Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
OBJECTIVES:
CJM: 6/07
State of Illinois
Trauma Nurse Specialist Program
HEAD TRAUMA
Connie J. Mattera M.S., R.N., TNS
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. Coma
b. Vegetative state
c. Persistent vegetative state
d. Minimally responsive state
e. Akinetic mutism
f. Locked-in syndrome
4. Head injury often does not occur alone; 75% are associated with multiple trauma
a. 30% - injuries limited to one body area
b. 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.
II. Patient destination and trauma team composition for optimal outcomes
A. Need 5 R's for optimal outcomes
1. Right patient, to the
State of Illinois TNS Program
Head Trauma - page 4
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.
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 post-
concussive 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 receptor-
mediated process.
V. 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 body’s 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
State of Illinois TNS Program
Head Trauma - page 7
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 brain’s 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 brain’s 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) Little effect on CBF when in physiologic ranges
(2) Hyperbaric levels result in vasoconstriction
(3) 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.
(4) PaO2 < 30 doubles the CBF
b. 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.
4. 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
(Cushing’s 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.
State of Illinois TNS Program
Head Trauma - page 8
D. Intracranial pressure: The intracranial volume is fixed in an adult (1200-1500 mL) and
does not vary
1. Three intracranial components
a. 80%: Cerebral tissue: Brain is 75% H2O; constant blood brain barrier
from intact cell wall membranes
b. 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.
c. 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) Child: 0-5 mmHg
(2) Adult: 5-12 mmHg
b. Intracranial hypertension: 15-20 mmHg
c. Malignant intracranial hypertension
(1) ≥ 20 mmHg sustained for 30 minutes
(2) ≥ 30 mmHg sustained for more than 15 minutes
(3) ≥ 40 mmHg sustained for more than 2 minutes
E. 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. Blood volume to brain must diminish,
b. The body must increase CSF resorption, decrease production, displace
fluid down the spinal cord, or
c. Brain tissue is displaced (herniation)/
F. 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) Cytotoxic – intracellular
(2) Vasogenic – extracellular edema (tumors)
(3) Hydrostatic – tissues surrounding ventricles
State of Illinois TNS Program
Head Trauma - page 9
d. Papilledema
e. Seizures
3. Levels of intracranial pressure with corresponding S&S
a. Cerebral cortex and upper brain stem involved
(1) BP rising and pulse rate begins to slow
(2) Pupils still midsize and reactive
(3) Cheyne-Stokes ventilations
(4) Initially tries to localize and remove painful stimuli, eventually
withdraws then abnormal flexion occurs
(5) All S&S should be reversible at this stage
b. Middle brain stem (pons) involved
(1) Wide pulse pressure and bradycardia
(2) Pupils pinpoint to mid-size, sluggish or non-reactive (CN III)
(3) Central neurogenic hyperventilation
(4) Abnormal extensor posturing
(5) Few patients function normally from this level
c. Lower portion of brain stem (medulla) involved
(1) Pupils both dilated and non-reactive
(2) Respirations ataxic or absent
(3) Flaccid, does not react to pain
(4) Irregular pulse rate
(5) QRS, ST, and T wave changes
(6) Decreased BP
(7) Not considered survivable
I. 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. 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.
b. Infratentorial herniation: Cerebellar (tonsilar) herniation – Cerebellar
tonsils herniate into the foramen magnum. Causes almost immediate
death.
State of Illinois TNS Program
Head Trauma - page 12
3. Signs of herniation
a. Deterioration in the level of consciousness. GCS decreases by 2 or more
points
b. BP and ICP shoot up
c. HR drops to 30-40
d. Respiratory pattern changes
e. 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
f. Motor abnormality (contralateral deficits) to extensor motor posturing
g. Brainstem dysfunction
4. 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.
VI. 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. 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.
B. 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.
State of Illinois TNS Program
Head Trauma - page 13
flow and may prevent cerebral ischemia, but no studies have yet shown
improved outcomes.
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: Drug-
assisted 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.
3. 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) Name, dose, route, and time of all medications administered
(2) Patient's responses to medications
(3) Pertinent monitoring data: BP, HR, ECG, SpO2 pre & post-
intubation
C. Ineffective breathing pattern; potential or actual
1. Assess general respiratory rate (very fast or slow), depth, pattern and effort.
State of Illinois TNS Program
Head Trauma - page 15
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) Adolescents and adults: 16-20 breaths/min
(2) Elementary school children 30 breaths/min
(3) Infants and toddlers 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.
D. 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%
State of Illinois TNS Program
Head Trauma - page 16
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
State of Illinois TNS Program
Head Trauma - page 17
Strengths Limitations
■ Simplicity ■ Variation in inter-rater reliability
■ Provides a common language to report ■ Inconsistent use by caregivers in prehospital and hospital settings
neurologic findings based on bedside ■ Decreased BP (if SBP < 80, can’t assess GCS with respect to
observations possible outcomes)
■ Ability to trend over time ■ 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
g. 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 patient’s eye opening, verbal, and motor
responses either spontaneously or in response to verbal or painful
stimuli (Healey et al, 2003). Always report the patient’s BEST
response, even if different on one side of the body from the other.
h. 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.
