment or ICP will rise (Monroe-Kellie hypothesis or
"No room in the inn theory").
3.
Intracranial pressure values

a.
Normal
(1)
(2)
b.
Intracranial hypertension: 15-20 mmHg
c.
Malignant intracranial hypertension

(1)
(2)
(3)
E.
20 mmHg sustained for 30 minutes

30 mmHg sustained for more than 15 minutes
40 mmHg sustained for more than 2 minutes
Volume pressure relationship:

1.
CBF is dependent on cardiac output (CO) and is independent of systemic arterial

resistance (TPR). If arterial pressure is > 160 torr, cerebral blood volume increases.
Initially, as volume increases, there is little or no increase in pressure due to
compensation, but as compliance is lost, small additions of volume result in large
increases in pressure.
2.
There is significant post-traumatic vasospasm as well as changes in pressure and

metabolic autoregulation. Cerebral vascular resistance is altered (often increased)
by trauma. There is increasing evidence that CBF is typically very low following TBI
and, in many cases, may be near the ischemic threshold. A low CPP may
jeopardize regions of the brain with preexisting ischemia. CBF in the vicinity of
posttraumatic contusions and subdural hematomas is reduced even further than
global CBF (BTF, 2003).
3.
To compensate for an elevated ICP, one of the following must happen:

a.
b.
c.
F.
Child: 0-5 mmHg

Adult: 5-12 mmHg
Blood volume to brain must diminish,

The body must increase CSF resorption, decrease production, displace
fluid down the spinal cord, or
Brain tissue is displaced (herniation)/
Evolution of pathology causing ICP: pressure + time are big killers!

1.
Increase in brain volume

a.
Mass: Brain tumor, abscess, blood clot, AV malformation; CSF, blood

and/or tissue
b.
Edema
(1)
(2)
(3)
Cytotoxic intracellular
Vasogenic extracellular edema (tumors)
Hydrostatic tissues surrounding ventricles

2.
3.
Increase in CSF volume (hydrocephalus)

a.
b.
CSF is produced in the ventricles by the choroid plexus (20 mL/hr)

It is reabsorbed in the arachnoid space by the arachnoid villi
c.
Communicating
(1)
Overproduction of CSF
(2)
Under reabsorption (blood in subarachnoid space)
d.
Non-communicating
(1)
Also called obstructive hydrocephalus
(2)
An obstruction causing the inability of CSF to circulate to the
arachnoid villi to be reabsorbed
Increase in blood volume: Cerebral blood flow is a function of

a.
b.
c.
d.
4.
5.
6.
7.
8.
G.
Influx pressures (systole)

Efflux pressure (venous pressure)
Vascular radius
Blood viscosity
ICP leads to compression of arteries cell ischemia edema

In the presence of ischemia/compression of medulla; the body will attempt to fix
itself (maintain cerebral perfusion) producing a CNS response called the Cushing
response (systolic hypertension, widened pulse pressure and reflex bradycardia)
Respiratory insufficiency; hypercapnia
Vasodilation/hyperemia; increased CBF
Rapid clinical deterioration and death
Cerebral perfusion pressure (CPP)

1.
Cerebral perfusion pressure is the physiologic variable that defines the pressure
gradient driving cerebral blood flow (CBF) and metabolic delivery and is, therefore,
closely related to ischemia (BTF, 2003).
2.
Factors that influence CPP

a.
b.
MAP = mean arterial pressure (MAP = Diastolic BP + 1/3 pulse pressure)

ICP = intracranial pressure
3.
CPP = MAP ICP

a.
Normal MAP = 90-100 mmHg
b.
Normal ICP in adults: 5-12 mmHg
c.
CPP = 100 10
d.
Normal CPP = > 60 mmHg but should be patient specific
(1)
Infants > 50
(2)
Children > 60
4.
As the ICP rises near the MAP, the gradient for CBF decreases and perfusion is
restricted. In a hypotensive patient, even a marginally elevated ICP can be harmful.
The body usually compensa tes for increased ICP by elevating the arterial BP to
maintain CPP.
5.
Ultimately, the adequacy of CPP is more important than increased ICP. A decrease
in CPP results in a reduction in cerebral blood flow. Decreased CPP = altered level
of consciousness. Need a minimum CPP gradient of 60 mmHg to be conscious.
6.
Never lower the BP in a head trauma patient!

a.
b.
c.
d.
e.
CPP < 60 = Impaired blood flow to brain

CPP < 50 = Critical reduction in brain tissue oxygen
CPP < 40 = CBF down 25%
CPP 30 = Irreversible brain ischemia
If ICP MAP: The patient is dead

H.
7.
Enhancing intravascular hydrostatic pressure by increasing the BP and CPP can

help to improve cerebral perfusion. In most cases, CPP is amendable to clinical
manipulation, and enhancement of CPP may help to avoid both global and regional
ischemia (BTF, 2003).
8.
There is no direct relationship between CBF and ICP. Studies have shown that ICP
changes very little when BP is increased by as much as 30 mmHg in head-injured
patients, and this is true regardless of the status of autoregulation. Thus moderate
increases in BP, as might be needed to maintain an adequate CPP should not be
expected to cause an increase in ICP in most patients (BTF, 2003).
9.
BTF Guideline for CPP (2003): CPP should be maintained at a minimum of 60

mmHg. In the absence of cerebral ischemia, aggressive attempts to maintain CPP
above 70 mmHg with fluid and pressor should be avoided because of the risk of
adult respiratory distress syndrome (ARDS).
Clinical signs of ICP

1.
Early to progressive signs

a.
b.
c.
2.
Pressure is exerted downward. Cerebral cortices and/or reticular activating

system and cranial nerves are affected producing the following:
(1)
Altered mental status: progressive restlessness, confusion,
disorientation and lethargy or combativeness; changes in speech
or loss of judgment
(2)
Amnesia of events before or after the injury
(3)
Increased severity of headaches
(4)
Visual abnormalities: Diplopia, blurred vision, visual field deficits
(lose sight in part of field)
(5)
Conjugate deviation of eyes or gaze palsies
(6)
Deterioration in motor function: Monoplegia, hemiplegia. First part
of boy to show an increase in ICP is the wrist that will over pronate
or supinate; pronator drift
(7)
Sensory loss
(8)
Oval pupils with hippus (pupil rapidly dilates and constricts when
stimulated with light so it looks like it is jiggling up and down)
Pressure on the hypothalamus: Vomiting (often without nausea); temp
changes
Nuchal (neck) rigidity
Later signs game over

a.
Further alteration in mental status; decreased responsiveness and level of

consciousness (coma)
b.
Pressure on brainstem
(1)
Cushing's triad (brainstem pressure):

(a)
(b)
(c)
c.
Systolic hypertension w/ widening pulse pressure

Bradycardia (Vagal nerve pressure)
Bradypnea or irregular respirations: pressure
respiratory centers
on
(2)
Pupillary changes (unilateral to bilateral dilation) and decreased

reactivity to light (CN III paralysis)
(3)
Further deterioration in motor function: flexor-extensor posturing

(non-purposeful movement that is a brain stem reflex)
(4)
Absent or decreased brainstem reflexes: cough, gag, corneal,

Doll's eyes and calorics
Wide fluctuations in core temperature

3.
d.
Papilledema
e.
Seizures
Levels of intracranial pressure with corresponding S&S

a.
Cerebral cortex and upper brain stem involved

(1)
(2)
(3)
(4)
(5)
b.
Middle brain stem (pons) involved

(1)
(2)
(3)
(4)
(5)
c.
Wide pulse pressure and bradycardia

Pupils pinpoint to mid-size, sluggish or non-reactive (CN III)
Central neurogenic hyperventilation
Abnormal extensor posturing
Few patients function normally from this level
Lower portion of brain stem (medulla) involved

(1)
(2)
(3)
(4)
(5)
(6)
(7)
I.
BP rising and pulse rate begins to slow

Pupils still midsize and reactive
Cheyne-Stokes ventilations
Initially tries to localize and remove painful stimuli, eventually
withdraws then abnormal flexion occurs
All S&S should be reversible at this stage
Pupils both dilated and non-reactive

Respirations ataxic or absent
Flaccid, does not react to pain
Irregular pulse rate
QRS, ST, and T wave changes
Decreased BP
Not considered survivable
Herniation syndromes; life threatening

1.
The brain tissue will treat itself if the pressure is not relieved. Folds of dura
compartmentalize the brain. Herniation occurs when increased volume, pressure
and/or decreased compliance causes a part of the brain to shift from one
compartment into another, causing compression of other structures. If the
compression results from a building mass along the central region of the cerebrum
(epidural or subdural hematoma), pressure is first directed to the midbrain, then the
pons, and finally, to the medulla. The S&S of this progressive pressure and
structural displacement are known as the central syndrome (Bledsoe, 2006). It is
often a life-threatening event.
2.
Types of herniation
a.
b.
Supratentorial herniation
(1)
Cingulate herniation: Cingulate gyrus herniated into the falx
(2)
Uncal herniation: Medial edge of the temporal lobe herniates

down through the tentorial notch into the posterior fossa. Ipsilateral
pupil dilates and fixes. Contralateral motor weakness or paralysis.
(3)
Transtentorial (central) herniation: Downward displacement of

the cerebral hemispheres, diencephalon, and midbrain through the
elongated tentorial notch. Both pupils are fixed and dilated;
bilateral motor posturing.
Infratentorial herniation: Cerebellar (tonsilar) herniation Cerebellar

tonsils herniate into the foramen magnum. Causes almost immediate
death.

3.
Signs of herniation
a.
b.
c.
d.
e.
f.
g.
4.
VI.
Deterioration in the level of consciousness. GCS decreases by 2 or more

points
BP and ICP shoot up
HR drops to 30-40
Respiratory pattern changes
Pupillary changes (unilateral to bilateral dilation and non-reactive to light).
Pupil first dilates on same side as the clot (ipsilateral dilation) then both
may dilate and become nonreactive
Motor abnormality (contralateral deficits) to extensor motor posturing
Brainstem dysfunction
Outcomes
a.
Have two minutes to act after herniation. If medulla brainstem function

is altered, the BP will drop to 40-20. HR will increase to 140-150. The brain
will not go back to its normal alignment. This is an indication for temporary
hyperventilation.
b.
Generally poor outcomes in the presence of hypoxia, hypotension,

hypercarbia, hyperglycemia (which usually means a clot), or increased Ca
levels. Check Mg; Mg runs with Ca.
Guidelines for assessing and managing patients with TBI

The American Association of Neurological Surgeons and the Brain Trauma Foundation (BTF)
published patient care guidelines for the management of severe head injury in 1995 with
widespread distribution in 1996. These were updated in 2000 and again in 2007. EMS Guidelines
were published by the BTF in 2000 under a grant from the U.S. DOT and NHTSA. The guidelines
address care of traumatic brain injury (TBI) patients with a GCS of 8 or less. Penetrating head
trauma guidelines were published in 2001. Pediatric guidelines came out in 2002, and Spinal Cord
injury guidelines were issued in 2001-2002. The BTF also maintains Guidelines for the Surgical
Management of Traumatic Brain Injury and Prognosis of Severe Traumatic Brain Injury. A full text of
the guidelines can be obtained from the BTF website: www.braintrauma.org.
A.
B.
Classifications of evidence (BTF, 2007)

1.
When assessing the value of therapies or interventions, the available data is

classified into one of three categories according to the following criteria:
2.
Class I evidence: Data from good quality, prospective randomized controlled trials
(RCT). The gold standard of clinical trials. .
3.
Class II evidence: Moderate quality RCT, Clinical studies that violated one or
more of the criteria for a good quality random controlled trial. Types of studies so
classified: good quality case-controlled or good quality cohort studies.
4.
Class III evidence: Poor quality RCT with major violations of the criteria for a good
or moderate quality RCT. Also included were moderate or poor quality cohort and
case-controlled studies, and case series, databases or registry data.
Level of recommendation (BTF, 2007)

1.
Level I Represent the strongest evidence for effectiveness based on accepted

principles of patient management that reflect a high degree of clinical certainty
usually based on Class I evidence.
2.
Level II: Represent a particular strategy or range of management strategies that

reflect a moderate clinical certainty based on class II evidence.
3.
Level III (opinions): Remaining strategies for patient management for which there
is unclear clinical certainty based on class III evidence.

VII.
Initial assessment and resuscitative interventions

A.
The first two hours post-injury are characterized by ischemia and a 3% decrease in CBF
that must be corrected. The first priority is rapid physiologic resuscitation and
prevention of secondary injury. No specific treatment should be directed at intracranial
hypertension in the absence of transtentorial herniation or progressive neurological
deterioration not attributable to extracranial explanations (BTF, 1995).
B.
Assess, establish and control a patent airway

1.
Maintain spine motion restriction, if indicated, while establishing airway access

a.
Check spine motion restriction devices applied in the field; maintain until
spine is cleared clinically or radiographically.
b.
If the airway is impaired from the tongue, secretion, trauma and/or edema,
use positioning, suction, and manual maneuvers to clear the airway of
obstructions. If repositioning opens the airway, secure with a NPA or OPA
depending on the presence or absence of a gag reflex.
c.
Vomiting precautions Airway tissues are extremely vascular, bleed

profusely and swell rapidly. Blood is a great gastric irritant that frequently
induces vomiting. If the patient is not paralyzed, anticipate vomiting from
the head injury or increased ICP with pressure on the medulla, although
uncommon in adults. May or may not have associated nausea.
d.
2.
(1)
Projectile vomiting is due to direct pressure on the medulla or

vagus nerve roots (CN X), which aborts normal sensory pathways
and results in violent contractions of abdominal and thoracic
muscles (Wooten, 1996). Seen more often in children.
(2)
Vomiting is especially dangerous in patients with head trauma who

have an altered gag reflex as they cannot protect their airways and
frequently aspirate. Gastric contents are extremely acidic and will
rapidly damage pulmonary tissues leading to a high patient
mortality.
Have large bore suction equipment available at all times. Suction as

necessary. Limit deep tracheal suctioning to 10-15 seconds to avoid
hypoxia. Oxygenate prior to and after suctioning.
Airway adjuncts
a.
The high incidence of hypoxia and risk of aspiration in patients with

traumatic brain injury have been used to justify an aggressive approach to
airway management, including intubation by EMS personnel (Davis et al,
2006). The Prehospital Guidelines recommend that patients with severe
TBI, who demonstrate hypoxia not corrected by supplemental oxygen and
those who lack the ability to maintain their own airway have advanced
airway management.
b.
Of concern, Wang et al (2004) found threefold increased odds of mortality

in those that were intubated in the field after adjustment for injury severity
and other cofounders. The high incidence of hyperventilation following
intubation, desaturation and bradycardia during tube placement, and
undetected esophageal intubation may be important contributors to
increased mortality in intubated patients. Laryngoscopy without benefit of
neuroprotective drugs may be harmful in this subset of patients. Positive
intrathoracic pressure caused by over ventilation may decrease venous
return and impair cardiac output in hypovolemic patients. High intrathoracic
pressures can also cause an increase in ICP.
c.
Hyperventilation results in hypocapneic cerebral vasoconstriction and brain

ischemia. Permissive hypercapnia results in an increase in cerebral blood

flow and may prevent cerebral ischemia, but no studies have yet shown
improved outcomes.
3.
d.
Davis et al (2006) report improved survival rates for intubated patients with
pCO2 values ranging between 30 and 49 mmHg with a rapid decrease in
survival for results less than 30 or over 49 mmHg. Non-intubated patients
did not show the same outcome differentials. In their study, most intubated
patients arrived with pCO2 values outside the optimal range especially with
use of manual ventilation. This underscores the potential dangers of
prehospital intubation associated with positive pressure ventilation and
hyperventilation. This data is important in the ED setting. The use of
ventilators or capnometry-guided ventilations for patients with moderate to
severe TBI is important.
e.
If intubated in the field, check pCO2, tube placement and patency.
f.
If not intubated and procedure is indicated: Prepare equipment for patients

with a GCS 8 as many have a pO2 < 60 torr and are hypercarbic.
(1)
If awake or responsive to pain and/or gag reflex present: Drugassisted intubation with in-line stabilization.
(2)
If unresponsive and/or apneic: Orotracheal intubation with in-line

stabilization.
(3)
Directed intubation: In some patients, facial and upper airway

trauma is such that airway landmarks are all but impossible to see.
Airway access in these patients may be very difficult. Patients may
need to be log rolled onto their side to keep tissues out of the way.
Copious suction is needed. A laryngoscope is used to attempt
glottic visualization, but if not immediately apparent, look for
bubbling air escaping from the trachea with expiration. Have an
assistant compress the chest to create bubbling if necessary.
Attempt to pass the tube through the bubbling source into the
trachea.
g.
If intubation attempts fail and the patient cannot be adequately ventilated

with a BVM, anticipate the need for a rescue airway or salvage airway
(needle or surgical cricothyrotomy).
h.
Gold standard in children may be NO intubation. Insert an oral airway and

attempt ventilations with a BVM.
Nursing participation in the procedure

a.
Monitor patient's hemodynamic baselines and responses during procedure

(BP; HR and rhythm; RR and depth; SpO2; skin color, temperature)
b.
Premedicate hypopharynx with topical anesthetic prior to intubation. Apply

in-line stabilization, lip retraction, Sellick's maneuver, thyroid cartilage
pressure and/or assist with intubation per local protocols.
c.
Observe patient for allergic reaction during and just after drug injection
d.
Document the following:

(1)
(2)
(3)
C.
Name, dose, route, and time of all medications administered

Patient's responses to medications
Pertinent monitoring data: BP, HR, ECG, SpO2 pre & postintubation
Ineffective breathing pattern; potential or actual

1.
Assess general respiratory rate (very fast or slow), depth, pattern and effort.

2.
Assist ventilations as needed with a BVM at 10-12 breaths/minute for adults; 15-20
BPM for children; and 30 BPM for infants (BTF, 2007). If long-term ventilatory
assist is necessary, prepare the patient for intubation and place on mechanical
ventilator.
3.
Current BTF indications for hyperventilation: In the absence of herniation,

routine prophylactic hyperventilation should be avoided during the first 24 hours as
it can compromise cerebral perfusion during a time when cerebral blood flow is
reduced by up to 2/3rds (BTF, 2007) causing cerebral ischemia.
a.
Hyperventilation produces a rapid decrease in the pCO2 that causes

vasoconstriction, decreased cerebral blood flow, and lowers the
intracranial pressure. For each 1 torr drop in pCO2, there is a
corresponding decrease in CBF of 3%.
b.
Hyperventilation may be necessary for brief periods when there is an ICP

25, signs of cerebral herniation such as unilateral or bilateral pupillary
dilatation, asymmetric pupillary reactivity, motor posturing, or neurologic
deterioration (decrease in GCS of more than 2 points when initial GCS was
< 9) after correction of hypotension or hypoxemia (BTF, 1995).
Hyperventilation may be indicated for longer periods if there is ICP
refractory to sedation, paralysis, CSF drainage, and osmotic diuretics.
c.
If hyperventilation is used, ventilate at 12-15 mL VT/kg augmented by 15 L

O2 to maintain pCO2 between 30-35 torr for as short a time as possible.
Allow time for exhalation. If patient fails this regimen, anticipate a poor
outcome. Excessive vasoconstriction can worsen cerebral ischemia. A
PaCO2 of 25 should be avoided.
d.
Aggressive hyperventilation may cause loss of autoregulation. Slight

hyperemia is probably preferable.
Hyperventilation rates
(1)
(2)
(3)
D.
Adolescents and adults:

Elementary school children
Infants and toddlers
16-20 breaths/min
30 breaths/min
35-40 breaths/min (BTF, 2007)
e.
Jugular venous O2 concentration (SvO2), arterial-jugular oxygen content

difference (AVdO2), and CBF monitoring may identify cerebral ischemia if
hyperventilation resulting in pCO2 values < 30 mm Hg is necessary.
f.
Don't hyperventilate or give PEEP in shock as it will increase intrathoracic

pressure and decrease venous return and cardiac output.
Inadequate gas exchange; potential or actual

1.
Level III recommendation: Oxygenation should be monitored and hypoxia (PaO2

< 60 mmHg or O2 saturation < 90% avoided (BTF, 2007).
2.
Clinically assess patient for signs of hypoxemia/hypoxia and hyper/hypocapnia.

Hypoxia (PaO2 <60) generates free radicals and must be corrected immediately.
Most hypoxia resistant cells: pupils; most hypoxia susceptible cells: temporal lobe.
3.
Hypoxemia (apnea, cyanosis, or arterial hemoglobin oxygen saturation < 90%)

must be avoided, if possible, or corrected immediately. Oxygen saturation should
be monitored on all patients with severe traumatic brain injury as frequently as
possible or continuously. Hypoxemia should be corrected by administering
supplemental oxygen to achieve an SpO2 of 90% or greater.
4.
Monitor capnography/end tidal CO2 (normal = 35). EtCO2 increases before ICP
goes up. Use as a monitor of pulmonary blood flow, correct placement of an ET
tube, and adequacy of ventilations and/or chest compressions. Anticipate 100%
FiO2 to achieve a PaO2 > 100 mmHg and SpO2 > 95%

5.
Monitor ABG results: pH, PaCO2; HCO3; BE; PaO2; O2 sat. Maintain normocarbia
or controlled hypercarbia in the absence of clinical signs of herniation (pupillary
dilation or asymmetric reactivity, motor posturing, coma).
E.
Assess for tension pneumothorax, open pneumothorax, or flail chest; resuscitate per Chest
Trauma outline if found.
F.
Alteration in vascular volume, cardiac output, cardiac rhythm, or cerebral perfusion

1.
Assess general rate (fast, normal, slow); presence and quality of peripheral pulses,
and skin condition. Assume hypotension if radial pulse is absent. Hypotension must
be avoided or corrected immediately to maintain CPP > 60 mmHg.
2.
Cold, moist skin suggests hypovolemic shock. Patients cannot loose enough blood
due to intracranial bleeding to cause hypotension except in infants. If pulses are
weak, thready, tachycardic, or absent at the radials and present at the carotids,
attempt to determine the reason. Look for large scalp hematomas or hemorrhage,
tension pneumothorax, hemothorax, pericardial tamponade, hemoperitoneum,
pelvic fracture, loss into an extremity, and retroperitoneal bleeding.
3.
While undressing the patient, quickly look for obvious wounds or deformities.
4.
If patient as altered mental status, maintain supine position to enhance CPP as

autoregulation may be lost. Do not elevate the head of the backboard.
5.
Control external hemorrhage with direct pressure and pressure dressings or

topical hemostatic agents. These are particularly effective for scalp injuries. Wrap
pressure dressings circumferentially above the ears over a vascular pressure point.
Do not apply pressure over a possible depressed skull fracture. Cover open
scalp/skull wounds as needed. Stabilize impaled objects.
6.
Cardiac monitor: 90% have dysrhythmias which are brainstem mediated due to
release of catecholamines
7.
Maintain euvolemia/mean arterial pressure. The prevention of shock and/or

prompt treatment of hypotension are important considerations in the patient with
TBI (BTF, 2007).
a.
Level I: There are insufficient data to support any treatment standard given
that it would be unethical to conduct prospective randomized trails
concerning the effects of hypotension and hypoxia on patients with TBI.
b.
Level II: Blood pressure should be monitored and hypotension (systolic

blood pressure in adults < 90 mmHg avoided. In children, hypotension can
be defined as systolic BP < the fifth percentile for age.
c.
Fluid resuscitation in patients with TBI should be administered to avoid

hypotension and/or limit hypotension to the shortest duration possible.
Fluid therapy is used to augment cardiac preload, support cardiac output,
blood pressure and peripheral oxygen delivery in an effort to maintain
adequate cerebral perfusion pressure limiting secondary brain injury.
d.
The most commonly used resuscitation fluid is an isotonic crystalloid

solution. This is administered in quantities necessary to support blood
pressure in the normal range, though there are little data to support a
specific target blood pressure. Inadequate volume resuscitation can
precipitate sudden hypotension and should be avoided. Fluid resuscitation
should be done in such as way that does not cause secondary blood loss
or hemodilution. Hyperosmolar resuscitation, generally using hypertonic
saline with or without Dextran, significantly increased BP and decreased
overall fluid requirements (BTF, 2007).
e.
Avoid dextrose containing solutions unless hypoglycemia is confirmed due

to their potential risk of worsening CNS lactic acidosis and cerebral edema

G.
f.
Administer volume expanders and blood products as prescribed.
g.
If a hypotensive trauma patient does not respond to fluids, the brain

becomes a secondary consideration (ATLS, 2005).
D = Disability: Mini-neurological exam: GCS, pupil size and response, gross motor
function, and possible glucose check. Coma is defined as a GCS 8 (ATLS, 2005).
Repeated assessments are crucial to monitor for presence of increased ICP.
1.
Glasgow coma score

a.
The GCS was published in 1974 and revised in 1977 by Drs. Graham
Teasdale and Bryan Jennett to serve as a rapid, objective, quantifiable and
reproducible tool to assess the depth and duration of impaired
consciousness and coma at the bedside 24-hours or so after brain injury or
brain surgery. Both Teasdale and Jennett were affiliated with the University
of Glasgow in Scotland, thus the citys name was incorporated into the title
of the scale (Fischer & Mathieson, 2001).
b.
It was not originally conceived to evaluate all trauma patients. However,

subsequent research has shown that severely traumatized patients who
are in a shock-like state will experience deterioration in the GCS as it really
measures brain function rather than brain injury and brain function can be
affected by many things, including shock.
c.
Originally known as the Coma Index, it reported three independent

subscores of motor, verbal, and eye. It evolved into the Glasgow Coma
Scale as the minimum score for each variable was changed to 1 and the
sum of the three components was reported as a single score.
d.
One huge advantage of this scoring system is its simplicity. With a little
practice, all caregivers can learn to accurately obtain and document this
aspect of the neuro assessment.
e.
Scale is used to
(1)
(2)
(3)
(4)
decide whether injury severity is sufficient to require or justify

certain types of treatment;
compare different series of injuries; and
predict the degree of the ultimate recovery to be expected
(Norwood et al, 2002).
Examples:
(a)
BTF Guideline: Class II data indicate that the prehospital

measurement of the GCS score is a significant and
reliable indicator of the severity of head injury, particularly
in association with repeated scoring and improvement or
deterioration of the score over time. A single
measurement of GCS does not predict outcome,
however, a decrease of 2 or more points with a GCS of 9
or lower suggests serious injury. Studies indicate that a
GCS of 3-5, as well as lack of improvement or
deterioration of GCS score by 2 points or more from the
field to the ED have at least a 70% positive predictive
value for a poor outcome.
(b)
Liberman et al (2003) reported that trauma patients

presenting with a GCS of 3 as well as fixed and dilated
pupils in the absence of paralysis, sedation, substance
abuse or the use of atropine have no reasonable chance
of functional recovery.

(c)
f.
Scoring systems that incorporate GCS into their calculations:

(1)
(2)
(3)
(4)
(5)
(6)
Revised Trauma Score (RTS)

Trauma and Injury Severity Score (TRISS)
Severity Characteristic of Trauma score
Acute Physiology and Chronic Health Evaluation (APACHE) II and
III scores
Circulation, Respiration, Abdomen, Motor, Speech Scale
Simplified Acute Physiology Score II
Strengths
Limitations
Simplicity
Provides a common language to report
neurologic findings based on bedside
observations
Ability to trend over time
g.
h.
American College of Surgeons (ATLS, 2005)

recommends intubation or a surgical airway for any
trauma patients with a GCS of 8 or less.
Variation in inter-rater reliability

Inconsistent use by caregivers in prehospital and hospital settings
Decreased BP (if SBP < 80, cant assess GCS with respect to
possible outcomes)
Hypoxia
Hypothermia
Hypoglycemia
Sedating or paralyzing drugs
Intubated patients
Patients with facial/ocular trauma
Hearing impairments
Language barrier
Children younger than 3 years
Alcohol/drug intoxication
Patients that speak a foreign language or have immature
language skills
GCS relationship to mortality differs considerably between blunt
and penetrating head trauma
Obtaining the GCS: GCS should be assessed through interaction with the
patient (i.e., by giving verbal directions or for patients unable to follow
commands, by application of a noxious or painful stimulus).
(1)
Ideally, GCS scoring should occur after a clear airway is

established, and after hypoxemia and hypotension have been
corrected, the patient has been resuscitated and before
administration of sedative or paralytic agents or after these drugs
have been metabolized (Livingston, 2000; BTF, 2007).
(2)
Components: Unconsciousness can be simplistically defined as

failure to respond appropriately to environmental stimuli. Coma is
defined as a state of unconsciousness from which the individual
cannot be awakened, in which the individual responds minimally or
not at all to stimuli, and initiates no voluntary activities (BIAA,
2004). The GCS is the sum of three independent coded values
that measure a patients eye opening, verbal, and motor
responses either spontaneously or in response to verbal or painful
stimuli (Healey et al, 2003). Always report the patients BEST
response, even if different on one side of the body from the other.
Best eye opening: Assesses both wakefulness, arousal mechanisms in

the brainstem, and content of behavioral response. Ask the patient, What
happened to you? If the patient opens his eyes, then ask the questions in
the verbal and motor section of the GCS to determine the total score.

(1)
If the patient does not open his or her eyes, apply a central pain
stimulus. Pinch the earlobe or apply pressure over the supraorbital
ridge. If the patient is spontaneously moving all four extremities,
apply blunt pressure to the nailbed or pinch the anterior axillary
skin. Alternative method of appropriate pain stimulus: pinch
muscles to top of shoulder.
(2)
Eye opening to command or speech is a higher level of stimulus

recognition and one can assume that the cerebral cortex is
processing information..
Spontaneous: Eyes are open or open spontaneously when a person approaches the bedside or
is observed while caring for the patient. Indicates an intact arousal mechanism.
To voice: Eyes open to either spoken or shouted verbal stimulation.
To pain: Eyes open to a painful stimulus. Use only when patient does not open eyes to verbal
stimulus. Opening to pain only represents a lower brain functioning.
No eye opening: despite painful stimuli
Confrounding
variables
Chemically sedated or paralyzed/or eyes swollen shut/orbital trauma; cranial nerve injury.
i.
Best verbal response: Assesses the eloquent cortex (where we speak)

by evaluating the content and context of speech. While this evaluates a
high level of cognitive function, its absence does not imply a total loss of
function. This is a difficult area to score with consistency, especially
between the options of 4 and 5.
Converses and is oriented to person, where he or she is located (place), time (approximate
date - at least month, season or year), and situation.
Converses but is confused or disoriented. Should have a good attention span, but responses
may be inaccurate.
Inappropriate words, poor attention span; does not converse. The patient may repeat random,
repetitive words, numbers, or profanity.
Incomprehensible sounds, moans, or cries
No sounds even after painful stimuli
Confounding
variables
Intubated, paralyzed, sedated, intoxicated or chemically impaired, maxillofacial trauma, grossly

swollen tongue, cricothyrotomy, tracheotomy, mutism, aphasia, hearing loss, language barrier,
dementia, and/or psychiatric disorders.
j.
Best motor response: Assesses both arousal and content of behavioral

response. This element is the least affected by trauma. It allows evaluation
of interface between sensing a stimulus, interpreting the information and
reacting to it. Note best response, even if seen only unilaterally.
Obeys commands: Ask a conscious patient to move his fingers or toes. Ideally, would obey a
motor command to move an extremity. If limbs are paralyzed due to high spine trauma, have the
patient blink eyes in response to a command.
Localizes (Protective response); Localizes pain stimulus and attempts to remove it or move
away from it with purposeful movement. This is best assessed by pinching the trapezius muscle or
the ear lobe and observing if the patient tries to move your hand away or to pull away from the
pain source. The hands should move across midline or above the nipples to confirm purposeful
movement. Behaviors that indicate this response: pt. tries to remove a c-collar or oxygen mask;
moves the arm in which a pain stimulus like an IV start or blood draw is being applied. This
response indicates that the parietal lobe is functioning to to interpret and localize the stimulus and
that it can communicate with the motor cortex in the frontal lobe for purposeful movement..

4
Withdraws: Generalized purposeful movements pulling both arms in toward the torso. Pt. knows
he is in pain, but cannot localize the stimulus. This response indicates that pain pathways to the
thalamus are intact, but the parietal lobe is not interpreting or localizing the pain source.
Abnormal flexion (old decorticate posturing): Adduction of upper extremities with flexion or the
wrist or elbows and extension of the legs in non-purposeful, reflexive movement. Indicates lesions
in the cerebral hemispheres or internal capsule (Fischer & Mathieson, 2001).
Abnormal extension (old decerebrate posturing): Adduction, hyperpronation and extension of

upper extremities, internal rotation of shoulders, extension and plantar flexion of the legs in
nonpurposeful movement. May progress to arching of the back (opisthotonos). Reflects midbrain
to upper pontine damage. Posturing is a brain stem reflex.
No response (movement) to pain
Confounding
variables
Chemically or traumatically paralyzed, peripheral nerve injury, extremity trauma with

immobilization, pain, inability to comprehend commands, dementia, psychiatric disorders,
alcohol/drug intoxication.
k.
There is currently debate over the sensitivity and specificity of GCS scoring
with evolving consensus that the motor component alone can predict
neurological outcomes (Gill et al, 2005).
l.
Recommended scoring for intubated, sedated, or paralyzed patients from

the National Trauma Data Bank:
(1)
Record the score exactly as it is measured (Legitimate, unaltered

value). In a separate field, add any of the following codes that
apply:
(a)
(b)
(c)
(d)
(2)
m.
Intubated
Intubated and paralyzed
Sedated
Untestable
The legitimate score is accurate if one is describing the results at

the moment, but it is highly skewed if using the score to determine
the seriousness of a head injury or if trying to predict prognosis.
When patients are sedated, using the GCS recorded before
sedation is preferable to the assumption of normalcy (Livingston et
al, 2000).
Young children: Champion et al described a better method to describe the

verbal responses of children younger than three years:
(1)
(2)
(3)
(4)
(5)
n.
T:
TP:
S:
U:
5:
4:
3:
2:
1:
Appropriate for age

Consolable cries
Persistent irritation
Restlessness and agitation
No verbal response
Interpreting the results: GCS severity distinctions can be debated

depending on full physical exam but management of brain injury is often
still determined by GCS (ATLS, 2005).
(1)
GCS 13-15 - Mild head injury: Should be awake with no

significant focal deficits. Increasingly, a GCS of 15 is considered a
mild head injury. Risk levels for those with a GCS of 15 can be
stratified as follows:
(a)
Low risk: No symptoms or previous symptoms of

dizziness, headache or vomiting.
(b)
Intermediate risk: Loss of consciousness or posttraumatic

amnesia.

(c)
o.
2.
VIII.
High risk: Severe headache, persistent nausea or more

than one vomit (Batchelor & McGuiness, 2002).
(2)
GCS 9-12 - Moderate head injury: Patient presents with altered

sensorium and/or focal deficits but is still able to follow simple
commands. Scores within this range represent 10% of all head
injuries. Up to 20% deteriorate to coma; 40% have abnormal CT
scans, and 8% require surgery (ATLS, 2005). Should be admitted
for observation, even if the CT is normal.
(3)
GCS 3-8 - Severe head injury: Patients within this range do not
follow simple commands after resuscitation and stabilization. They
are at risk for secondary brain injury from hypoxia, hypotension,
and anemia.
Accurate Glasgow Scoring is essential in determining the need for

resuscitative interventions, selecting the appropriate receiving hospital,
trending a patient over time, and calculating a RTS.
Treating the causes of altered mental status (AMS): Hypoglycemia and drug
toxicity have been reported as the cause of traumatic events. As with brain injury,
hypoglycemia and drug intoxication may present with AMS with or without focal
neurologic deficits. It is recommended that patients with AMS of undetermined
etiology have a rapid glucose determination (BTF, 2007). Evidence exists that
patients with ischemic brain injury with hyperglycemia (>200) have worse outcomes
than those with normal serum glucose levels. An injured brain is hypermetabolic
and glucose intolerant. If glucose levels or available, do not give dextrose unless
they are hypoglycemic. Use clinical assessments when making treatment
decisions. Consider the presence of drug toxidromes that may be reversible.
H.
Expose to examine and recover to maintain warmth
I.
Adjuncts to primary survey

1.
Place urinary catheter as ordered; carefully monitor and record intake and output.
2.
Insert an NG or OG tube depending on the nature of the trauma to prevent gastric

distention and to decrease the risk of vomiting and aspiration.
Secondary survey
A.
Chief complaint and SAMPLE history: What are the patients current symptoms?
1.
2.
Nursing diagnosis: Pain. Headache may be due to cerebral edema, vascular

dilation, traction on bridging veins, or stretching of the arteries at the base of the
brain.
a.
Ask the patient about the onset, provocation/palliation efforts, quality

(throbbing, constant/intermittent etc.) region/radiation/recurrence, severity
(0-10), and time (how long has this lasted?)
b.
Ask about associated S&S such as visual disturbances, nausea, vomiting,

sinus congestion, photophobia, etc.
c.
If the patient has a known hematoma, contusion, cerebral edema,

aneurysm, or AV malformation, worsening headache may signal an
increase in the size of the lesion, additional bleeding, or brain tissue
swelling. Notify a physician immediately.
SAMPLE history
a.
If the patient is conscious, ask if they lost consciousness (or remember

waking up)
b.
Did the patient vomit?

B.
c.
Allergies
d.
Has the patient ingested any drugs or alcohol?
e.
Medications: Patients on warfarin (Coumadin) who sustain a traumatic

intracranial hemorrhage have a mortality rate that is 5 times that of patients
not anticoagulated and is a common cause of preventable death (Ivascu et
al, 2006). These authors recommended a very aggressive approach to
anticoagulated patients: immediate triage; rapid ED physician evaluation;
head CT with immediate reading; and 2 units of fresh frozen plasma (FFP)
thawed while patient is in CT. If CT is positive, give FFP and vitamin K, and
then an additional 2 units of FFP two hours later. Admit to ICU or take to
surgery if required. If CT is negative, admit for 24 hours of observation
(Sutphen, 2006).
f.
Significant underlying illnesses
g.
Last oral intake
h.
Ask about mechanism of injury and events surrounding the trauma
Vital signs: The vital signs may provide very valuable information about the patients
underlying injuries. Obtain a full set of manual vital signs before hooking the patient up to
automated devices. Repeat at least every 15 minutes while unstable or as indicated by
local protocols.
1.
2.
Respiratory rate, patterns, and depth. Provides more clues as to the location of
pathology than any other vital sign. Be particularly alert for sudden apnea and be
prepared to assist ventilations. Look for diaphragmatic breathing, an indication of
intercostal muscle paralysis.
a.
Eupnea: Normal pattern of ventilations.
b.
Bradypnea: Decreased rate. Respiratory rate may slow initially after an

acute increase in ICP.
c.
Cheyne-Stokes: Crescendo/decrescendo respirations (waxing and

waning depth and rate) with periods of apnea up to 20 seconds; seen with
increased ICP. Due to increased sensitivity to CO2 that results in a change
in depth and rate and decreased stimulation from respiratory centers that
results in apnea. Lesions are most often located bilaterally deep within the
cerebral hemispheres, diencephalon (thalamus and/or hypothalamus) or
basal ganglia.
d.
Central neurogenic hyperventilation: Regular, sustained, increased rate

and depth of respirations with forced inspiration and expiration. Thought to
be due to release of the reflex mechanisms for respiratory control in the
lower brainstem and results in decreased CO2 and alkaline pH. Giving
oxygen does not change the pattern. Lesion location unclear, often in the
midbrain and upper pons.
e.
Apneustic: A pause of 2-3 seconds noted after a full or prolonged gasping

inspiration followed by an inefficient, brief expiration. May alternate with an
expiratory pause. Lesion located in the lower pons, usually due to a basilar
artery occlusion.
f.
Cluster: Clusters of slow irregular breaths with periods of apnea at

irregular intervals (gasping breathing has features similar to cluster
breathing). Lesion in the lower pons or upper medulla.
g.
Ataxic (Biot's) breathing: Complete irregular, unpredictable pattern with

deep and shallow random breaths and pauses. Lesion in the medulla.
Pulse: Count rate, evaluate rhythmicity, quality, location; compare equality.

3.
BP
a.
Blood pressure should be measured using the most accurate system

available under the circumstances. It should be obtained as often as
possible and, if possible, continuously by trained medical personnel.
b.
Hypotension (SBP < 90) must be avoided or corrected immediately to

maintain a CPP > 60 (BTF, 2007).
c.
A single prehospital BP < 90 was associated with a doubling of

mortality as compared with a matched group of patients without
hypotension (Traumatic Coma Data bank). A combination of hypoxia and
hypotension increases mortality to 75% (ATLS, 2005).
d.
It is possible that SBP needs to be significantly higher than 90 to maintain

CPP but no studies have been performed to determine an ideal number.
Once ICP monitoring has been established, manipulation of BP should be
guided by CPP management (BTF, 2007).
e.
In children, the following SBPs have been linked to poor outcomes:

(1)
(2)
(3)
(4)
f.
C.
SBP, widened pulse pressure

P
RR
Decompensatory alterations
(1)
(2)
(3)
4.
65 mmHg
70-75 mmHg
75-80 mmHg
80-90 mmHg
Compensatory alterations in vital signs: Cushing's triad

(1)
(2)
(3)
g.
0-1 years:
1-5 years:
5-12 years:
12-16 years:
Hypotension (Chesnut et al, 1998)

Tachycardia (grave sign)
ECG changes:
(a)
Q wave with ST depression
(b)
Prolonged QT interval
(c)
Dysrhythmias: atrial: PACs, biphasic Ps, A-Fib
Evaluate core temperature for hyper or hypothermia. Note: The anterior

hypothalamus keeps us from getting too hot (radiator). It sits right next to the
pituitary stalk and is directly stimulated at 42 C. The posterior hypothalamus is the
heater. It sets the hypothalamic set point and raises the body temp. The patient will
change temps without sweating or gooseflesh. Each degree increase in temp. =
6% increase in CBF.
Review of systems - See Patient Assessment module

Focused exam of head should include inspection for deformities, asymmetry, contusions,
abrasions, puncture wounds, bruising, lacerations, swelling/edema, bleeding, and drainage
of CSF from eyes, nose (rhinorrhea), mouth or ears (otorrhea). Inspect eyes, nose, mouth,
and ears for signs of injury.
D.
Focused neuro exam: Extent of exam depends on the patient's level of consciousness
and acuity. If awake, alert and cooperative, can perform detailed assessment. If comatose,
the nursing exam is usually limited to GCS, pupillary check, and pain responses.
1.
Level of consciousness: Most sensitive indicator of neurological status. In a

conscious patient, altered mental status (AMS) is the first sign of deterioration. To
provide consistency, describe patient's response in specific behavioral terms.
a.
Arousal
(1)
Alert: Awake, responds immediately to commands

b.
2.
3.
Lethargic: Response to commands may be incomplete or slow.

Needs stimuli, but obeys. Returns to sleep.
(3)
Stuporous: Decreased awareness. Does not obey commands.

Spontaneous or purposeful movements may be noted.
(4)
Comatose: Unable to arouse. Abnormal flexion or extension to

stimuli. May be flaccid (Wooten, 27).
Awareness: Orientation to person (himself and/or loved ones), place and

time. Determine if changes are new or if they pre-date the trauma (e.g.,
dementia)
Mental status exam

a.
Assess for short-term memory (amnesia); shortened attention span;

difficulty following simple/complex commands.
b.
Determine if affect and behavior reveal restlessness, agitation, irritability

or combativeness. Evaluate cognition by determining if the patient's
responses to questions are appropriate or inappropriate.
c.
Ask a conscious patient if they are experiencing audio or visual

hallucinations.
d.
Evaluate cognition and their ability to process information: A study by

de Kruijk et al (2002) found that the most prevalent symptoms reported in
those admitted to an ED with mild TBI are forgetfulness, drowsiness,
headache, dizziness, trouble concentrating and lightheadedness and will
need cognitive retraining. Determine if the patients responses to questions
are appropriate or inappropriate. Anticipate slowing of thought processing
speed.
Nursing diagnosis: Alteration in cognitive function

a.
b.
4.
(2)
Attempt to orient patient to person, place, time and situation.

Restrain patient only as necessary to provide safety.
Cranial nerve exam: see Neuro A&P study guide

a.
b.
I: Olfactory (smell detection and interpretation): Probably the least tested

and least helpful in neurological testing because of changes that occur from a
wide rage of influences, i.e., rhinitis, craniofacial trauma, smoking. Evaluate in
patients with suspected anterior basilar skull fractures, those who complain of
taste disturbances, seizures, or headaches. Do not use ammonia capsules as
they trigger pain receptors of the trigeminal nerve.
(1)
Ask patient to close eyes. Testing one nostril at a time, put a

freshly opened alcohol wipe or a bar of soap near their nose and
ask them to tell you what they smell.
(2)
Results: Lost entirely - anosmia. Lost some - hyposmia.
II: Optic Transmits visual information to occipital lobe for processing (visual
acuity; visual fields):
(1)
Visual acuity: Ability of the eyes to perceive visual detail (near

and/or far). Ask patient if they wear corrective lenses or contacts.
Testing one eye at a time, have them read your name badge or a
near car, count fingers at 6 inches, detect the movement of your
hand, or detect the projection of light in descending order of visual
acuity. Worst visual acuity is an NLP (no light perception) eye.
Assess for double vision, visual deficits.
(2)
Visual fields: peripheral vision

(3)
(a)
Exam: Have the patient cover one eye and sit facing you.
Extend your arm out perpendicularly and wiggle a finger in
each of the visual quadrants. Ask patient to identify what
quadrant the movement is in.
(b)
Results: Visual fields can be impaired in head

injury/stroke. With one hemisphere disease, neither eye
sees the contra-lateral environment (hemianopsia).
Funduscopic exam
(a)
(b)
(c)
Evaluate appearance of optic disk

Assess for venous pulsations
Look for retinal hemorrhages
III: Oculomotor (regulates pupil size; constriction and reactivity; eye

movement up, down and in to the nose; lifts eye lid). There are insufficient
data to draw conclusions on the diagnostic and prognostic value of findings
on the pupillary exam. Conditions that affect pupil size and reactivity
besides brain stem or CN III trauma: hypoxia, orbital trauma, drugs
diabetes mellitus (affects blood supply to the nerve); alcohol; aneurysms;
and hypothermia. Pupils should be assessed and documented for each
eye after the patient has been resuscitated and stabilized. The duration of
pupillary dilation and fixation should also be documented (BTF, 2007).
c.
(1)
Size - Normal range: 3-4 mm. Unilaterally or bilaterally dilated

pupils unresponsive to light in an unconscious patient may indicate
transtentorial uncal herniation due to ipsilateral compression of CN
III. This patient is in need of emergent interventions to lower the
intracranial pressure. A unilaterally fixed and dilated pupil may also
reflect direct injury to the orbit or globe.
(a)
(b)
(c)
(d)
Midrange bilaterally reactive

Midrange, bilaterally non-reactive
Pin point bilaterally non-reactive
Dilated, bilaterally non-reactive
= midbrain OK
= midbrain lesion
= pontine lesion
= medullary lesion
Drugs and toxins that affect pupil size/reactions

Constriction
Dilation
Sympathetic blockade: beta blockers, MAO inhibitors
Parasympathetic stimulant: acetylcholine, narcotics,

methadone, neostigmine, nicotine, physostigmine,
pilocarpine, tetraethyl ammonium
Sympathetic stimulants: Cocaine,

epinephrine, phenylephrine, tyramine
Parasympathetic
blockers:
Alpha-methyldopa,
atropine, botulinus toxin, chlorpheniramine maleate,
clonidine, curare, dopamine, doxepin hydrochloride,
ibopamine, imipramine hydrochloride, jimson weed,
methantheline bromide, scopolamine, toadstool toxin,
wild sage.
Early and late barbiturate intoxication
High blood alcohol levels over 300 mg/dl
Narcotics
(2)
ephedrine,
Shape Pupils are generally round. Assess and report changes

immediately.
(a)
Ipsilateral oval pupil frequently heralds the early stages of

transtentorial herniation with compression of CN III. If
unreversed, the pupil will continue to dilate and become
nonresponsive to light.
(b)
(c)
Tear drop: often means ruptured globe

Key hole: old iridectomy during cataract surgery

(3)
Equality Inspect simultaneously before checking the light reflex.

Some people have naturally unequal pupils with less than a 20%
difference (1 mm) (anisocoria) with no pathologic significance.
Others show unequal pupils due to an earlier injury or neck surgery. If
comatose, attempt to find their picture from a driver's license or ask
significant others to determine if pupils were always unequal or
whether it is a new development. If condition is physiologic, the pupils
should maintain their relative sizes in both bright and dim light.
Greater than a 1 mm difference in a patient with AMS is significant.

If a disparity is accentuated in dim light, suspect Horner's Syndrome
(CN III deficit). If > 3 years of age with a dilated pupil after trauma oxygenate and assume brain shift.
(4)
Reactivity (CN II & III): The light reflex depends on an intact

afferent system that carries the light impulse on the Optic nerve
(CN II) to the occipital lobe to be interpreted as too much light and
parasympathetic fibers on the outside of CN III from the midbrain
to the pupil. A bright light shined into one eye should result in brisk
constriction of at least 1 mm of both the ipsilateral eye (direct
response) and the contralateral eye (consensual response). The
Oculomotor nerve has its nuclei adjacent to the midbrain areas
controlling consciousness. Assessing pupils is essential in all
patients with altered mental status. The nerve exits the midbrain
under the medial portion of the temporal lobe called the uncus. It is
susceptible to compression from edema, intracerebral
hemorrhage, and epidural or subdural hematomas. Unilateral CN
III compression compromises the efferent pathway, thus blocking
the direct light response, while preserving the consensual
response (swinging light test) (BTF, 2007). See note under size for
significance of non-reactivity.
(a)
(b)
(c)
(d)
(e)
(f)
d.
Have patient look straight ahead in as dim a light as

possible
Bring light in from the side (out of the visual axis) and
shine into one eye.
Observe that pupil for its response (direct response). Note
as brisk, sluggish, or non-reactive. Should briskly constrict
at least 1 mm.
Bring light in again from the side and shine into the same
eye. Observe the opposite pupil for its response
(consensual response).
Repeat the procedure on the other eye.
If a dilated, non-reactive pupil is due to injury inside or
outside of the brainstem, it is likely that this will be
accompanied by other prominent neurologic symptoms,
like diplopia or altered consciousness (Goldberg, 31).
(5)
Accommodation: Pupil should constrict when the focus changes

from a distant object to a nearby object. Argyll-Robertson's or
"prostitute's pupil" - accommodates, but does not respond.
(6)
Hippus: Pupil spontaneously dilates and constricts after a light

stimulus. Indicates ICP. Seen in pre/postictal patients. Both eyes
= herniation.
(7)
Observe eye lid for ptosis.
Gaze palsies: CN III, IV, VI Control lateral and vertical gaze. Examine
together as they collectively control ocular motility. When stimulated, these
muscles shorten.

(1)
(2)
e.
Exam: Extra ocular movements (EOM's) - Have patient follow a

finger in all six directions of gaze. Eyes should move together. Assess
conjugate or dysconjugate gaze.
(a)
IV (Trochlear) innervates superior oblique muscles that

depress the adducted eye and help move the eye in other
positions.
(b)
VI (Abducens) innervates lateral rectus muscle and

normally pulls eye towards ear; most sensitive nerve (first to
become dysfunctional) in the presence of ICP.
(c)
III (Oculomotor) supplies all the other ocular muscles

(superior rectus, medial rectus, inferior rectus, inferior oblique
and levator palpebrae).
Results: May have traumatic III, IV, and VI nerve palsies

(a)
If large pupil, ptosis and eye pulled to ear: assess for

complete 3rd nerve loss. Eyes look towards a lesion as
neither can move to the contralateral side. Sign generally
first seen just before herniation.
(b)
If eyes deviate toward the nose, anticipate loss of CN VI

and ICP.
(c)
Pupils fixed in the midline indicate compression of CN III

or the brain stem. Tested in unconscious patient (see
Dolls-Eyes maneuver).
(d)
Roving eyes = frontal lobe dysfunction
(e)
(Pearl: before 6 or 7 months old, nerves are unmyelinated,

that is why infants often look cross-eyed
(f)
Nystagmus may be horizontal or vertical. Slight nystagmus

at the extreme lateral position is normal. Marked nystagmus
on extreme lateral gaze or forward gaze is abnormal. Jerk
nystagmus with a fast and slow component suggests CNS or
PNS lesion. Vertical nystagmus suggests brain stem lesion.
(g)
Diplopia or double vision should disappear when one eye is

covered. Exception: dislocated lens, retinal detachment.
V: Trigeminal: Sensation to facial skin, cornea, and various mucous

membranes (ocular, nasal, and oral) by way of three branches: ophthalmic,
maxillary, and mandibular. Mandibular branch also supplies motor ability to
muscles of mastication.
f.
(1)
Sensory component: Test by whisping cotton swab across midline of

forehead, upper lip/cheeks and chin. Alternate with broken tip of cotton
swab to distinguish sharp from dull. Blink reflex: With eyes closed,
gently stroke lashes or tap forehead between the eyebrows (glabellar
tap) to check for a blink reflex.
(2)
Motor component: Have patient bite down and clench teeth to test
occlusion and strength of temporalis and masseter muscles.
(3)
Results: Cerebral lesion results in full loss of sensation on opposite

side of the face. Peripheral nerve damage will result in deficit on one
branch. Unilateral weakness or the inability to contract the jaw
muscles suggests a trigeminal nerve lesion. Bilateral dysfunction
suggests motor neuron involvement.
VII: Facial: : Motor to muscles of facial expression; closes eye lids

g.
h.
i.
(1)
Exam: Inspect face during conversation for any asymmetry, tics, or

abnormal movements. Have patient smile, frown, open and close
eyelids against resistance, puff out cheeks, whistle - observe for
asymmetry or weakness on one side or flattening of the nasolabial
fold. When lids are tightly closed, assess if one side shows more
lashes than the other. If so, motor deficit on that side.
(2)
Taste from the anterior 2/3rd of the tongue (salt, sour, sweet) and
sensory from the soft palate and salivary glands. Not usually tested.
(3)
Results: Lesions generally result in contralateral paralysis of the lower

face (below the eye) due to bilateral connections to the forehead and
eyelids from each hemisphere. Typical stroke results in weakness in
elevating the corner of the mouth, but no significant weakness in
wrinkling the forehead. Bell's palsy or peripheral nerve damage results
in total ipsilateral hemi-facial paralysis.
VIII: Vestibulocochlear: Two separate nerves purely sensory: vestibular

function and cochlear (auditory) function.
(1)
Exam: Check auditory reception/equality through whispered speech.

Softly whisper a phrase, word or number in each ear and ask the
patient to repeat it. Have patient hum. If a conductive defect, the
poorly hearing ear hears the hum louder. Can test on self by occluding
one ear and humming.
(2)
Results: Auditory information is processed bilaterally, so may not be

affected. If CN VII has dysfunction, check CN VIII very carefully as
they run together.
IX & X: Glossopharyngeal & Vagus: Examine together; lifts palate, provides

gag reflex
(1)
Exam: Have patient say, "Ah" or repeat "Ha, ha, ha". Look for
elevation of the palate (normal) or deviation of uvula (abnormal).
(2)
Results: Vagal dysfunction will result in hoarseness or vocal cord

paralysis. Not significantly affected by unilateral cerebral lesions.
XI: Spinal accessory: Supplies sternocleidomastoid muscles and the upper

portion of the trapezius muscles. Sternocleidomastoids on each side of the
neck turn the face to the opposite side. An isolated XI nerve does not exist
(Henry, 2004)
(1)
j.
5.
Exam: Have patient turn head against your hand and shrug shoulders
with and without resistance. Assess equality of strength, bulk of
muscle.
XII: Hypoglossal: Supplies most of extrinsic lingual muscles.

speaking normally, do not test XII separately.
If patient is
(1)
Exam: Have patient stick out tongue. Observe any asymmetry,

deviation or atrophy. Tongue usually points to side of a lesion. Have
patient push tongue into cheek against resistance, assess for
strength.
(2)
Result: Weakness on one side of the tone will cause the tongue to
deviate to that side. Rare for this nerve to be affected.
Motor exam
a.
Assess spontaneous, purposeful movement, muscle tone & strength to

gravity and against resistance. Have patient extend arms in front of them
with palms up and eyes closed. Watch for pronator drift to indicate
unilateral weakness.

b.
Conscious patient: Assess ability to shrug shoulders, flex and extend

elbows and wrists, hold fingers spread open against resistance and to
open fingers against resistance; flex and extend knees, plantar and
dorsiflex feet; wiggle toes.
c.
If unconscious: Observe spontaneous or purposeful movements and then

begin applying stimuli from least noxious to pain. Assess for weakness by
holding up both upper extremities and releasing them simultaneously. A
weak extremity will fall more quickly. To check lower extremities, bend the
knees and place feet together flat on the cart. Hold the knees together and
release at the same time. A weak or paralyzed limb will fall immediately.
d.
Grading function
(1)
(2)
(3)
(4)
(5)
(6)
e.
Movement/strength abnormalities
(1)
(2)
(3)
(4)
f.
8.
Decreased: flaccid/atonic
Increased: spasticity, rigidity
Sensory exam
a.
b.
c.
d.
e.
7.
Paresis (weakness)
Paralysis (inability to move at all)
Posturing: Abnormal flexion or extension
Clonus: Spasm in which contraction and relaxation alternate in
rapid succession
Muscle tone abnormalities

(1)
(2)
6.
5 = normal muscle strength

4 = normal range of motion against some resistance
3 = normal range of motion against gravity only
2 = weak contraction; unable to overcome gravity
1 = slight muscle contraction; no joint movement
0 = complete paralysis
Superficial touch
Superficial and deep pressure/pain
Sensitivity to heat and cold
Sensitivity to vibration
Proprioception: joint position sense
Cerebellar exam
a.
Have patient rapidly turn their hands palm up and palm down (rapid
alternating movements), rotate their hands in concentric circles (posting),
touch their finger to your finger (light on an object), and run the heel of one
foot down the shin of the opposite leg.
b.
An inability to smoothly start and stop or coordinate motion is called ataxia

and may indicate cerebellar dysfunction
Reflex exam
a.
DTRs, anal wink
b.
Babinski: upper motor neuron (UMN) lesion
c.
Brainstem
(1)
Doll's eyes (oculocephalic reflex): Done only after C-spine is

cleared in a comatose patient
(a)
Lift both eyelids. Rapidly turn the head from midline to one
side.

(2)
(b)
Normally, the eyes continue to look upward at the ceiling,

so they appear to move in a direction opposite to the way
the head is turned, i.e., when head is rapidly turned to
right, eyes appear to move left.
(c)
Record as normal response, abnormal response

(dysconjugate or asymmetrical eye movement), or
pathologic response (no movement of either eye so they
move in the direction the head is turned - like eyes painted
on a doll).
Calorics; oculovestibular reflex

(a)
(b)
(c)
(d)
(e)
IX.
Performed when the oculocephalic test is equivocal or

contraindicated
Verify integrity of the tympanic membrane
Irrigate the tympanic membrane with ice water
Normal response: slow deviation of eyes toward the side
of the stimulus followed by rapid override by the cortical
centers to direct eyes back toward the midline. Creates
impression of nystagmus away from cold.
Abnormal response: eye does not move
Definitive interventions
A.
Currently, there is no treatment that can prevent nerve damage or promote nerve healing.
After ABCs are addressed, management is aimed at early CT scanning, immediate
evacuation of intracranial mass lesions, followed by aggressive management in an ICU that
includes ICP monitoring. This is done to maintain cerebral perfusion and oxygenation and
to control and prevent complications of secondary injury including increased intracranial
pressure.
B.
Monitor/maintain cerebral perfusion

1.
2.
3.
4.
C.
ICP monitoring: The only way to reliably determine CPP and cerebral
hypoperfusion is to continuously monitor ICP and BP (BTF, 2007).
Transcranial Doppler
Jugular venous oxygen extraction
Direct or indirect cerebral blood flow monitors
Intracranial pressure (ICP) monitoring

1.
Recommendations: (BTF, 2007)

a.
Level I: There are insufficient data to support a treatment standard for this
topic.
b.
Level II: Intracranial pressure (ICP) should be monitored in all salvageable

patients with severe traumatic brain injury (TBI); Glasgow Coma Scale
(GCS) score of 3-8 after resuscitation) and an abnormal computed
tomography (CT) scan. An abnormal CT scan of the head is one that
reveals hematomas, contusions, swelling, herniation, or compressed basal
cisterns.
c.
Level III: ICP monitoring is indicated in patients with severe TBI with a
normal CT scan if two or more of the following features are noted at
admission:
(1)
(2)
(3)
d.
Age over 40 years

Unilateral or bilateral motor posturing
Systolic BP < 90 mmHg
Post-op w/ significant brain swelling

2.
3.
e.
Routine ICP monitoring is not indicated in patients with mild or moderate

head injury. However, it may be undertaken in certain conscious patients
with traumatic mass lesions at the discretion of the treating physician.
f.
Of note, 78% of trauma centers now comply with the BTF guidelines and
monitor ICP (BTF, 2007). It is questionable as to whether one can
prognosticate from the readings. For example, one can only speculate that
if the pressure is greater than 25 for 24 hours, the patient can't be normal
upon recovery.
ICP data use

a.
ICP data can be used to predict outcome and worsening intracranial

pathology, calculate and manage CPP, allow therapeutic CSF drainage
with ventricular ICP monitoring and restrict potentially deleterious ICP
reduction therapies (BTF, 2007).
b.
Can be the first indicator of worsening status and evolving mass lesions
requiring surgery.
c.
Treatment of ICP without ICP monitoring carries risk

(1)
Prolonged hyperventilation significantly reduces CBF.
(2)
Prophylactic paralysis increases pneumonia and ICU stay.
(3)
Barbiturates have a significant risk

prophylactic use is not recommended.
(4)
Mannitol has a variable ICP response in extent and duration of

ICP reduction.
of
hypotension
and
Types of ICP monitoring systems (BTF, 2007)

a.
The Association for Advancement of Medical Instrumentation (AAMI) has

developed the American National Standard for Intracranial Pressure
Monitoring Devices in association with a Neurosurgery committee.
According to the AAMI, an ICP device should have the following
specifications:
(1)
(2)
(3)
Pressure range 0-100 mmHg

Accuracy: 2 mm Hg in range of 0-20 mmHg
Maximum error 10% in range of 20-100 mmHg
b.
Intraventricular fluid-coupled catheter with an external strain gauge

transducer or catheter tip pressure transducer is the most accurate, low
cost, and reliable monitor and is the established reference standard. The
monitor is set to a prescribed maximum pressure and an alarm sounds
when that pressure is reached. It can be recalibrated in situ. ICU nurses
are authorized to drain CSF for about 10 seconds to relieve the pressure.
An external transducer must be consistently maintained at a fixed
reference point relative to the patients head to avoid measurement error
(BTF, 2007).
c.
ICP transduction via fiberoptic or micro strain gauge devices placed in

ventricular catheters provide similar benefits but at a higher cost.
d.
Parenchymal: Camino catheter: Closed fiberoptic system placed using

micro strain pressure transducers through 18 gauge needles, read tissue
pressures and provides results similar to ventricular ICP. Monitoring at 30
is best. No head turning! Have the potential for measurement differences
and drift due to the inability to recalibrate.
e.
Less accurate

(1)
Subdural devices: Catheter tip pressure transducer of fluidcoupled catheter with an external strain gauge.
(2)
Subarachnoid: Fluid-coupled device with an external strain gauge
(3)
Epidural devices
4.
Normal ICP = 5-12 torr. Initiate ICP interventions at an upper threshold of 20-25
mm Hg. Manage patient care according to ICP readings, frequent clinical exams,
and CPP data.
5.
May treat ICP by draining CSF through monitoring system
6.
Nursing responsibilities for patients with ventriculostomy and ICP monitors

a.
b.
c.
d.
e.
f.
g.
h.
i.
j.
k.
l.
7.
Explain need for monitor to patient and family.

Gather and assemble equipment.
Flush the lines and calibrate equipment.
Perform neurological assessment.
Administer sedation/analgesia as prescribed.
Place head of bed at 30 degrees if prescribed in a hemodynamically stable
patient.
Prepare operative site, establish sterile field, assist physician as needed.
Connect monitoring catheter to transducer or monitor.
Observe the numeric reading and wave patterns; adjust characteristics to
obtain visual reading.
Cover site with sterile dressing.
Adjust alarm system to unit parameters.
Obtain frequent checks of neuro status and patency of system. Irrigate
system using sterile technique to maintain patency according to unit policy
(Bourg, 2007).
Risk/complications:
a.
If left in place for longer than 4-5 days, infected is a risk - give antibiotics as
ordered.
b.
Hemorrhage: Rare in ventriculostomy catheters.
c.
Malfunction or obstruction: In fluid coupled ventricular catheters,

subarachnoid bolts, or subdural catheters has been reported in up to 16%
of patients (BTF, 2007). No publications on the complication rate of
fiberoptic transducer in populations studied since 1999. Malfunctions of
microstrain gauge devices are reported as 0%.
d.
Malposition
D.
Transcranial dopplers: Common carotid branches into the external carotid that perfuses
the face and the internal carotid that perfuses scalp and brain. The velocity of the middle
carotid artery (MCA)/ext. carotid = 1.7; > 3 = vasospasm.
E.
Systemic jugular venous oxygen saturation (SjVO2 or SjO2), arterial-jugular venous

oxygen content differences (AVdO2) (extraction ratios), and CBF monitoring may help to
identify cerebral ischemia if hyperventilation values < 30 mmHg are necessary.
2.
3.
4.
5.
Monitor patients with TBI, SAH in vasospasm, and post-op patients with suspicious
pathology of significant brain swelling or intracranial hemorrhage.
Tests are less expensive
Assess oxygen availability to brain
Depend on CBF and HbO2 content
Normal SjO2 = 65-75%; goal: keep above 55%
6.
SjO2 decreases with
1.
a.
decreased CBF which increases O2 extraction;

b.
c.
d.
7.
Cerebral blood flow decreases with

a.
b.
c.
d.
F.
anemia; and
a decrease in arterial oxygen extraction.
If SjO2 is < pO2 27 - look for above
increased ICP and decreased CPP;
excess hyperventilation;
cerebral spasm; and
systemic hypotension.
Anti-cerebral edema measures

1.
Hyperosmolar therapy: Mannitol and hypertonic saline

a.
Recommendations (BTF, 2007)

(1)
Level I: There are insufficient data to support a Level I

recommendation for this topic.
(2)
Level II: Mannitol is effective for control of raised intracranial

pressure (ICP) at doses of 0.25 gm/kg to 1 gm/kg body weight.
Arterial hypotension (systolic blood pressure < 90 mmHg) should
be avoided.
(3)
Level III: Restrict mannitol use prior to ICP monitoring to patients

with signs of transtentorial herniation or progressive neurological
deterioration not attributable to extracranial causes.
b.
Mannitol is a hypertonic simple sugar - super oxide (free radical)

scavenger. It creates an osmotic gradient that pulls fluid from the
intracellular and parenchymal spaces into the vascular space thereby
decreasing cerebral edema, lowering blood viscosity to increase cerebral
blood flow, and increasing oxygen delivery to the cells.
c.
Mannitol reduces ICP within 15-30 minutes of its administration while

osmotic gradients are established between plasma and cells. Effects last
from 90 minutes to six hours or more depending on the patients clinical
condition (BTF, 2007).
d.
Indications for use (BTF, 2007)

(1)
Management of TBI with suspected or actual raised intracranial

pressure.
(2)
Single administration for short-term benefits while further

diagnostic procedures (CT scan) and interventions (surgical
evacuation of an intracranial mass) can be accomplished.
(3)
Prolonged therapy for increased ICP.
e.
Mannitol should not to be used prophylactically. Caution in CHF. Mannitol

may be used prior to ICP monitoring in the presence of transtentorial
herniation or progressive neuro deterioration not attributable to systemic
pathology, but only under conditions of adequate volume resuscitation
(BTF, 2007).
f.
Don't dehydrate the brain! Avoid hypovolemia by providing fluid

replacement. If you decrease blood volume you decrease cerebral blood
flow.
(1)
There may be a lot of cerebral swelling, but not a lot of free water.
An indwelling urinary catheter is essential in these patients.
(2)
Maintain serum sodium levels at 145 to 150.

g.
2.
3.
(3)
Osmoles normally = 2 X Na (143) = 286. Keep serum osmoles

320 mOsml if concerned about renal failure. Serum sodium and
serum osmoles are good tests to follow, as a 10 mOsml gradient
(296) is needed to get fluid out of brain.
(4)
Arterial hypotension, sepsis, nephrotoxic drugs, or preexisting

renal disease place patients at risk for renal failure with hyperosmolar therapy (BTF, 2007).
Hypertonic saline (HS)

(1)
Effect on ICP is due to the osmotic gradient that moves water

across an intact blood-brain barrier reducing the cerebral water
content of mainly non-traumatized brain tissue. HS also
dehydrates endothelial cells producing vessel dilation and shrinks
RBCs that increases their deformability (ability to perfuse through
capillaries) leading to plasma volume expansion and improved
blood flow. It also reduces WBC adhesion in traumatized brain
(BTF, 2007).
(2)
Side effects: Risk of central pontine myelinolysis when given to

patients with preexisting chronic hyponatremia. Risk of inducing or
aggravating pulmonary edema in patients with underlying cardiac
or pulmonary problems (BTF, 2007).
(3)
Current evidence is not strong enough to make recommendations

on the use, concentration and method of administration of
hypertonic saline for the treatment of traumatic intracranial
hypertension (BTF, 2007).
Prophylactic hypothermia
a.
Level I: There are insufficient data to support a Level I recommendation for

this topic.
b.
Level II: There are insufficient data to support a Level II recommendation

for this topic.
c.
Level III: Pooled data indicate that prophylactic hypothermia is not

significantly associated with decreased mortality when compared with
normothermic controls. However, preliminary findings suggest that a
greater decrease in mortality risk is observed when target temperatures
are maintained for more than 48 h. Prophylactic hypothermia is associated
with significantly higher Glasgow Outcomes Scale (GOS) scores (46%
better chance of a good outcome) when compared to scores for
normothermic controls (BTF, 2007).
d.
Target temperatures with best outcomes: 32-33C and 33-35C.
Sedation & pain management

a.
Patients with TBI often require sedation for agitation, restlessness,

mechanical ventilation, or pain (Bourg, 2007) to decrease metabolic
requirements, decrease ICP, facilitate effective ventilations, and provide
comfort.
b.
IV narcotics (morphine, fentanyl), benzodiazepines, e.g., lorazepam

(Ativan) or midazolam (Versed), or short-acting anesthetic agents
(propofol) can facilitate management of patients who are agitated, thus
helping to keep their ICPs down. Benzodiazepines minimally affect ICP,
cerebral oxygen demand or cerebral blood flow (Bourg, 2007). Propofol
can markedly reduce BP and may not be the best choice until
hemodynamic stability is assured to prevent a drop in CPP. Sedation does
not provide pain management. Need to treat both if necessary.

c.
Barbiturates induce an anesthesia-like state to provide cerebral protection

if ICP cannot be reduced. High dose barbiturate therapy may be
considered in hemodynamically stable salvageable severe head injury
patients with increased ICP refractory to maximal medical and surgical ICP
lowering therapy (Origitano, 1996).
Barbs may also be beneficial for near drowning but are contraindicated in
hypotensive patients (ATLS, 2005). Attempt to rule out other causes of
agitation including hypoxia or electrolyte imbalance. Use extreme caution
in monitoring ventilatory status.
d.
4.
Maintain venous outflow from cranium

a.
Maintain patient's head and neck in neutral alignment to facilitate venous

drainage.
b.
Assess airway securing and spine motion restriction devices for JV

constriction.
5.
Reduce environmental stimuli: Dim lights and decrease noise as much as

possible
6.
Evaluate patient's response to pain and consider need for analgesics.
7.
Avoid increased intrathoracic or intra-abdominal pressure

a.
b.
c.
d.
8.
Minimize time in Trendelenburg position during central line placement.

Attempt to prevent the elicitation of a Valsalva maneuver, cough, gag,
vomiting or sneezing.
Avoid hip flexion and isometric muscular activity.
Minimize activities that stimulate posturing.
Avoid rapid and wide fluctuations in BP

a.
b.
c.
d.
G.
Neuromuscular blockade may be employed when sedation alone proves

inadequate and short-acting agents should be used when possible (BTF,
1995). Unfortunately, pharmacologic relaxation has the undesirable effect
of limiting the neurologic examination to the pupils and CT scan. Therefore,
its use in the absence of evidence of herniation should be limited to
situations where sedation alone is not sufficient to optimize safe and
efficient patient transport and resuscitation.
Beware of sudden decreases in BP - notify physician immediately.

Titrate medications slowly.
Space nursing procedures that ICP such as suctioning.
Limit environmental stimuli as indicated.
Anticonvulsant medications
1.
In the acute period, seizures may precipitate adverse events in the injured brain
due to elevations in intracranial pressure, BP changes, changes in oxygen delivery,
and also excess neurotransmitter release (BTF, 1995).
2.
Give only to prevent early post-traumatic seizures in high risk patients

a.
b.
c.
d.
e.
f.
g.
h.
GCS < 10
Cortical contusion
Depressed skull fracture
Subdural hematoma
Epidural hematoma
Intracerebral hematoma
Penetrating head wound
Seizure within 24 hours of injury

3.
Ativan (lorazepam) 0.1 mg/kg or Versed (midazolam). Versed can be given

intranasally using a mucosal atomizer device (MAD) at 0.2 mg/kg up to 1 mL/nostril
or 10 mg total single dose.
4.
Fosphenytoin (Cerebyx) 10-20 mg PE (phenytoin sodium equivalents)/kg IVPB

not faster than 150 PE/min. If patient is in status, the loading dose of fosphenytoin
is 15-20 mg PE/kg infused at 100-150 mg PE/min. Side effects of fosphenytoin:
nystagmus, pruritus, paresthesia, dizziness, somnolence, ataxia, tinnitus, nausea,
vomiting, and headache. Incidence and severity of side effects are dose and rate
dependent.
5.
After termination of initial seizure activity, Dilantin (phenytoin) can be used to

prevent further tonic-clonic and temporal lobe seizures. Dose: No more than 50 mg
per min IVP through a filter up to 18 mg/kg. Monitor ECG during infusion (Bourg,
2007).
6.
Prophylactic use of fosphenytoin, carbamazepine, or phenobarbital is not

recommended for preventing late (occurring after 7 days following injury) posttraumatic seizures.
H.
Narcotic antagonists if suspected overdose: Naloxone 0.4 to 2 mg IVP
I.
Infection prophylaxis (BTF, 2007)
J.
1.
Level I: There are insufficient data to support a Level I recommendation for this
topic.
2.
Level II: Periprocedural antibiotics for intubation should be administered to reduce

the incidence of pneumonia. However, it does not change length of stay or
mortality. Early tracheostomy should be performed to reduce mechanical ventilation
days. However, it does not alter mortality or the rate of nosocomial pneumonia.
3.
Level III: Routine ventricular catheter exchange or prophylactic antibiotic use for
ventricular catheter placement is not recommended to reduce infection.
4.
Risks of infection and aspects of care

a.
As many as 70% of mechanically ventilated patients can develop

pneumonia and ICP monitor infection rates can be as high as 27% (BTF,
2007).
b.
Risk of infection is affected by the duration of external ventricular drainage,

use of prophylactic parenteral antibiotics, presence of concurrent other
systemic infections, presence of intraventricular or subarachnoid
hemorrhage, open skull fracture, including basilar skull fractures with CSF
leak leakage around the ventriculostomy catheter, and flushing of the
ventriculostomy tubing (BTF, 2007).
c.
Ventriculostomies and other ICP monitors should be placed under sterile

conditions to closed drainage systems, minimizing manipulation and
flushing. There is no support for routine catheter exchanges as a means of
preventing CSF infections. There is also no support for use of prolonged
antibiotics for systemic prophylaxis in intubated TBI patients, given the risk
of selecting for resistant organisms. Early tracheostomy or Extubation in
severe TBI patients have not been sown to alter the rates of pneumonia,
but may reduce the duration of mechanical ventilation (BTF, 2007).
d.
If suspected basilar skull fracture, prophylactic administration of

Pneumovax is sometimes recommended.
Deep vein thrombosis (DVT) prophylaxis (BTF, 2007)

1.
Level I: There are insufficient data to support a Level I recommendation for this
topic.

2.
Level II: There are insufficient data to support a recommendation for this topic.
3.
Level III:
a.
Graduated compression stockings or intermittent pneumatic compression

(IPC) stockings are recommended, unless lower extremity injuries prevent
their use. Use should be continued until patients are ambulatory.
b.
Low molecular weight heparin (LMWH) or low dose unfractionated heparin

should be used in combination with mechanical prophylaxis. However,
there is an increased risk for expansion of intracranial hemorrhage.
c.
There is insufficient evidence to support recommendations regarding the

preferred agent, dose, or timing of pharmacologic prophylaxis for DVT.
4.
In the absence of prophylaxis, patients with severe TBI are at high risk for
developing DVT with embolic events.
5.
Methods used for detection: clinical evidence; or Duplex scanning, venography,

radiolabeled fibrinogen scans in asymptomatic patients.
6.
Treatment in neurosurgical patients is complicated by the uncertainty of the safety

of anticoagulant therapy (BTF, 2007).Prevention is critical.
7.
Mechanical agents: Graduated compression stockings, intermittent pneumatic

compression stockings. Do not increase BP, ICP or CVP. Lower extremity injuries
may limit their use or application may limit ambulation and physical therapy.
8.
Pharmacological agents
a.
b.
c.
Low-dose heparin
Low-molecular weight heparin
Risks associated with both include intracranial and systemic bleeding that
may lead to morbidity and death.
K.
The use of glucocorticoids is not recommended for improving outcome or reducing

intracranial pressure in patients with severe head injury (BTF, 1995)
L.
Impaired verbal communication: Create alternative methods to communicate for those

who need intubation and are awake
M.
Alteration in thermoregulation
1.
2.
3.
4.
N.
Adjust room temperature as needed

Adjust patient covering as needed
Monitor for fluctuations in temp and alert physician if either occurs
Administer hypothalamic depressants as ordered
Surgical management: Operative considerations

1.
Prepare patient for craniotomy if they have an extracererbral hematoma > 1 cm

thickness. Neurosurgeon will consider acute removal of intracerebral hematomas
causing substantial mass effect.
2.
Unstable comatose patients who are taken to surgery for thoracic or abdominal
injury may be candidates for diagnostic bur holes or insertion of ICP monitoring if
there is a significant scalp injury or signs of herniation.
3.
Temporal Bur Hole: Only to be used in situations where immediate neurosurgical

care is not available by a surgeon properly trained in the procedure. Indications:
hemiplegia, dilated pupil; 85% dilate on side of mass; 15% dilate contralateral to
mass (Kernohan's Phenomenon). Need to remember that 1) most head injured
patients do not have hematomas, 2) a burr hole may fail to locate the hematoma, 3)
only a small portion of the hematoma can be evacuated through a burr hole, 4) the
procedure may produce brain damage, 5) the procedure may not be life-saving,
and 6) the time involved in performing the procedure may equal the time to get the

patient to a neurosurgeon (ATLS, 2005). Should only be done with the advice and
consent of a neurosurgeon.
4.
X.
Lab profiles
A.
B.
C.
D.
E.
F.
G.
H.
I.
J.
K.
XI.
In extreme cases of cerebral edema, surgeons may remove a portion of the skull to
allow for brain swelling to prevent herniation and death. Patients may be fitted with
a protective helmet until the skull defect can be reconstructed or repaired.
H&H or CBC
Glucose (injured brain is hypermetabolic and glucose intolerant; levels increase in
intracranial hemorrhage and decrease in secondary ischemia. If glucose > 200 = poor
outcome)
Serum lactate
Electrolytes
Drug/tox screen
ABG, SpO2, AVdO2, SjO2.
Creatinine, blood urea nitrogen (BUN)
International normalized ratio (INR)
Prothrombin time (PT) and partial thromboplastin time (PTT)
Urine electrolytes, urea and glycerol q. 6 hours. Monitor Na levels for SIADH.
Serum osmolarity: diagnoses injury to hypothalamus which may result in diabetes insipidus
as indicated by serum osmolarity > 295 mOsm/kg, or syndrome of inappropriate ADH
secretion (SIADH) with serum osmolarity less than 280 mOsm/kg.
Neuro diagnostic radiography

A.
A normal PE, normal CT, and a normal MRI DO NOT mean a normal patient
B.
X-Rays: Lateral C-Spine must show all 7 cervical vertebrae to presumptively clear neck for
emergency procedures. Need AP, bilateral obliques and open-mouth odontoid views ASAP
when patient is stabilized and all emergency procedures are completed; portable chest if
prepping for OR. Skull films are not needed if CT is planned. Note: Pencil lead doesn't show
up on X-ray.
C.
C-T scan: Probably the most important diagnostic tool in the emergent treatment
period. Shows neurons or gray matter (not axons), hematomas, contusions, fluid-filled
ventricles, mass lesions of localized injury, and associated bony structures. They do not
detect diffuse injury. ICP cannot be reliably predicted by CT alone.
1.
2.
High-yield criteria for identifying adult patients at risk for significant intracranial
injuries after blunt head trauma (defined as any injury that led to neurosurgical
intervention, rapid clinical deterioration, or had the potential for long-term
neurologic impairment) and need for CT BEAN BASH (Mower et al, 2005):
a.
b.
c.
d.
B Behavior abnormal
E Emesis intractable
A Age > 65
N Neurological deficit
e.
f.
g.
h.
B Bleeding disorder
A Altered mental status
S Skull fracture
H Hematoma scalp
Other criteria that suggest the need for CT

a.
b.
c.
d.
e.
f.
Loss of consciousness > 5 minutes

Combativeness
Facial injury
Penetrating skull injury
Acute pupillary inequality
Skull films reveal IC air or shift of the pineal gland from midline

g.
h.
i.
3.
A meta-analysis done by the World Health Organization Centre Task Force (Borg
et al, 2004) studied the diagnostic tools available to detect mild brain injury and
found that CT could reveal unsuspected lesions in patients with MBI. Only 8% of
those with GCS scores of 15 had an abnormal CT, but 30% of patients with a GCS
of 13 had abnormal CT results.
4.
NO CONTRAST in most cases. If basal cistern is absent anticipate 88% mortality

in 24 hours
5.
Need iron in blood to see it on CT. There are some isodense subdurals. If there is
anemia from trauma with a Hct, won't see the clot on CT.
D.
Air ventriculography: If CT not possible due to multiple injuries and need for immediate
operative intervention, the neurosurgeon may perform a ventriculostomy while other
surgeons stabilize the patient (ATLS, 1997). Ten ml of CSF are drained and replaced with
air. A portable AP skull film is taken to look for the presence of midline shift. Shift indicates
a possible mass lesion requiring immediate evacuation. Rarely used.
E.
MRI/MRA: Forty-one percent of TBI patients with a normal CT will have an abnormal MRI.
Increased sensitivity reveals small or subtle lesions. More useful in subacute and chronic
phases of head injury. More time consuming than other imaging studies. Magnetic field may
make it incompatible with monitoring and resuscitative equipment; access to patient limited
during study.
F.
SPEC scan: Single Photon Emission Scan: measures metabolism of the brain. They can
see if the brain is "idling" and try to determine if it is a biochemical or electrical event.
G.
PET scan
H.
Cerebral angiography: used if CT unavailable and vascular injury is suspected.

Transfemoral approach preferred.
I.
Other studies
1.
2.
3.
4.
XII.
Lumbar puncture
EEG
Evoked potentials; visual, brain stem auditory, and somatosensory
Xenon blood flow studies
Ongoing patient monitoring

A.
B.
C.
D.
E.
A patient is considered in coma until they can obey commands and localize pain.
VS as ordered.
Mentation, orientation, responses and GCS
Neuro signs including pupils, motor strength and sensory response to stimuli
Report any change from previous assessments
F.
A patient is deteriorating if:

1.
2.
3.
XIII.
Alcohol or other drug intoxication is a confounding factor

Anticoagulant use
Amnesia, particularly antegrade
GCS drops by 2-3 points;

there is a unilateral pupil change; or
there is lateralized extremity weakness.
Sequelae of head trauma

A.
Glasgow Outcome Scale

1.
Good recovery
2.
Moderate disability
3.
Severe disability: never return to work
4.
Persistent vegetative state (very costly care) - awake but unaware
5.
Death

XIV.
B.
Mild head injury: May have prolonged problems with memory, dizziness, headaches,
attention deficits and other CNS dysfunctions. Initial GCS 13-15 = 4% morbidity.
C.
Moderate and severe injuries may have significant cognitive deficits requiring an
aggressive approach to PT, occupational and speech therapy.
D.
Poor outcomes can be anticipated in the presence of

1.
hypoxia;
2.
shock (hypotension) with ICP;
3.
hypercarbia;
4.
hyper (Michaud et al, 1991) or hypoglycemia;
5.
hypercalcemia;
6.
hypermagnesemia;
7.
drop in cerebral blood flow;
8.
CPP < 50 and ischemic brain injury;
9.
40% mass lesions;
10.
GCS that drops 2-3 points;
11.
pupil asymmetry; and/or
12.
unilateral extremity weakness and drift leg lag.
E.
MPX Scores (Mamelak et al, 1996)

1.
Age, best motor score and pupillary reactivity at admission and 24 hours are
significant predictors of outcome
2.
Extraocular motility predictive at 24 hours only
3.
Age most important independent predictor with an inverse relationship between
age and survival. There is an approximate 10% decrease in survival each decade
after the 20's.
4.
24 hour MPX data is generally a better predictor of six-month outcomes and more
specific in predicting negative outcomes than admission findings.
F.
Rehabilitation: Comprehensive neuropsychological rehabilitation involves combination

therapies for persons with cognitive, emotional, interpersonal and motivational deficits
associated with TBI and is beneficial for symptom management, community reintegration,
and return to work.
Specific traumatic brain injuries (TBI)

A.
Morphology of injury (ATLS, 1997)

1.
Skull fractures: Involve the cranial vault or basilar skull bones. Classified as linear,
stellate, open/closed; vertex/basilar
2.
Intracranial lesions
a.
Focal injuries: Specific, grossly observable lesions, e.g., structural or

expanding mass lesions with local brain damage. Brain shifting causes
coma from brain stem compression. Twenty seven to 60% of patients with
severe head injury (unable to speak or follow commands) have focal injury
(mass lesions) requiring operative intervention (Wagner, 1996). They
cause 50% of all admits and 66% of all deaths.
Produced by contact or non-movement forces and/or accelerationdeceleration forces.
b.
Diffuse injuries: There is no macroscopic brain injury that can be seen on

skull film or CT scan. There is wide-spread microscopic disruption of both
structure and function due to shearing, stretching, or tearing forces applied
to nerve fibers. Coma is due to direct damage of brainstem or cortex, but
no brainstem compression. Examples are cerebral concussions and
diffuse axonal injuries.

B.
Extracranial scalp injuries: There are five layers to the scalp and it is well vascularized.
The blood vessels do not constrict as well as in other areas of the body, so are at risk for
bleeding profusely when injured. Common injuries:
1.
Lacerations: Due to blunt trauma that can tear skin and underlying connective
tissue causing it to separate. This can leave elevated borders surrounding a
depression that mimics a depressed skull fracture (Bledsoe, 2006).
2.
Incisions: Smooth wound margins as if cut with a knife
3.
Hematomas: Closed injury causing blood to accumulate within the layers of the
scalp. May bleed enough over a depressed skull fracture to fill the depression and
conceal the injury.
Abrasions, contusion, burns
4.
5.
6.
C.
Avulsions: Scalp tissue is only loosely attached to the skull. Shearing forces may
tear a flap of tissue, exposing a portion of the skull. This can create serious
contamination and bleeding.
A scalp hematoma or laceration may suggest deeper injury beneath. Always have
a high index of suspicion for skull fracture. Danger: blood loss that can put the
patient into shock. Must be controlled as soon as possible.
Skull fractures
1.
2.
Epidemiology
a.
There are approximately 111,000 skull fractures/year in the U.S.
b.
The frontal and occipital are the thickest bones. The temporal bone is the
thinnest; 50% of fractures occur here. Keystones of the skull base are the
sphenoid bones and petrous processes of the parietal bone, which bear
lateral forces when the head is hit. They, and the cribriform plate, are often
the bones that are injured in a basilar skull fracture.
c.
Only 5% of people who hit their heads sustain a skull fracture, but 20% of
patients with skull fractures had a major head injury. Skull fractures make
the brain more susceptible to trauma.
d.
A compound fracture with neuro impairment > 4 hours has a 25 times

greater chance of deterioration. Skull fracture with obtundation = major
head injury. 25% will develop a surgically significant lesion.
e.
Little growth of new skull bone occurs after two years of age and places
patients at risk for post-injury infections. They must have all openings
covered with sterile dressings followed later by split thickness grafts.
Vertex fractures
a.
Linear
(1)
Definition: An inbending of the skull at the point of injury with

simultaneous outbending around the region of impact which
dissects both tables of bone causing a crack.
(2)
Etiology: Low-velocity, blunt or compression trauma
(3)
Incidence: 80% of all skull fractures. Occur most frequently in

children and elderly.
(4)
Pathogenesis: 50% involve temporal and parietal bones
(5)
Morbidity/mortality
(a)
(b)
Most are essentially benign

A diastatic (sprung suture) is the biggest predictor of who
will deteriorate from a linear fracture

(c)
b.
c.
(6)
Clinical presentation: External soft tissue trauma, subgaleal

hematoma, and pain
(7)
Diagnostic radiography: standard skull film or CT
(8)
Emergency intervention: Usually requires no treatment. If

fracture extends into orbit, paranasal sinus or crosses a major
vascular channel, admit to observe. Fracture line usually
disappears in 6 months (children) and 3-4 years in adults.
Stellate/comminuted
(1)
Definition: Skull fractures into multiple fragments that may

penetrate the meninges and damage structures beneath
(2)
Etiology: Moderate-velocity blunt or compression trauma
Open: See penetrating injuries

(1)
Definition: Combination of a depressed skull fracture and a scalp

laceration. The dura may be torn.
(2)
Pathogenesis
(a)
Blunt and/or penetrating trauma
(b)
AK 47 with Teflon bullet produces 2100 lbs/in2 of force that
explodes the inside of the head
(3)
Morbidity/mortality: High
(4)
Clinical presentation: Depends on site
(5)
Diagnostic radiography: Standard skull films; CT

Emergency intervention: OR
(6)
d.
A fracture over the temporal/parietal bones should cause

suspicion for an epidural hematoma
Depressed
(1)
Definition: Fracture with inward displacement of a bony segment
(2)
Etiology: High velocity contact over a small surface area results in

compression trauma
(3)
Pathogenesis: Results from direct applied forces. Frequently

seen in MVCs and violence. Ex: Hammer creates 1600 lb/in2.
(4)
Classifications
(a)
(b)
(c)
Closed with scalp intact

Compound with scalp open but dura intact
Complex with scalp and dura lacerated by bone fragments
= cortical laceration and hemorrhage
(5)
Morbidity/mortality: Causes intracranial damage like contusion

and laceration; infections and seizures
(6)
Clinical presentation: Can usually see or feel depression unless

covered by a scalp hematoma. May present with focal brain
injuries.
(7)
Diagnostic radiography: standard skull films, CT
(8)
Emergency intervention: If open, greater than 1 cm depressed,

or associated with neurological deficit: surgical debridement,
evacuation of clots and bone fragments, and elevation of
depressed bone and repair of lacerated dura. Prophylactic
anticonvulsants and antibiotics.

e.
3.
Growing fracture
(1)
Unique to pediatric population
(2)
Brain under 5 torr pressure; will pulsate through linear fracture
Basilar skull fractures

a.
Definition: A fracture that involves the base of the skull
b.
Location: Anterior, middle or posterior fossa bones, cribriform plate,

sphenoid wings, and/or petrous bones. This area is rough and ridged and
has many foramina (openings) for the spinal cord (foramen magnum),
cranial nerves, ear (auditory canal), and blood vessels. It forms the roof of
the orbits and nasal sinuses. These spaces weaken the skull and make it
vulnerable to fracture.
c.
Pathogenesis: Caused by blunt trauma to the head, especially to the

mandible, or when the vertebral column is driven against the occipital
condyles, e.g., fall on the buttocks.
d.
Morbidity/mortality: Risk for meningitis/encephalitis or a cerebral

abscess.
e.
Clinical presentation: Varies by location. However, if the patient has been

supine and develops a headache when they sit up, suspect basilar skull
fracture.
(1)
(2)
Anterior fossa (Cribriform plate, fovea ethmoidalish, sphenoid

sinus)
(a)
Telecanthus - Medial eyelids spread out towards ear

causing the bridge of the nose to appear widened and
flattened. This is the first sign EMS personnel are likely to
see.
(b)
CSF Rhinorrhea: 25% of these injuries tear the dura and

arachnoid, allowing CSF to leak out through the fracture
site into the nasal cavity. Because CSF is high in sodium
(159 mEq in CSF compared to 142 in blood), patients may
c/o a salty taste in the back of their mouth.
(c)
Epistaxis
(d)
Raccoon eyes: Classic triangular bruising of the lower

eye lids. Appears later.
(e)
May be associated with facial fractures and bleeding into

the orbit causing subconjunctival hemorrhages of lateral
sclera giving it a blood red appearance w/o evidence of
direct trauma (ocular Battle Sign).
(f)
Anosmia: CN I (Olfactory nerve) deficit. One third of

patients with an anterior basilar skull fracture will
permanently lose their ability to smell, and therefore the
ability to "taste" most foods.
(g)
(h)
(i)
Visual field deficits: CN II (Optic)

Pneumocephalus
Sinus air-fluid levels
Clinical presentation: Middle fossa also involves middle ear

(a)
CSF otorrhea: Glucose oxide reaction to glucose test

tape or check for B2 transferin
(b)
Hemotympanum or ear drum perforation

D.
8th
nerve
(c)
Conductive
hearing
deficit:
(Vestibulocochlear) involvement
(d)
Dizziness; look for nystagmus
(e)
Facial weakness/paralysis on the affected side: Facial

nerve (CN VII) runs right next to CN VIII as they exit
through the base of the skull to surface structures. They
are often both injured in a middle fossa fracture.
(f)
Battle sign: Mastoid ecchymosis that presents 24-36 hrs

after injury
f.
Diagnostic radiography: May not see on skull films
g.
Emergency interventions
(1)
Semi-Fowler's position. Avoid nose blowing, straining, and

sneezing. Avoid iatrogenic contamination.
(2)
Usual cause for persistent bleeding from ear is canal laceration
(3)
CSF leak may be helping to blunt a rise in ICP and limit brain
damage. Do not try to stop it. Place nothing in the nose or ear.
Collect drainage from nose on a rolled 4 X 4 (moustache dressing)
taped over the upper lip. Place a loose dressing over the ear to
collect drainage. If mixed with blood, look for the characteristic
"halo" sign as blood cells are heavier and will stay in the middle
while CSF wicks out to the perimeter causing a larger strawcolored ring. This sign is most reliable if fluid is leaking from the
ear (Bledsoe, 2006).
(4)
Don't always start on prophylactic antibiotics. Eighty percent of

CSF leaks self-seal. If it persists longer than 7-14 days, may need
dura repair. Starting to see prophylaxis with Pneumovax.
Focal intracranial injuries

Anatomy review: All central nervous system tissue is surrounded by three layers of
meninges: dura (outer layer attached to the inner table of skull bone and inner layer folding
to surrounding all CNS structures); arachnoid; and pia (attached to brain surface). There
are potential spaces between these layers into which bleeding may occur, creating a
hematoma or hemorrhage.
1.
Epidural hematomas
a.
Definition/incidence: Blood clot between skull and dura that doesn't

involve the brain.
b.
Etiology: Falls, direct blows to the head, MVC, sports injuries
c.
Pathogenesis: Classically, epidurals are associated with a linear fracture

in the temporal area that can tear the middle meningeal artery (which is
encased in a groove o the skull bone after the age of 3). They can occur in
other sites due to brisk oozing of blood from diploic vessels (those
contained in the spongy middle layer of skull bone) injured by skull
fractures. They may be venous in origin if fracture crosses a dural sinus
(usually under a skull suture line).
The arterial bleeding must "peel" the dura away from the inner table of
skull in order to form the hematoma. This creates a contained clot.
However, there is no room for extra bleeding inside the skull, so
intracranial pressure rises rapidly. The clot will compress cerebral
structures (shutting them down) and may eventually shift the brain onto
midline structures (brainstem and cranial nerves).

d.
Morbidity/mortality data: Five to 28% overall mortality. Mortality of 3-4% if

caught before coma. Needs to get to OR before coma evolves, otherwise
mortality starts doubling.
e.
Peds considerations: Clots not common in children but they experience

epidurals more frequently than subdurals except in infant child abuse.
Intracranial blood loss may precipitate shock in young children < 3 years.
More common bilaterally in children. May tend to watch longer before
operative intervention.
f.
Clinical presentation: Depends on the source and rapidity of bleeding

(1)
Palpate temple for boggy hematoma indicating trauma to the

vessels that spread out to the temporalis muscle.
(2)
Unequal pupils: Ipsilateral (same side) dilated pupil that becomes

fixed due to pressure on CN III.
(3)
Change in consciousness: GCS drops by 2-3 points. May have a

lucid interval (9%-33%).
(4)
Headache of increasing severity
(5)
Possible seizures, vomiting
(6)
Localized contralateral extremity weakness. Very important sign.

Look for pronator drift.
(7)
Beware posterior fossa epidural hematoma

(a)
(b)
(c)
(d)
(e)
(f)
(g)
(h)
2.
Occipital skull fracture

Cranial nerve dysfunction
Cerebellar signs
Abnormal extraocular movements
Motor dysfunction
Nausea/vomiting
VS and respiratory arrest
May be delayed in appearance
g.
Diagnostic radiography: Looks like a lens or is C-shaped on CT. Brain is

70% water, cannot be compressed so shift compresses ventricles.
h.
Emergency interventions: Surgical evacuation if S&S of brain shift. Don't

operate on all, may resolve in a couple of days if small.
Acute subdural hematomas

a.
Definition/incidence: Blood accumulation in the potential space between

the dura and arachnoid meningeal layers. Incidence: 17-29% of head
injuries. Most common traumatic mass lesion (51%-68%). Three times
more common than an epidural with the worst prognosis. Two times more
common in adults than children due to increased violence.
b.
Etiology: MVCs, falls, assaults, industrial and sports injuries. Occur from
frontal or occipital impacts more often than from lateral impact.
c.
Populations at risk: Elderly, alcoholics, and infants as their brains are

chronically dehydrated, smaller due to degeneration of cortical tissue, or
smaller due to immature development. This places tension on the veins
that bridge the cerebral cortex with the dural sinuses (venous outflow
tracts) attached to the skull and makes them vulnerable to injury.
d.
Pathogenesis
(1)
Classified as acute (within 48 hrs), subacute (2-14 days), and

chronic (>14 days) depending on symptoms onset after injury

e.
(2)
Bridging veins which traverse the space between the cerebral

cortex and venous sinuses shear and tear. Rare arterial cause.
(3)
Beneath the clot, the cortex may be damaged by contusion,

ruptured veins and arteries
(4)
Bilateral in 8%-21% of cases
(5)
If less than 72 hours old, may be liquid or clotted blood
Morbidity/mortality: 28%-73% die as clot is under dura and almost

directly against brain. Represents 33%-75% of mass lesion mortality.
(1)
Attributed to primary brain damage underlying the clot, vascular

injury, hyperemic response leading to increased intracranial
volume, ipsilateral hemispheric or total brain swelling, and ICP.
(2)
Factors predictive of functional recovery

(a)
(b)
(c)
(d)
f.
3.
Evaluation within 4 hours of injury

Post-op ICP < 20 mmHg
Normal post-op evoked potentials
GCS > 5
Clinical presentation
(1)
Acute: Headache, drowsiness, agitation, slow cerebration,

confusion. If brain is shifting: ipsilateral dilated and fixed pupil,
contralateral hemiparesis. Lucid interval in 13%.
(2)
Subacute: Similar to acute with failure to regain consciousness
(3)
Chronic: Headache that progresses in severity, slow cerebration,

confusion, drowsiness, giddiness, possible seizure, papilledema,
and contralateral hemiparesis. Hematoma may reaccumulate or
calcify.
g.
Diagnostic radiography: Looks like a smudge covering the brain surface

on CT
h.
Emergency interventions: Surgical evacuation of clot if 3 mm or more

thick, hemorrhage control, or need for resection of the contused, nonviable
brain.
Subarachnoid hemorrhage (SAH)

a.
Definition: Blood in the subarachnoid space
b.
Pathogenesis: Most common cause is trauma. Traumatic SAH is usually

diffuse, does not form a definite hematoma and does not create a mass
effect. Bleeding occurs from superficial cortical vessels, an AV
malformation, or leaking congenital intracranial aneurysm and is often
associated with subdural hematoma. Causes swelling around the brain
stem (not good). Twelve percent of females and 7% of males have
unsuspected cerebral aneurysms.
c.
Morbidity/mortality data: If system is filled with blood, outcome is poor
d.
(1)
(2)
(3)
Severe headache Intense pain (worst headache of their life)

becoming occipital, aggravated by any movement worse lying
down. Can mimic migraine and tension headaches. A majority of
non-traumatic SAH patients have a premonitory leak and
headache days to weeks before major rupture with neuro damage.
Optic fundi have pre-retinal hemorrhages; visual disturbances
Ipsilateral dilated pupil

(4)
(5)
(6)
(7)
e.
Diagnostic radiography: CT; arteriography. CT changes may not appear

for up to 4 hours (longer with a minimal bleed). Appear as high-density fluid
collections within the cerebrospinal fluid spaces.
f.
(1)
(2)
g.
4.
Blood in CSF causes intense vasoconstriction leading to extensive

infarction - therefore no hyperventilation
ICP monitoring may be indicated
(3)
If CT scan is negative, but clinical suspicion is strong physician will

do an LP
(4)
Surgical evacuation, nimodipine (60 mg q. 4 hours PO or per NG

tube) for vasospasm, and standard treatment for cerebral edema
Complications: Extensive SAH puts patient at risk for communicating

hydrocephalus
Intracerebral hemorrhage
a.
Definition: A deep contusion or tear in blood vessels that result in

hemorrhage in the brain parenchyma
b.
Pathogenesis: Single or multiple hemorrhages may occur from blows to

the skull, rotational acceleration, missile-type injuries, and coup-contrecoup
lesions. Sixty percent are associated with skull fractures, especially
depressed fractures, and 60% appear under contusions. The majority
(85%) are located in the frontal and anterior temporal lobes at the anterior
base of the brain. They may take some time to develop. Sudden
deceleration or head rotation causes these regions to impact the rough
surface of the basilar skull.
c.
Morbidity/mortality: Depends on size. Mortality 65% if at a point around a

contusion or complicated by progressive focal edema and mass effect.
Majority of deterioration occurs within first 48-72 hours. Delayed
hemorrhage is a risk.
d.
Clinical presentation: Similar to contusions; depends on location. Will

often share S&S of a stroke.
(1)
Headache
(2)
Deteriorating consciousness to deep coma
(3)
Contralateral hemiplegia
(4)
Ipsilateral dilated pupil
(5)
Speech deficits
e.
Diagnostic radiography
(1)
(2)
f.
5.
Meningeal irritation signs: nuchal rigidity requires 12-24 hours to

develop and is not a reliable early sign
Deterioration of mental status
Hemiparesis; R/O c-spine injury
Seizures
CT can determine the volume of blood. If 35-40 cc or if they are

located in the posterior temporal lobe OR
Cerebral arteriography
Surgical indications:
coup/contrecoup lesion
Size
>
30
ml,
temporoparietal
clot,
or
Cerebral contusions
a.
Definition: Actual bruising of, or cortical bleeding into, cortical tissue,

generally without puncture of the pial covering. Classified as coup (found at

the site of impact), contrecoup (in a line directly opposite the point of
impact which is the worse of the two impacts), gliding, and petechial. May
involve laceration of vessels and brain tissue with tissue necrosis, pulping
and infarction. With most contusions, there is any area of brain cells that
are destroyed and will not regenerate. But the surrounding tissue
(penumbra) that is being affected by the swelling can be saved with
appropriate management.
b.
Pathogenesis: Temporal and frontal lobes are the primary sites of coup
lesions. The frontal lobes bang on the frontal bone. Temporal lobes hit the
middle cranial fossa (sphenoid wings) and start to bruise and swell. After
the initial impact, the brain "sloshes" backward, again impacting the
internal skull structures. If hit on the forehead, the contrecoup lesion is
often in the occipital lobes producing visual disturbances (seeing stars).
Often multiple and occur in combination with other lesions.
The blood-brain barrier in the area of the contusion may lose its integrity,
which can lead to the development of an intracerebral hematoma.
Contusions and hematomas that are initially small may increase in size
causing rapid worsening of a previously stable patient's condition.
6.
c.
Morbidity: Worsens with ICP 20-25 mmHg. Goal: ICP 10 mm Hg.

Significant due to associated hemorrhage, edema, and brain swelling.
d.
Clinical presentation: Depends on involved structures but often presents

with localizing personality, behavior, motor, speech. memory, or visual
deficits. Temporal lobe contusions especially severe due to close proximity
of the midbrain.
e.
Diagnostic radiography: CT
f.
Emergency interventions: Monitor patient with small lesion (<5-7 mm of

brain shift on CT) for ICP. Extensive contusion with hemorrhage and
mass effect require surgery.
Impalement/penetrating injuries
a.
Definition: Open head injuries due to a projectile
b.
Pathogenesis
(1)
Bullets and other projectiles destroy a path of brain tissue along

their trajectory (primary injury). Trauma to cerebral vessels may
cause large hematomas. Bone fragments, imploded debris, and
the breach in cranial integrity may result in the development of
infections and cerebral abscesses. Large fragments that lodge in
the ventricles or on the brain surface may migrate with
catastrophic results.
(2)
High velocity injuries: Large shock waves and zones of negative

pressure result in significant cavitation. Swelling of adjacent tissue
may result in fatal ICP.
c.
Morbidity/mortality: High (50%) due to structural damage, massive brain

swelling and uncontrolled ICP
d.
Clinical presentation: Depends on sites of injury
e.
Impaled objects:
Patient presentation depends on the structures
involved. Some patients are awake and aware with rather large objects
impaled into their skull. Do not move or remove.
f.
Diagnostic radiography: skull film, CT

g.
7.
Brain stem hemorrhage

a.
Definition: Bleeding into the midbrain, pons, or medulla
b.
Pathogenesis
c.
E.
Emergency interventions: Stabilize impaled objects in place pending

removal in OR. Prophylactic antibiotics; anticonvulsants may be ordered.
(1)
Primary: Direct impact or torsion injuries of the brain stem
(2)
Secondary: Compression from ICP, cerebral edema, or

laceration of temporal lobes
(1)
Midbrain: Deep coma, midpoint fixed pupils, ophthalmoplegia,

abnormal extension response to pain
(2)
Pons: Coma, pin-point pupils,

extension response to pain
(3)
Medulla: Pupils bilaterally dilated and fixed; death
d.
Morbidity/mortality: Almost 100% if comatose
e.
Diagnostic radiography: CT; MRI
ophthalmoplegia,
abnormal
Diffuse injuries: 50% of all admits; 1/3 of all TBI deaths

1.
Concussion
a.
Incidence: 2-4 million/yr - most common head injury
b.
Definition: Traumatic, microscopic damage to cells deep in the white

matter of the brain causes reversible physiologic disturbance of
neurological function that occurs at the instant of trauma.
c.
Pathogenesis
d.
(1)
Linear motion of the brain "stuns" the affected cells and puts them
on "idle". While in this state, the cells are not dead, but they do not
function as they should.
(2)
Traumatic forces cause transient ischemia, neural depolarization

following sudden acetylcholine release, or microscopic axonal
disruption of fibers in upper brain stem (ascending reticular
activating system) and temporal lobe producing the classic S&S.
(3)
Patients don't have to hit their head or lose consciousness
(4)
They may report seeing stars or flashes of light. (Note: seeing

stars is K related. Linear motion causes K to run out of cells and
short circuits the occipital lobe.)
(5)
Most neurons stain blue. Neurons in temporal lobe following a

concussion stain red from damage.
Clinical presentations
(1)
Grade I
(a)
(b)
(c)
(2)
Short-lived confusion
No loss of consciousness
Post-traumatic amnesia less than 30 minutes
Grade II
(a)
Loss of consciousness less than 5 minutes
(b)
Post-traumatic amnesia greater than 30 minutes
(c)
Retrograde amnesia 5-10 minutes after impact

e.
f.
g.
(3)
Grade III
(a)
Loss of consciousness greater than 5 minutes but < 6
hours
(b)
Post-traumatic amnesia greater than 24 hours
(c)
Retrograde amnesia
(4)
Emotional lability; may be crying and weeping
(5)
May be associated with more severe structural lesions, most

common is cerebral contusion.
Post concussive syndrome in peds patients - observe carefully

(1)
Alert; no initial loss of consciousness
(2)
Minutes to hours later, child becomes sleepy, somnolent, irritable,

pale, tachycardic and clammy
(3)
Vomits then shows rapid improvement in 24 hours
Post concussive syndrome (PCS) in adults

(1)
Between 20% and 80% of people with mild head injury continue to
experience S&S six months after the injury (de Kruijk et al, 2002).
Concussions are cumulative. Memory cells in temporal lobe are
most subject to damage. Repetitive concussions will cause recent
memory loss.
(2)
The American Psychological Association defines PCS as

quantifiable deficits in memory or attention and the onset or
worsening of any three of the following symptoms: tiring easily,
disordered sleep, headaches, vertigo/dizziness, irritability,
anxiety/depression/affective lability, changes in personality, or
apathy. Neuropsychological deficits detectable after resolution of
neuro symptoms . Recovery may take 6-12 mos.
(3)
Patients may also have problems with sunlight, coffee,

nervousness, irritability, negative energy syndrome, difficulty with
abstract thinking and judgment, loss of inhibition and libido, and
avoidance of crowds.
(4)
Preinjury factors (age, education, emotional adjustment) and postinjury factors (pain, family support, stress) interact with cognitive
functioning and significantly affect recovery from TBI (McCauley et
al, 2001).
(1)
(2)
(3)
2.
Reorient patient to time and place

Analgesia for headache
Prophylactic anticonvulsants controversial - not generally used
Diffuse axonal injuries (DAI)

a.
Definition: Shearing, tearing, or stretching force on nerve fibers causing

widespread disruption of neurologic function without any focal lesions
noted.
Characterized by white matter degeneration as the axon is disrupted close
to the cell body resulting in progressive focal axonal abnormalities in the
cerebral hemispheres, brainstem, and less frequently in the cerebellum
over 12 - 24 hours (Wagner, 1996).
b.
Pathogenesis: During rotation, mechanical forces act on the long axonal

fibers and cause certain axons to experience structural failure as they are
physically separated (stretched, sheared) into distal and proximal

segments. The distal segment degenerates resulting in profound deficits.
Frequent targets: temporal lobe and brainstem.
See reactive astrocytes 4-6 hours after the injury. Dead neurons stain red
and can never recover.
c.
Morbidity/mortality: Results in global neurologic dysfunction and diffuse

swelling. Coma is due to brain stem dysfunction. Accounts for of all
admissions and 2/3 of all TBI deaths. May have residual neurologic
deficits. Recovery dependent on amount and location of neuronal damage.
Currently no effective treatment for severed axons.
d.
e.
(1)
Mild DAI (Grade 1): Widespread axonal damage in the

parasagittal white matter of the cerebral hemispheres and is found
in those who have a brief loss of consciousness and do not
experience come or those with milder injuries. Mortality 15%.
(2)
Moderate DAI (Grade 2): Tissue tear hemorrhages and axonal

abnormalities in the cerebral hemispheres and corpus callosum.
Coma 24 hours, may have abnormal posturing. Mortality 20%24%.
(3)
Severe DAI (Grade 3): Grade II findings plus abnormalities in the

upper brain stem, and an increased degree of axonal hemispheric
abnormalities. Point of maximum stress where tissues of different
density interface (between gray and white matter). Coma is
immediate, lasting longer than 24 hours with positive brain stem
signs (posturing) and incomplete recovery. Mortality 60% due to
direct hemorrhage in brain stem.
(4)
Classic picture: For patients with milder injuries, the clinical

presentation can be unclear (Bay & McLean, 2007). In more
severe injuries, immediate, deep, prolonged coma may last weeks
to months, accompanied by ICP, persistent brain stem reflexive
posturing (flexion or extension), hypertension, temperature
(104-105 F), and hyperhidrosis indicating diencephalon
involvement. No mass lesions or S&S on CT; no brain stem
compression - so no pupil signs. May be associated with a
persistent vegetative state.
(5)
Interventions: Support ABCs. At present, there is no effective

curative treatment for DAI. If an axon is injured but not severed,
providing an optimum environment for healing may enable it to
recover. If secondary injury occurs the loss will be permanent
(Feliciano, 269).
Diagnostic radiography
(1)
CT may show characteristic small hemorrhagic lesions in the

corpus callosum, superior cerebellar peduncles, or periventricular
region
(2)
Visualized better on MRI with contrast.

Centers for Disease Control and Prevention Screening Instrument for Detection of MBI
Question
1.
At the time of your trauma, did you experience any period of transient confusion,
disorientation, or impaired consciousness?*
YES
No
2.
At the time of your trauma, did you experience any dysfunction of memory (amnesia)?*
YES
No
3.
Did you experience any of the following in relation to your trauma: seizures, headache,
dizziness, irritability, fatigue, or poor concentration?**
YES
No
At the time of your trauma, did you experience any loss of consciousness lasting 30
minutes or less?*
YES
No
4.
* Answer of yes on any of these items indicates mild traumatic brain injury
** If yes, must answer yes on one other item.
Source: J Neurosci Nurs 2007 American Association of Neuroscience Nurses
Sample discharge instructions for patients with mild head injury

1.
2.
3.
4.
5.
6.
7.
No serious brain or skull injuries have been found on your initial examination. However, it is possible
for more serious signs or symptoms to develop later. If possible, have a responsible adult stay with
you for 24 hours after the injury. This person should wake you every 4 hours to look for the
symptoms listed below.
You may take acetaminophen (Tylenol) every 4 hours to relieve pain. DO NOT take aspirin or
ibuprofen until approved by a physician. Take only your normal medications and those prescribed
for you at this time. If you are on any blood thinners, follow the physicians instructions about taking
them.
NO alcoholic beverages for 24 hours. It is better to avoid alcoholic beverages until all symptoms
from the injury resolve.
Rest for the next 24 hours and resume normal activities as tolerated. Fatigue following mild head
injury is normal.
Do not drive, operate machinery, or make important legal decisions until symptoms resolve.
Contact your physician if you experience any of the following symptoms within the next few weeks:
Inability to answer simple questions, such as What day is it? or What happened to you?
Increased headache or the inability to wake up completely
Nausea and vomiting three or more times
Problems with walking or stumbling or difficulty with coordination
Slurred speech
Seizures or convulsions
Weakness or the arms or legs
Vision changes
NORMAL signs and symptoms following mild head injury may be experienced for some time (up to
six months to one year). If they increase in severity or persist to the extent that your daily activities
are disrupted, contact your physician.
Trouble remembering things
Difficulty with concentration, sequencing tasks, making decisions
Headache
Mood changes: irritability
Fatigue
Difficulty sleeping or a noticeable change in the number of hours you are sleeping
Adapted from Bourg, 2007
CJM: 8/97; Rev. 1/03; 6/07

References
American Association of Neurological Surgeons and the Brain Trauma Foundation (1996). Guidelines for the
management of severe head injury (in press).
ACS Committee on Trauma. (2005). Advanced Trauma Life Support Course. ACS: (in press).
Batchelor, J. & McGuiness, A. (2002). A meta-analysis of GCS 15 head-injured patients with loss of
consciousness or post-traumatic amnesia. Em Med J, 19, 515-519.
Bay, E. & McClean, S.A. (2007). Mild traumatic brain injury: an update for advanced practice nurses. J
Neurosci Nurs, 39(1), 43-51.
Bazarian, J., McClung, J., Shah, M.l, Cheng, Y., Flesher, W., & Kraus, J. (2005). Mild traumatic brain injury
in the United States 1998-2000. Brain Injury, 19(2), 85-91.
Bledsoe, B.E., Porter, R.S., & Cherry, R.A. (2001). Head, facial and neck trauma. In Paramedic Care:
Principles & Practice Trauma Emergencies (pp. 263-315). Upper Saddle River: Brady.
Borg, J., Holm, L., Cassidy, D., Peloso, P.;, Carroll, L., Holst, H., et al. (2004). Diagnostic procedures in mild
traumatic brain injury: Results of the WHO Collaborating Centre Task Force on mild traumatic brain
injury. J of Rehabilitation Medicine, 43, 61-75.
Bourg, P. (2007). Head and face trauma. In Oman, K.S. & Koziol-McLain, J. (Eds), Emergency Nursing
nd
Secrets (2 ed) (288-297). St. Louis: Mosby.
Brain Trauma Foundation (2007). Guidelines for the management of severe traumatic brain injury. J of
Neurotrauma, 24(suppl), S-1-106.
Brain Trauma Foundation (2003). Update notice: Guidelines for the management of severe traumatic brain
injury: cerebral perfusion pressure. Jointly published by The Brain Trauma Foundation, The
American Association of Neurological Surgeons, The Congress of Neurological Surgeons, and The
Joint Section on Neurotrauma and Critical Care.
Chesnut, R.M., Gautille, T., Blunt, B.A. et al. (1998). Neurogenic hypotension in patients with severe head
injuries. J of Trauma, 44, 958-964.
Chesnut, R.M. (1997). Avoidance of hypotension: condition sine qua non of successful severe head-injury
management. J of Trauma: Injury, Infection, and Crit Care, 42(5), S5-S9.
Davis, D.P., Idris, A.H., Sise, M.J., Kennedy, F., Eastman, A.B., Velky, T., Vilke, G.M., & Hoyt, D.B. (2006).
Early ventilation and outcome in patients with moderate to severe traumatic brain injury. Crit Care
Med, 34(4), 1202-1208.
De Kruijk, J., Leffers, P., Menheere, P., Meerhoff, S., Rutten, J., & Twijnstra, A. (2002). Prediction of posttraumatic complications after mild traumatic brain injury: Early symptoms and biochemical markers.
J of Neurology, Neurosurgery and Psychiatry, 73, 727-732.
Dries, D.J. (1995). Permissive hypercapnia. J of Trauma: Injury, Infection, and Crit Care, 39, 984-989.
Gill, M., Windemuth, R., Steele, R., & Green, S. (2005). A comparison of the Glasgow Coma Scale score to
simplified scores for the prediction of traumatic brain injury outcomes. Annals of Em Med, 45(1), 2742.
Harders, A., Kakarieka, A., Braakman, R. et al. (1996). Traumatic subarachnoid hemorrhage and its
treatment with nimodipine. J of Neurosurgery, 85, 82-89.

Harrahill, M. (1996). Glasgow coma scale: A quick review. JEN, 22(1), 81-83.
Hrtl, R., Gerer, L.M., Iacono, L., Quanhong, N., Lyons, K., & Ghajar, J. (2006). Direct transport within an
organized state trauma system reduces mortality in patients with severe traumatic brain injury. J of
Trauma, 60(6), 1250-1256.
Henzler, D., Cooper, D.J., Tremayne, A.B., Rossaint, R., & Higgins, A. (2007). Early modifiable factors
associated with fatal outcome in patients with severe traumatic brain injury: A case control study.
Crit Care Med, 35(4), 1027-1031.
Ivascu, F.A., Janczyk, R.J., Junn, F.S., Bair, H.A., Bendick, P.J., & Howells, G.A. (2006). Treatment of
traumatic patients with intracranial hemorrhage on preinjury warfarin. J of Trauma, 61, 318-321.
Kibby, M.Y. & Long, C.J. (1996). Minor head injury: attempts at clarifying the confusion. Brain Injury, 10(3),
159-186.
Lehmkuhl, L.D. (1996). Brain injury glossary. The Traumatic Brain Injury Model System Research Program
of The Institute for Rehabilitation and Research.
Maddocks, D. & Saling, M. (1996). Neuropsychological deficits following concussion. Brain Injury, 10(2), 99103.
Mamelak, A.N., Pitts, L.H. & Damron, S. (1996). Predicting survival from head trauma 24 hours after injury: a
practical method with therapeutic implications. Journal of Trauma, 41(1), 91-99.
Michaud, L.J., Rivara, F.P., Longstreth, W.T. et al. (1991). Elevated initial blood glucose levels and poor
outcome following severe brain injuries in children. J of Trauma, 31, 1356-1362.
Newell, D.W., Weber, J.P., Watson R. et al. (1996). Effect of transient moderate hyperventilation on dynamic
cerebral autoregulation after severe head injury. Neurosurgery, 39, 35-44.
Sutphen, S.K. (2006). Trauma update from the 2006 annual scientific assembly of the American college of
emergency physicians. Available on line: www.medscape.com/viewarticle/547419. Accessed 12/297/06.
Valadka, A.B. & Narayan R.K. (1996). Injury to the cranium. In Feliciano, D.V., Moore, E.E., & Mattox, K.L.
(Eds.) Trauma (3rd ed.) (pp. 267-278). Stamford: Appleton & Lange.
Wang, H.E., Beitzman, A.B., Cassidy, L.D., Adelson, P.D., & Yealy, D.M. (2004). Out-of-hospital
endotracheal intubation and outcome after traumatic brain injury. Annals of Em Med, 44(5), 439450.
Wooten, C. (1996). The top ten ways to detect deteriorating central neurological status. J Trauma Nursing,
3(1), 25-27.
Resources:
TBI-trac.ed: An internet-based distance learning program designed to provide healthcare professionals with
the most current evidence-based treatment strategies for TBI care.
Brain Trauma Foundation: www.braintrauma.org
Brain Injury Association of America: www.BIAUSA.org
National Institute of Neurological Disorders and Stroke (NINDS) Traumatic Brain Injury information:
www.ninds.nih.gov/health_and_medical/disorders/TBI_doc.htm

Brain & Spine Trauma Glossary
A
Accident
An event causing loss, which takes place without being expected. In most cases, the accident can
be characterized with regard to time and place of occurrence. The public commonly associates this
term with an unavoidable event. Therefore, when referring to injuries caused by motor vehicles, the
preferred term is motor vehicle "crash" rather than accident as virtually all crashes are preventable.
Acuity
Sharpness or quality of a sensation.
Acute
Sharp, severe, having sudden onset, sharp rise and short course; lasting a short time; seriously
demanding urgent attention.
Affect
The observable emotional condition of an individual at any given time.
Alert
State of being watchful or ready.
Amnesia
Lack of memory about events occurring during a particular period of time.
Aneurysm
A balloon-like deformity in the wall of a blood vessel. The wall weakens as the balloon grows larger,
and may eventually burst, causing a hemorrhage.
Anosmia
Loss of the sense of smell.
Aphasia
Loss of the ability to express oneself and/or to understand language. Caused by damage to brain
cells rather than deficits in speech or hearing organs.
Apraxia
Inability to carry out a complex or skilled movement; not due to paralysis, sensory changes, or
deficiencies in understanding.
Arousal
Being awake. Primitive state of alertness managed by the reticular activating system (extending
from medulla to the thalamus in the core of the brain stem) activating the cortex. Cognition is not
possible without some degree of arousal.
Ataxia
A problem of muscle coordination not due to apraxia, weakness, rigidity, spasticity, or sensory loss.
Caused by lesion of the cerebellum or basal ganglia. Can interfere with a person's ability to walk,
talk, eat, and to perform other self care tasks.
Awareness
Conscious of stimulation, arising from within or from outside the person.
B
Behavior
The total collection of actions and reactions exhibited by a person.
Bilateral
Pertaining to both right and left sides.
Brain injury
A more specific term than head injury. Damage to the brain that results in impairments in one or
more functions, including: arousal, attention, language, memory, reasoning, abstract thinking,
judgment, problem-solving, sensory abilities, perceptual abilities, motor abilities, psychosocial
behavior, information processing and speech. The damage may be caused by external physical
force, insufficient blood supply, toxic substances, malignancy, disease-producing organisms,
congenital disorders, birth trauma, or degenerative processes.
Brain injury, closed
Occurs when the head accelerates and then rapidly decelerates or collides with another object (for
example the windshield of a car) and brain tissue is damaged, not by the presence of a foreign
object within the brain, but by violent smashing, stretching, and twisting, of brain tissue. Closed brain
injuries typically cause diffuse tissue damage that results in disabilities which are generalized and
highly variable.
Brain injury, mild
A patient who has had a traumatically-induced physiological disruption of brain function, as

manifested by at least one of the following: 1) any loss of consciousness, 2) any amnesia for events
immediately before or after the incident, 3) any alteration in mental state at the time of the incident
(e.g., feeling dazed, disoriented, or confused, 4) focal neurological deficit(s) which may or may not
be transient; but where the severity of the injury does not exceed the following: a) loss of
consciousness 30 minutes or less; b) after 30 minutes, an initial GCS score of 13-15 (now under
debate to only include a GCS of 15); and c) post-traumatic amnesia not greater than 24 hours.

Brain injury, moderate A GCS of 9-12 during the first 24 hours
Brain injury, severe
Produces at least 6 hours of coma; GCS of 8 or less during the first 24 hours
Brain stem
The lower extension of the brain where it connects to the spinal cord. Neurological functions located
here include those necessary for survival (breathing, heart rate) and for arousal (being awake and
alert).
C
Cerebellum
The portion of the brain (located inferior and posterior to the cerebrum) which helps coordinate
movement. Damage may result in ataxia.
Chronic
Marked by long duration or frequent recurrence.
Cognition
The conscious process of knowing or being aware of thoughts or perceptions, including

understanding, and reasoning.
Cognitive impairment Difficulty with one or more of the basic functions of the brain: perception, memory, attentional
abilities, and reasoning skills.
Coma
A state of unconsciousness from which the patient cannot be awakened or aroused, even by
powerful stimulation; lack of any response to one's environment. Defined clinically as an inability to
follow a one-step command consistently; GCS of 8 or less.
Complete injury
Used to describe an absence of sensory and motor function in the lowest sacral segment.
Comprehension
Understanding of spoken, written or gestural communication.
Concussion
The common result of a blow to the head or sudden deceleration usually causing an altered mental
state, either temporary or prolonged. Physiologic and/or anatomic disruption of connections
between some nerve cells in the brain may occur.
Confusion
A state in which a person if bewildered, perplexed, or unable to self-orient.
Conjugate movement Both eyes move simultaneously in the same direction. Convergence or the eyes toward the midline
(crossed eyes) is a dysconjugate movement.
Consciousness
The state of awareness of the self and the environment.
Contralateral
Opposite side
Cortical blindness
Loss of vision resulting from a lesion of the primary visual areas of the occipital lobe. Light reflex is
preserved.
Contrecoup
Bruising of brain tissue on the side opposite where the blow was struck.
Coup damage
Damage to the brain at the point of impact.
D
Dermatome
Refers to the area of the skin innervated by the sensory axons within each segmental nerve (root).
There are 28 dermatomes on each side of the body.
Diffuse axonal
A shearing injury of large nerve fibers (axons covered with myelin) in many areas of the brain.
injury (DAI)
It appears to be one of the two primary lesions of brain injury, the other being stretching or shearing
of blood vessels from the same forces, producing hemorrhage.
Diplopia
Seeing two visual images of a single object; double vision.
Disinhibition
Inability to suppress (inhibit) impulsive behavior and emotions.
Disorientation
Not knowing where you area, who you are, or the current date.
F
Flaccid
Lacking normal muscle tone; limp
Frontal lobe
Front part of the brain; involved in planning, organizing, problem solving, selective attention,
personality, and a variety of "higher" cognitive functions.

G
Glasgow Coma Scale A standardized system used to assess the degree of brain impairment and to identify the
seriousness of injury in relation to outcome. The system involves the patient's BEST responses
involving: eye opening, verbal ability, and motor activity all of which are evaluated independently
according to a numerical value that indicates the level of consciousness and degree of dysfunction.
Score run from a high of 15 to a low of 3.
H
Hematoma
The collection of blood is tissues or a space following the rupture of a blood vessel. May refer to an
epidural, subdural, subarachnoid or intracerebral collection of blood.
Hemianopsia
Visual field cut. Blindness for one half of the visual field in each eye.
Hemiplegia
Paralysis of one side of the body as a result of injury to neurons carrying signals to muscles from the
motor areas of the brain.
Hemiparesis
Weakness of one side of the body.
Hydrocephalus
Enlargement of fluid-filled cavities in the brain, not due to brain atrophy.
Hypertonicity
The ability of a hyperosmolar solution to redistribute fluid from the intra- to the extracellular
compartment. Urea, for example, may be hyperosmotic but since it equilibrates rapidly across
membranes, it is not hypertonic.
I
Impairment
Loss and/or abnormality of cognitive, emotional, physiological, or anatomical structure of function;

including all losses or abnormalities, not just those attributable to the initial pathophysiology.
Incomplete injury
Partial preservation of sensory and/or motor function found below the neurological level including
the lowest sacral segment. Sacral sensation includes sensation at the anal mucocutaneous junction
as well as deep anal sensation. The test of motor function is the presence of voluntary contraction of
the external anal sphincter upon digital examination.
Incoordination
A problem with coordination of movement of parts of the body, resulting from dysfunction of the
nervous system rather than weakness of muscles.
Intracranial pressure
Cerebrospinal fluid (CSF) pressure measured from a needle or bolt introduced into the CSF space
surrounding the brain. It reflects the pressure inside the skull.
Ipsilateral
Same side of the body.
Ischemia
A severe reduction in the supply of blood to body tissues.
J
Judgment
Process of forming an opinion, based upon an evaluation of the situation at hand in comparison with
personal values, preferences, and insights regarding expected consequences. The ability to make
appropriate decisions.
K
Kinesthesia
The sensory awareness of body parts as they move. See proprioception.
L
Leg bag
A small, thick plastic bag that can be tied to the leg and collects urine. It is connected by tubing to a
catheter inserted into the urinary bladder.
Lethargic
Awakens with stimulation; drowsy but awake.
Lucid interval
A period shortly after injury when the patient was reported to have talked.
M
Memory
The process of organizing and storing representations of events and recalling these representations
to consciousness at a late time.

Memory, long term
In neuropsychological testing, this refers to recall 30 minutes or longer after presentation. requires
storage and retrieval of information that exceeds the limit of short-term memory.
Memory, remote
Information an individual correctly recalls from the past, stored before the onset of brain injury.
There is no specific requirement for the amount of elapsed time, but it is typically more than six
months to a year. Preserved information from delayed memory becomes part of remote memory.
Memory, short term
Primary or "working" memory; its contents are in conscious awareness. A limited capacity system
that holds up to seven chunks of information over a period of 30 seconds to several minutes,
depending upon the person's attention to the task.
Mental competence
The quality or state of being competent; having adequate mental abilities; legally qualified or
adequate to manage one's personal affairs. An individual found by a court to be mentally
incompetent has a guardian appointed to make personal and/or economic decisions on their behalf.
Monoplegia
Paralysis of one arm or one leg.
Muscle tone
Used in clinical practice to describe the resistance of a muscle to being stretched. When the
peripheral nerve to a muscle is severed, the muscle becomes flaccid (limp). When nerve fibers in
the brain or spinal cord are damaged, the balance between facilitation and inhibition of muscle tone
is disturbed. The tone of some muscle may become increased and they resist being stretched - a
condition called hypertonicity or spasticity.
Myotome
Refers to the collection of muscle fibers innervated by the motor axons within each segmental nerve
(root). There are 10 myotomes on each side of the body.
N
Neurological level,
sensory level,
and motor level:
The first of these terms refers to the most caudal segment of the spinal cord with normal sensory
and motor function on both sides of the body. In fact, the segments at which normal function is
found often differ by side of the body and in terms of sensory vs. motor testing. Up to four different
segments may be identified in determining the neurological level: R-sensory; L-sensory; R-motor; Lmotor. It is strongly recommended to separately record each segment rather than a single level as
this can be misleading. When the term sensory level is used, it refers to the most caudal segment of
the spinal cord wit normal sensory function on both sides of the body. The motor level is similarly
defined with respect to motor function.
Non-purposeful
movement
Movement that a person may make which has no apparent goal. Ex. Flexor or extensor posturing.
Nystagmus
Involuntary horizontal, vertical, or rotary movement of the eyeballs.
O
Occipital lobe
Region in the back of the cerebrum which processes visual information. Damage to this lobe can
cause visual deficits.
Oncotic pressure
A small portion of the total osmotic pressure that is due to the presence of large protein molecules.
Osmolality
The osmotic concentration of a solution expressed as osmoles of solute per kg of solution
Osmolarity
The osmotic concentration of a solution expressed as osmoles of solute per L of solution.
Osmotic pressure
The pressure exerted by a solution necessary to prevent osmosis into that solution when it is
separated from the pure solvent by a semipermeable membrane. Osmotic pressure (mmHg) = 19.3
X osmolality (mOsm/kg).
Orientation
Awareness of one's environment and/or situation, along with the ability to use this information
appropriately in a functional setting. See disorientation.
P
Paresis
Weakness of a muscle
Paraplegia:
Refers to impairment or loss of motor and/or sensory function in the thoracic, lumbar or sacral (but
not cervical) segments of the spinal cord, secondary to damage of neural elements within the spinal
canal. With paraplegia, arm functioning is spared, but, depending on the level of injury, the trunk,

legs and pelvic organs may be involved. The term is used in referring to cauda equina and conus
medullaris injuries but not to lumbosacral plexus lesions or injury to peripheral nerves outside the
neural canal.
Parietal lobe
One of the two paired lobes of the brain located behind the frontal lobe at the top of the brain.
Interprets and localizes sensory stimuli.
Damage to the right parietal lobe can cause visual-spatial deficits causing the person to have
difficulty finding their way around new or even familiar places.
Damage to the left parietal lobe may disrupt a person's ability to understand spoken and/or written
language.
Pathology
Interruption or interference of normal bodily processes or structures.
Perception
The ability to make sense of what one sees, hears, feels, tastes, or smells. Perceptual losses are
often very subtle and the patient and/or family may be unaware of them.
Post traumatic
amnesia
A period of hours, weeks, days, or months after the injury when the patient exhibits a loss of
day-to-day memory. The patients is unable to store new information and therefore has a decreased
ability to learn. Memory of the PTA period is never stored, therefore things that happened during
that period cannot be recalled. May also be called antegrade amnesia.
Problem solving
Ability of the individual to bring cognitive processes to the consideration of how to accomplish a
task.
Problem
solving skill
Ability to consider the probable factors that can influence the outcome of each of various
solutions to a problem, and to select the most advantageous solution. Individuals with deficits in this
skill may become "immobilized" when faced with a problem. By being unable to think of possible
solutions, they may respond by doing nothing.
Proprioception
The sensory awareness of the position of body parts with or without movement. Combination of
kinesthesia and position sense.
Ptosis
Drooping of a body part, such as the upper eyelid, from paralysis or drooping of visceral organs
from weakness of the abdominal muscles.
Purposeful movement Motor activity with an apparent goal

Q
Quadriplegia
Paralysis of all four limbs (from the neck down). Now more commonly referred to as tetraplegia,
meaning four.
R
Retrograde amnesia
Inability to recall events that occurred prior to the accident; may be a specific span of time or type of
information.
S
Skeletal level:
Refers to the level at which, by radiographic examination, the greatest vertebral damage is found.
Somatic
Relating to, or affecting the body.
Stimulus
That which causes sensation (i.e., light for vision, sound for hearing). When a patient begins to
emerge from coma, an organized program of controlled stimulation is sometimes used to begin
"exercising" the brain. However, when a patient becomes agitated, the amount an intensity of
simulation should be limited (only one task for one sense at a time).
Stupor
Deep sleep; unresponsive but can be awakened with repeated, noxious stimulation. Awareness is
depressed but present.
T
Temporal lobes
Two paired lobes located about the level of the ears. They allow one to tell the difference between
one smell from another and one sound from another. They also help in sorting new information and
are responsible for short-term memory. The right lobe is primarily involved with visual memory
(pictures and faces). The left lobe is involved in verbal memory (words and names).

Tetraplegia
Preferred to quadriplegia: Refers to impairment or loss of motor and/or sensory function in the
cervical segments of the spinal cord due to damage of neural elements within the spinal canal.
Tetraplegia results in impairment of function in the arms as well as in the trunk, legs, and pelvic
organs. it does not include brachial plexus lesions or injury to peripheral nerves outside the neural
canal.

STUDY QUESTIONS
1.
List four major initial complication of TBI that should be anticipated and prevented if at all possible:
2.
If a patient presents with a MAP of 70 and an ICP of 30; what is the cerebral perfusion pressure?
Would this indicate adequate perfusion or cerebral ischemia?
3.
If a patient presents with oval pupils and hippus, what should a TNS suspect?
4.
List the three findings of the Cushing's triad:
5.
List two defining signs and symptoms of brain shift or herniation:
6.
All patients with a severe traumatic brain injury and a Glasgow Coma Score of 8 should have their
airway secured via:
7.
True or False: The BTF Guidelines state that normocarbia or controlled hypercarbia should be
maintained in the absence of clinical signs of herniation.
8.
Why must all uncontrolled bleeding and hypotension be avoided or corrected immediately in a
patient with TBI?
9.
What abnormal ventilations are described as crescendo/decrescendo with periods of apnea?

A.
B.
C.
D.
10.
Central Neurogenic Hyperventilation.

Apneustic.
Cheyne Stokes.
Cluster.
A patients only verbal utterances are random, repetitive words or profanity. How should this verbal
response be scored?
A.
B.
C.
D.
Converses
Confused speech
Inappropriate words
Incomprehensible sounds

11.
An adult cannot localize pain and generally pulls up or withdraws both arms in purposeful
movement when a pain stimulus is applied. How should the GCS motor response be rated?
A.
B.
C.
D.
12.
5
4
3
2
Protective response
Withdrawal response
Abnormal flexion
Abnormal extension
When assessing a comatose adult, you note that the patient flexes their right arm and extends left
arm extends when a pain stimulus is applied. When scoring the motor aspects of the Glasgow
Coma Score, which number would you select?
A.
B.
C.
D.
5
4
3
2
Protective response
Withdrawal response
Abnormal flexion
Abnormal extension
13.
What is the most sensitive test of unilateral motor weakness in a head injured patient who can
cooperate with your motor commands?
14.
Name two brainstem reflexes a physician may evaluate to determine presence of absence of
brainstem function:
15.
Why is hyperventilation to be avoided during the first 24 hours after TBI?
16.
Under what three circumstances may brief periods of hyperventilation be indicated?
17.
Which osmotic diuretic serves as a free radical scavenger and is given to patients with head trauma
to control ICP w/ signs of neurological deterioration?
18.
Under what circumstances are barbiturates considered for TBI patients?
19.
Under what circumstances should anticonvulsant medications be administered?
20.
List two TBI patients who should be prepared for emergent surgery:

21.
Why is serum glucose at the time of injury or in the ED an important consideration for the patient's
morbidity?
22.
List three TBI patients who need cranial CT scanning to r/o significant injury:
23.
List three cardinal signs of neurological deterioration in a TBI patient:
24.
How do basilar skull fractures damage cranial nerves or cause leaks of cerebral spinal fluid?
25.
What is one of the earliest, specific or defining signs that a patient has sustained an anterior basilar
skull fracture that you can assess while inspecting the face?
26.
Why is insertion of a nasopharyngeal airway or an NG tube contraindicated if a patient has midface

or above fractures?
27.
What two cranial nerves frequently present with dysfunction in a middle fossa basilar skull fracture?
28.
A patient who sustains a linear fracture to the temporal or parietal bones from blunt trauma and
experiences disruption of the middle meningeal artery, a rapidly deteriorating level of
consciousness, and clinical signs of brain shift should be suspected of having a(n):
29.
Name the type of hematoma associated with venous bleeding, commonly encountered in the elderly
or alcoholic population:
30.
Which hematoma has the greater morbidity and mortality: epidural or subdural? Why???

31.
List three specific signs and symptoms of subarachnoid hemorrhage:
32.
A blow to the head causing actual bruising of cortical tissue is called a
33.
What clinical signs could suggest that a comatose patient had a brain stem hemorrhage at the level
of the pons?
34.
A diffuse injury causing transient loss of cerebral function following a deceleration injury to the brain
where loss of consciousness (if one occurs) does not exceed 6 hours is called a/n:
35.
Why is the hallmark of this injury amnesia?
36.
Any patient who remains comatose over six hours after TBI with no demonstrable lesion evident on
C-T should be suspected of having a/n:
37.
In what range would you expect the physician to maintain a head-injured patient's pCO2 who has an
increase in intracranial pressure? _________________________________________________
38.
A 72-year-old male was cleaning the gutters on his house when he became dizzy and fell to the
ground. On assessment, you note he withdraws to deep, painful stimuli, does not open his eyes,
and is silent. RR: 10 and shallow with periods of apnea. There is thin, bloody fluid draining from his
nose. Which is contraindicated in this situation?
A.
B.
C.
D.
39
An adult has severely elevated intracranial pressure from an acute TBI. VS: BP 210/100; P 50; R
12 and irregular. Which of these is contraindicated?
A.
B.
C.
D.
40.
Transilluminated intubation with sedation

An oropharyngeal airway prior to BVM ventilation
Nasotracheal intubation
Drug-assisted intubation
Administer IV fluids to ensure brain perfusion.

Administer Nipride to reduce the blood pressure.
Control seizure activity quickly with Valium/Ativan.
Oxygenate well before suctioning the patient.
Patients with cerebral hematomas are more likely to dilate a pupil on the (same/opposite) side as
the lesion and lose motor function on the (same/opposite) side when the brain begins to shift.

Notes:

Head Trauma PDF

Hochgeladen von

Dokumentinformationen

Originaltitel

Copyright

Verfügbare Formate

Dieses Dokument teilen

Dokument teilen oder einbetten

Freigabeoptionen

Stufen Sie dieses Dokument als nützlich ein?

Sind diese Inhalte unangemessen?

Copyright:

Verfügbare Formate

Head Trauma PDF

Hochgeladen von

Copyright:

Verfügbare Formate

State of Illinois

Trauma Nurse Specialist Program

Time allotment: 2 hours

Epidemiology of head trauma

Incidence: Estimated at 200/100,000 population which translates to one every 21 seconds

Behaviors that increase the risk of sustaining head trauma

General categories of injury

Head injuries can be classified according to

Severity of the injury

State of Illinois TNS Program

Penetrating (open) trauma: A penetrating injury produces an opening through the

Mechanisms of injury: Brain injury is usually due to a combination of forces

Acceleration: Stationary head is hit by a moving object as in car vs. pedestrian,

Acceleration/deceleration injury: Moving head hits a moving object

The challenge of improving outcome rests on advances in prehospital

State of Illinois TNS Program

Moderate brain injury results in a loss of consciousness usually lasting minutes to

Three databases provide information about severe head injuries

TBI-trac: Interactive database designed as a Q/A program to track prehospital and

Patient destination and trauma team composition for optimal outcomes

Need 5 R's for optimal outcomes

Right patient, to the

State of Illinois TNS Program

Right hospital, in the

Traumatic brain injury care team should include the following:

EMS providers: ground and/or air transport

Hypoxia: Hypoxia, defined as apnea/cyanosis or PaO2 <60 (SpO2 < 90%)

State of Illinois TNS Program

Hypotension: Almost 1/3 of head injured patients present in shock with

Electrolyte imbalances (Na, K, Ca)

Hypercarbia (respiratory acidosis): also

Intracranial causes: Intracranial hypertension, delayed intracerebral hematoma

Secondary injury causes breakdown of the blood brain barrier, disruption of

Secondary injury is often preventable. The "secondary" brain damage opens a

Pathophysiology of traumatic brain injury

State of Illinois TNS Program

State of Illinois TNS Program

The fluctuating tone of cerebral arterioles depending on the brains changing

Metabolic or chemical influences: A change in metabolic rate will lead to a change

Little effect on CBF when in physiologic ranges

1 mmHg change = 2%-3% change in CBF between 20-80 mmHg

A pCO2 > 45 (hypercarbia) causes cerebral blood vessels to dilate

Conversely, low levels of CO2 cause pronounced vasoconstriction

Impaired CO2 reactivity impairs O2 reactivity.

Impaired autoregulation in TBI

Autoregulation is often compromised in the TBI patient. There is a

The brain now becomes dependent on BP for perfusion. If arterial pressure

State of Illinois TNS Program

Three intracranial components

Any increase in volume in one compartment must be matched by a similar

Intracranial pressure values

Intracranial hypertension: 15-20 mmHg

Malignant intracranial hypertension

20 mmHg sustained for 30 minutes

Volume pressure relationship:

CBF is dependent on cardiac output (CO) and is independent of systemic arterial

There is significant post-traumatic vasospasm as well as changes in pressure and

To compensate for an elevated ICP, one of the following must happen:

Child: 0-5 mmHg

Blood volume to brain must diminish,

Evolution of pathology causing ICP: pressure + time are big killers!

Increase in brain volume

Mass: Brain tumor, abscess, blood clot, AV malformation; CSF, blood