State of Illinois TNS Program
Head Trauma - page 19
(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..
4 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.
2 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.
Confrounding Chemically sedated or paralyzed/or eyes swollen shut/orbital trauma; cranial nerve injury.
variables
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.
4 Converses but is confused or disoriented. Should have a good attention span, but responses
may be inaccurate.
3 Inappropriate words, poor attention span; does not converse. The patient may repeat random,
repetitive words, numbers, or profanity.
2 Incomprehensible sounds, moans, or cries
1 No sounds even after painful stimuli
Confounding Intubated, paralyzed, sedated, intoxicated or chemically impaired, maxillofacial trauma, grossly
variables swollen tongue, cricothyrotomy, tracheotomy, mutism, aphasia, hearing loss, language barrier,
dementia, and/or psychiatric disorders.
6 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.
5 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..
State of Illinois TNS Program
Head Trauma - page 20
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.
3 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).
2 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.
1 No response (movement) to pain
Confounding Chemically or traumatically paralyzed, peripheral nerve injury, extremity trauma with
variables 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) T: Intubated
(b) TP: Intubated and paralyzed
(c) S: Sedated
(d) U: Untestable
(2) 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).
m. Young children: Champion et al described a better method to describe the
verbal responses of children younger than three years:
(1) 5: Appropriate for age
(2) 4: Consolable cries
(3) 3: Persistent irritation
(4) 2: Restlessness and agitation
(5) 1: No verbal response
n. 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.
State of Illinois TNS Program
Head Trauma - page 21
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
B. Vital signs: The vital signs may provide very valuable information about the patient’s
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. 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.
2. Pulse: Count rate, evaluate rhythmicity, quality, location; compare equality.
State of Illinois TNS Program
Head Trauma - page 23
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) 0-1 years: 65 mmHg
(2) 1-5 years: 70-75 mmHg
(3) 5-12 years: 75-80 mmHg
(4) 12-16 years: 80-90 mmHg
f. Compensatory alterations in vital signs: Cushing's triad
(1) ↑ SBP, widened pulse pressure
(2) ↓P
(3) ↓ RR
g. Decompensatory alterations
(1) Hypotension (Chesnut et al, 1998)
(2) Tachycardia (grave sign)
(3) ECG changes:
(a) Q wave with ST depression
(b) Prolonged QT interval
(c) Dysrhythmias: atrial: PACs, biphasic Ps, A-Fib
4. 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.
C. 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
State of Illinois TNS Program
Head Trauma - page 24
(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).
(3) Funduscopic exam
(a) Evaluate appearance of optic disk
(b) Assess for venous pulsations
(c) Look for retinal hemorrhages
c. 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).
(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) Midrange bilaterally reactive = midbrain OK
(b) Midrange, bilaterally non-reactive = midbrain lesion
(c) Pin point bilaterally non-reactive = pontine lesion
(d) Dilated, bilaterally non-reactive = medullary lesion
(2) 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) Tear drop: often means ruptured globe
(c) Key hole: old iridectomy during cataract surgery
State of Illinois TNS Program
Head Trauma - page 26
(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.
g. 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.
h. 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.
i. 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) Exam: Have patient turn head against your hand and shrug shoulders
with and without resistance. Assess equality of strength, bulk of
muscle.
j. XII: Hypoglossal: Supplies most of extrinsic lingual muscles. If patient is
speaking normally, do not test XII separately.
(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.
5. 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.
State of Illinois TNS Program
Head Trauma - page 29
b. anemia; and
c. a decrease in arterial oxygen extraction.
d. If SjO2 is < pO2 27 - look for above
7. Cerebral blood flow decreases with
a. increased ICP and decreased CPP;
b. excess hyperventilation;
c. cerebral spasm; and
d. systemic hypotension.
F. 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 patient’s 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.
State of Illinois TNS Program
Head Trauma - page 34
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. Low-dose heparin
b. Low-molecular weight heparin
c. 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. Adjust room temperature as needed
2. Adjust patient covering as needed
3. Monitor for fluctuations in temp and alert physician if either occurs
4. Administer hypothalamic depressants as ordered
N. 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
State of Illinois TNS Program
Head Trauma - page 38
patient to a neurosurgeon (ATLS, 2005). Should only be done with the advice and
consent of a neurosurgeon.
4. 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.
X. Lab profiles
A. H&H or CBC
B. Glucose (injured brain is hypermetabolic and glucose intolerant; levels increase in
intracranial hemorrhage and decrease in secondary ischemia. If glucose > 200 = poor
outcome)
C. Serum lactate
D. Electrolytes
E. Drug/tox screen
F. ABG, SpO2, AVdO2, SjO2.
G. Creatinine, blood urea nitrogen (BUN)
H. International normalized ratio (INR)
I. Prothrombin time (PT) and partial thromboplastin time (PTT)
J. Urine electrolytes, urea and glycerol q. 6 hours. Monitor Na levels for SIADH.
K. 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.
XI. 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. 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 Behavior abnormal
b. E Emesis intractable
c. A Age > 65
d. N Neurological deficit
e. B Bleeding disorder
f. A Altered mental status
g. S Skull fracture
h. H Hematoma scalp
2. Other criteria that suggest the need for CT
a. Loss of consciousness > 5 minutes
b. Combativeness
c. Facial injury
d. Penetrating skull injury
e. Acute pupillary inequality
f. Skull films reveal IC air or shift of the pineal gland from midline
State of Illinois TNS Program
Head Trauma - page 39
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.
XIV. 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 acceleration-
deceleration 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.
State of Illinois TNS Program
Head Trauma - page 41
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.
4. Abrasions, contusion, burns
5. 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.
6. 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.
C. Skull fractures
1. 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.
2. 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) Most are essentially benign
(b) A diastatic (sprung suture) is the biggest predictor of who
will deteriorate from a linear fracture
State of Illinois TNS Program
Head Trauma - page 42
e. Growing fracture
(1) Unique to pediatric population
(2) Brain under 5 torr pressure; will pulsate through linear fracture
3. 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) 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) Visual field deficits: CN II (Optic)
(h) Pneumocephalus
(i) Sinus air-fluid levels
(2) 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
State of Illinois TNS Program
Head Trauma - page 44
(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
e. 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) Evaluation within 4 hours of injury
(b) Post-op ICP < 20 mmHg
(c) Normal post-op evoked potentials
(d) GCS > 5
f. 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.
3. 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. Clinical presentation
(1) 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.
(2) Optic fundi have pre-retinal hemorrhages; visual disturbances
(3) Ipsilateral dilated pupil
State of Illinois TNS Program
Head Trauma - page 47
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.
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.
6. 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
State of Illinois TNS Program
Head Trauma - page 49
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, YES No
disorientation, or impaired consciousness?*
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
4. At the time of your trauma, did you experience any loss of consciousness lasting 30
minutes or less?* YES No
* 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
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 post-
traumatic 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), 27-
42.
Harders, A., Kakarieka, A., Braakman, R. et al. (1996). Traumatic subarachnoid hemorrhage and its
treatment with nimodipine. J of Neurosurgery, 85, 82-89.
State of Illinois TNS Program
Head Trauma - page 54
Harrahill, M. (1996). Glasgow coma scale: A quick review. JEN, 22(1), 81-83.
Härtl, 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), 99-
103.
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), 439-
450.
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 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.
State of Illinois TNS Program
Head Trauma - page 56
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.
State of Illinois TNS Program
Head Trauma - page 57
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.
State of Illinois TNS Program
Head Trauma - page 58
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, The first of these terms refers to the most caudal segment of the spinal cord with normal sensory
sensory level, and motor function on both sides of the body. In fact, the segments at which normal function is
and motor level: 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; L-
motor. 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 that a person may make which has no apparent goal. Ex. Flexor or extensor posturing.
movement
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,
State of Illinois TNS Program
Head Trauma - page 59
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 A period of hours, weeks, days, or months after the injury when the patient exhibits a loss of
amnesia 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 Ability to consider the probable factors that can influence the outcome of each of various
solving skill 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).
State of Illinois TNS Program
Head Trauma - page 60
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.
State of Illinois TNS Program
Head Trauma - page 61
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?
3. If a patient presents with oval pupils and hippus, what should a TNS suspect?
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?
10. A patient’s only verbal utterances are random, repetitive words or profanity. How should this verbal
response be scored?
A. Converses
B. Confused speech
C. Inappropriate words
D. Incomprehensible sounds
State of Illinois TNS Program
Head Trauma - page 62
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. 5 Protective response
B. 4 Withdrawal response
C. 3 Abnormal flexion
D. 2 Abnormal extension
12. 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. 5 Protective response
B. 4 Withdrawal response
C. 3 Abnormal flexion
D. 2 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?
20. List two TBI patients who should be prepared for emergent surgery:
State of Illinois TNS Program
Head Trauma - page 63
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:
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???
State of Illinois TNS Program
Head Trauma - page 64
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:
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. Transilluminated intubation with sedation
B. An oropharyngeal airway prior to BVM ventilation
C. Nasotracheal intubation
D. Drug-assisted intubation
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. Administer IV fluids to ensure brain perfusion.
B. Administer Nipride to reduce the blood pressure.
C. Control seizure activity quickly with Valium/Ativan.
D. Oxygenate well before suctioning the patient.
40. 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.
State of Illinois TNS Program
Head Trauma - page 65
Notes: