CONTINUING EDUCATION

Traumatic Brain Injury and Increased

Intracranial Pressure
Kim A. Noble, PhD, RN, CPAN

Traumatic brain injury (TBI) affects approximately 1.4 million individ-

uals and has a mortality rate greater than 30% in the first 72 hours after
injury. The patient with TBI can present a significant challenge for the
perianesthesia nurse in the acute care setting. Increased intracranial
pressure is a common consequence of TBI and the rapid assessment
and management can affect the long term outcome of the patient with
TBI. New monitoring modalities have been developed to monitor cerebral
blood flow and nutritional supply to neurologic tissues. A case scenario
will be used to identify priorities for the perianesthesia nurse caring for
this challenging patient.
2010 by American Society of PeriAnesthesia Nurses

ObjectivesdAfter reading this article, the partici-
pant should be able to: (1) Describe the alterations
in neurologic function found in the patient with
a TBI, (2) discuss new technological forms of intra-
cranial monitoring that are available, and (3) de-
scribe assessment and patient care priorities for
the perianesthetic patient with a TBI.
TRAUMATIC BRAIN INJURY (TBI) patients with
a Glasgow Coma Score (GCS) greater than 9 are
classified as having a severe brain injury and have
a mortality risk of more than 30% in the first 72
hours after the injury. Despite changes in monitor-
ing and treatment modalities, there has been very
little improvement in the mortality rate of TBI
in the last 20 years.1 Patients who have sustained
a severe TBI often have polytrauma with additional
injuries, which further complicates their treat-
ment and prognosis. TBI affects approximately
1.4 million individuals annually in the United
States and carries annual health care costs that
Kim A. Noble, PhD, RN, CPAN, is an Associate Professor,
Widener University, Chester, PA.
Address correspondence to Dr. Kim A. Noble, Department of
Nursing, Widener University, One University Place, Chester,
PA 19013; e-mail address: kimnoble@verizon.net.
2010 by American Society of PeriAnesthesia Nurses
1089-9472/$36.00
doi:10.1016/j.jopan.2010.05.008
exceed $100 billion.2 TBI is associated with 50%
of all trauma-related deaths leading to refractory in-
tracranial hypertension and herniation.3 Addition-
ally, one-third of the deaths associated with
Operation Iraqi Freedom and the Vietnam conflict
were caused by TBI.2
Perianesthesia nurses working in facilities with a
trauma center designation are on the front line to
deliver care to critically ill patients with severe TBI.
Secondary brain injuries significantly increase with
episodic hypotension, increased intracranial pres-
sure and hypoxia,4 leading to neuronal death from
cerebral edema, ischemia, and acute inflammation.2
Secondary brain injuries are associated with in-
creased rates of mortality and long-term disability.
For every person who dies from a trauma-related
injury, three are permanently disabled. Long-term
health care and rehabilitation expenses, as well as
loss of wages for patients, were $600 billion in
2006.3 Using rapid assessment and monitoring skills,
the perianesthesia nurse can intervene rapidly to
modulate the development of a catastrophic second-
ary brain injury.
Tessie Trauma (TT) is a 16-year-old female who was
driving with her father when her foot slipped off of
the brake and hit the gas pedal; she crossed the me-
dian of a large, busy street, resulting in a head-on

242 Journal of PeriAnesthesia Nursing, Vol 25, No 4 (August), 2010: pp 242-250

INCREASED ICP
collision with another car moving at a high rate of
speed. TT had refused to wear a seatbelt. Her fore-
head struck the windshield of the car and she sus-
tained a TBI, blunt injury to her abdomen,
fractures of her left humerus and collarbone, and
a crush injury of the left forearm.
It took the emergency personnel 25 minutes to ex-
tract TT from the car. She was initially conscious at
the scene, but by the time she was removed from
the car she was completely unresponsive and had
a GCS of 3. TTs father reported that she has a past
medical history of smoking and her only current
medication is oral contraceptives.
Upon admission to the emergency department,
TT had a right pupil that was 2 mm and a left of
4 mm; both were sluggishly reactive. She was
taken to radiology and had a computed tomogra-
phy scan of the head, which revealed a left-sided
contusion with a large epidural hematoma. She
was immediately taken to the operating room
(OR) for hematoma evacuation and stabilization
of her orthopedic injuries.
TT was taken to the OR, and anesthesia and surgery
began as planned. She was induced with 100%
oxygen, midazolam 2 mg, 100 micrograms fentanyl,
200 mg propofol, and succinylcholine for rapid
sequence induction. Anesthesia was maintained
with a continuous propofol infusion and incremen-
tal doses of midazolam, fentanyl, and vecuronium.
TT was not reversed at the end of the evacuation
of a large epidural hematoma, open reduction
with the insertion of an external fixator on the left
forearm, rodding of the left humerus, and closed
reduction of the left clavicle. Overnight, TT was to
remain on paralytics for facilitation of mechanical
ventilation and a propofol infusion to reduce
cerebral metabolic rate and improve cerebral blood
flow (CBF) and ICP. She received 3,200 mL of lac-
tated Ringers solution for a procedure that took
approximately 2 hours. Her blood loss for the proce-
dure was 550 mL. A nasogastric tube was inserted
during anesthesia and drained 200 mL of dark,
bilious material during the surgical procedure.
TT arrived in the Phase I PACU unresponsive and in-
tubated, and was placed on a tidal volume of 450
mL, assist-control 12, and FiO2 of 1.0 via a 6.0 oral
endotracheal tube taped at the 14-cm lip mark. TT
had a right-sided intracranial pressure (ICP) monitor
243
that reads 21 to 23 mm /Hg. Her admission vital
signs were blood pressure 86/44 mm Hg (mean
blood pressure [MBP] 62); heart rate 180 bpm;
respiratory rate 10 breath/min; temperature 101 F.
The following lab values were sent and results ob-
tained: Ph 7.28, PCO2 55, PO2 304, HCO3 18; Sat-
uration 1.0 on 100% FiO2; Na1 157 meq/L, K1
5.7 meq/L, Cle 117 meq/L, CO2 28 mmol/L, serum
osmolarity 312 mOsm/kg H2O; urine output for
the procedure 1,200 mL, blood loss 100 mL.
TT was unresponsive to verbal or light, painful stim-
uli. She had no spontaneous movement and her
pupils were 2 mm and sluggishly reactive. Her
head dressing was dry and intact with the protrusion
of the intracranial monitor. She had clear bilateral
breath sounds. She was in a sinus tachycardia on
the monitor without ectopy. Her skin was pale
and dry, with thready palpable pulses. The nasogas-
tric tube was patent and placed to low continuous
wall suction. TT had a Foley catheter, which drained
large amounts of dilute urine. She had bilateral large-
bore intravenous catheters with normal saline and
lactated Ringers solution infusing. Her left arm
had a plaster splint with a dry, intact dressing. The
external fixation was in place and x-ray studies
were completed at the end of the surgical procedure
and cleared by the orthopedic surgeon.
Anesthesia was consulted for lab results. Blood
gas analysis indicated a mixed respiratory and meta-
bolic acidosis. Her FiO2 was decreased to .6, her ven-
tilator rate increased to 14 breaths/minute, and her
tidal volume increased to 500 mL. Blood gasses
were to be repeated every 30 minutes. A 500-mL
fluid challenge was ordered over 15 minutes and
urine output was to be measured every 30 minutes
and replaced with crystalloid intravenous fluid. Vaso-
pressors were to be added to maintain a mean blood
pressure .70 mm Hg as needed. Urine-specific
gravity was sent to rule out diabetes insipidus. The
neurosurgeon was also contacted and TTs ICP was
reported. TTs parents were allowed to visit briefly
and were updated with her current status.
Intracranial Physiology and the Monro-
Kellie Hypothesis
The brain has a tremendous level of metabolic activ-
ity and requires a continuous supply of glucose and
oxygen to function. The greatest energy use drives
244
the active pumps that restore and maintain the in-
tracellular and extracellular ion concentration
gradients, allowing for polarized or charged cell
membranes. The central nervous system represents
only 2% of our body tissues; it receives 15% of the
total cardiac output and uses approximately 20%
of the total oxygen consumed by the body.5 The
blood flow and the delivery of oxygen and nutrients
to brain tissues are primarily controlled by the pro-
duction and release of CO2 by the working cells. As
cellular metabolism increases, CO2 production in-
creases, leading to a dilation of local blood vessels
and an increase in the delivery of oxygen. The re-
verse is also true; if the cellular activity of the brain
decreases, CO2 production will decrease, leading to
local vasoconstriction of intracranial blood vessels.
Cerebral hypoxia, or a decline in the supply of
oxygen, leads to a global depression of cellular
activity and decreased brain function. Symptoms
associated with cerebral hypoxia are agitation, eu-
phoria, drowsiness, reduced problem solving, and
unconsciousness. A situation causing a significant
decrease or loss of blood flow will cause cerebral
ischemia. Cerebral ischemia can be local, as would
be seen in a stroke, or global as would be present
with cardiac arrest. With global cerebral ischemia,
unconsciousness occurs in seconds and restoration
of blood flow to the brain is essential. There is
a rapid depletion of intracranial energy stores;
with glucose stores depleted in 2 to 4 minutes,
and adenosine triphosphate (ATP) exhaustion in 4
to 5 minutes.5 As the activity of the ATP-dependent
active pumps, Na1, water, and Ca11 move from the
extracellular to the intracellular spaces and cerebral
edema forms. The movement of Ca11 triggers the
release of DNA-based and intracellular enzymes,
triggering the initiation of the inflammatory cas-
cade, protein and fat destruction, and cellular injury
and destruction. Reperfusion can further increase
cellular damage as the restoration of blood flow
distributes inflammatory mediators and enzymes.5
According to the Monro-Kellie hypothesis, the
skull is a rigid bowl that offers little flexibility
for changes in the size of the three intracranial
components. Found in this rigid bowl are three
constituents: 80% represented by brain tissue
and the remaining 20% represented by the intra-
cranial fluid volumes (10% blood volume and
10% of cerebrospinal fluid). To maintain normal
pressure in the skull, any increase in the size of
KIM A. NOBLE
one component initially will lead to a compensa-
tory decrease in one or both of the other two. Nor-
mal intracranial pressure ranges between 0 and 15
mm Hg.5 When there is an increase in any one
component that overpowers compensation, in-
creased ICP is seen. Examples of compartmental
volume increases that would elevate ICP include
cerebrospinal fluid volume increases, as would
be present in acute hydrocephalus; increased
blood volume associated with subarachnoid hem-
orrhage; or cerebral edema leading to an increase
in the brain tissue volume.
Also of importance is the pressure required to per-
fuse the brain, termed cerebral perfusion pressure
(CPP), which is the difference between the mean
blood pressure (MBP) and the opposition to flow
provided by the ICP (CPP 5 MBP 2 ICP). Normal
CPP ranges between 70 and 100 mm Hg5 and ische-
mia is associated with pressures less than 40 mm
Hg. CPP is very important in patients with TBI
because it represents the pressure that is required
to bring oxygen and nutrients to neuronal cells,
and decreases in CPP may increase the probability
of a secondary brain injury, reducing long-term
prognosis.2 The worst situation for a patient with
a TBI would be when the ICP approaches and
then exceeds the MAP, blood flow ceases, and herni-
ation of the intracranial contents then follow. The
cortical neurons are very sensitive to hypoxia, and
the first sign of a reduction in neurologic function
is a decrease in the level of consciousness, as would
be seen in a patient who is awake and alert and then
becomes confused.5 As CPP declines, CO2 will
accumulate, leading to vasodilation and an increase
in blood volume, further increasing ICP. Symptoms
would progress and the patient would become
lethargic, stuporous, and lapse into a coma. As the
pressure is referred downward onto the brain
stem, changes would be present in respiratory
rate and cranial nerve function.
Anesthetic Management of the Patient
with a TBI
Research is currently under way for clarification
and evidence-based recommendation(s) for the se-
lection of anesthetic agents that could improve
neurologic outcomes for the patient with a TBI.
Emergent patient stabilization preoperatively and
anesthetic agent selection is based on a common
goal of treatment of the reduction of secondary
INCREASED ICP
brain injury. There are currently two methods of
anesthetic approach for the TBI patient: the use
of volatile gas anesthetics (VGAs) or total intrave-
nous anesthesia (TIVA). VGAs have been shown
to decrease CPP while at the same time increasing
cerebral perfusion pressure (CPP), and decrease
the neurologic demand for oxygen, termed cerebral
metabolic rate for oxygen (CMRO2). In comparison,
intravenous anesthetic agents have even more brain-
protective outcomes, including decreased CPP, the
preservation of CBF, cerebral vasoconstriction, and
decreases in ICP and CMRO2.2 Finally, the use of
ketamine, desirable for use in the unstable trauma
patient with multiple injuries because of its preser-
vation of cardiovascular function, has been contro-
versial in patients with TBI. The use of TIVA with
ketamine was found to be at least as efficacious as
VGA in severely injured patients with combat-
related TBI.2
Intracranial Monitoring: Future
Possibilities
Although the gold standard for monitoring neuro-
logic function remains the bedside examination,
methods of monitoring ICP hold a close second
for patients with severe TBI. Flaws exist with
both of these monitoring methods in their inability
to detect subtle changes in brain injury. New devel-
opments in neuromonitoring procedures have
provided data regarding cerebral metabolic func-
tion, including CBF monitoring, cerebral micro-
dialysis, measurement of brain tissue oxygen
tension (PbtO2), and jugular bulb venous oxygen
saturation (SjVO2).6
CBF is considered to be of vital importance in mon-
itoring the patient with a TBI because CBF gives an
estimation of nutrient delivery to brain tissue. Av-
erage CBF in a human is 55 mL/100 g of brain
per minute, but this average value differs based
on the type of tissue being monitored (ie, gray or
white matter). As mentioned previously, CBF is
coupled to metabolic rate via local blood flow con-
trol. Areas of brain tissue with high metabolism re-
ceive increased CBF from an increase in the local
production of CO2. Cerebral ischemia occurs if
the CBF decreases to less than 18 mL/100 g/min
and irreversible injury is present with CBF de-
creases to less than 10 mL/100 g/min of blood
flow. There are currently three options for CBF
monitoring: (1) continuous monitoring with ther-
245
mal diffusion flowmetry, which measures differ-
ences in temperature between two probes and
converts to a readout of CBF; (2) laser Doppler
flowmetry, where a probe is inserted into brain tis-
sue and measures the density of moving blood; and
(3) transcranial Doppler ultrasonography, where
blood flow through large intracranial vessels is
used predominately for the detection of vascular
spasm. CBF may also be measured in a spiral
dynamic perfusion computed tomography, where
a patient receives contrast and CBF, cerebral blood
volume, and mean transit times are measured.6
Cerebral microdialysis uses a catheter to measure
capillary-based levels of glucose as a measure of nu-
trient delivery and the lactate/pyruvate ratio and
glutamate, which are reflective of local ischemia.
For this monitoring system, a microdialysis cathe-
ter (a small tube within a semipermeable dialysis
membrane) allows the diffusion of substances
along the catheter into a small container for analy-
sis. This technology is still on the research stage
and although there have been several published tri-
als using cerebral microdialysis, additional research
is recommended.
PbtO2 has been well studied and uses a device
similar to pulse oximetry to measure focal oxygen
tension in a specific area of brain tissue. This device
is inserted via an intracranial bolt directly into
the white matter of the brain, providing a disease-
independent ischemic threshold.6 PbtO2 may be
influenced by CBF, CPP, and inspired oxygen con-
centration, but it is generally accepted that levels
below 10 to 15 mm Hg have a reduced prognosis
for recovery. PbtO2 has also been shown to decrease
with hyperventilation theorized to be caused by
vasoconstriction and the reduction in the delivery
of oxygen and nutrients to the brain tissue.
Finally, the measurement of SjVO2 provides the
venous saturation of blood leaving the brain as
a measurement of the delivery of oxygen to the
brain. The goal of this monitoring tool is to rapidly
identify and prevent a secondary brain injury. Mon-
itoring is completed with the retrograde place-
ment of a catheter of the internal jugular vein
with a fiberoptic sensor to continuously measure
oxygen saturation. SjVO2 has been well studied
and shows accuracy in numerous studies.6 Normal
SjVO2 is approximately 60% but may be lower in
TBI patients as the damaged neurologic tissue is
246
unable to appropriately extract oxygen, leading to
a higher level of SjVO2. A SjVO2 as high as 90% may
be found in TBI, indicating the inability of brain tis-
sue to unload oxygen. Decreased oxygen delivery,
or ischemia, may also lead to alterations in SjVO2. A
SjVO2 less than 50% for longer than 10 minutes
may be caused by ischemic desaturation, generally
large areas of brain tissue are affected before de-
clines in venous saturation are seen. The best use
of this technology is to trend venous saturation
over time in the brain-injured patient.6
Implications for the PACU Patient
The emergent care for the critically ill, multiple-
trauma patient with a TBI is challenging at best
for perianesthesia nursing. Patient care priorities
focus on rapid assessment and monitoring and
the stabilization as the patient emerges from anes-
thesia and recovers from surgery. A thorough un-
derstanding of the physiologic implications of
increased ICP allows the perianesthesia nurse to
anticipate, assess, and assist in the rapid treatment
of the highly time-dependent prevention of a sec-
ondary brain injury.
Alteration in Respiratory Function
The immediate and ongoing management of the
patient with TBI should always start with the assess-
ment of oxygenation and ventilation for the preven-
tion of hypoxemia. The occurrence of hypoxia and
hypovolemia in the patient with TBI can double the
mortality rate because of the development of a sec-
ond brain injury.1 TT should be adequately venti-
lated upon transport from the OR and placed on
the ventilator using the settings ordered by anesthe-
sia. She should only be suctioned if necessary and
receive sedation to control coughing. Retained
CO2 must be avoided because it may lead to intracra-
nial vasodilation and increase ICP.7 Arterial blood
gas analysis and frequent assessment for breath
sounds and ventilatory status are imperative. Serial
arterial blood gas analyses, with timely reporting
of abnormalities and implementation of ordered
ventilator setting changes, is important. In TTs situ-
ation, a pCO2 of 55 obtained upon admission to the
Phase I PACU will contribute to her increased ICP by
increasing the volume of blood in the cranium from
vasodilation of intracranial vessels. By increasing
both the ventilatory rate and tidal volume, TTs
pCO2 will return to a more normal value.
KIM A. NOBLE
If TTs blood pressure is adequate, the head of the
bed should be elevated at least 10 to 15 degrees to
promote the gravity-driven drainage of venous
blood from the cranium. A rapid respiratory assess-
ment is completed upon admission to the Phase I
PACU, including rate, expansion of ventilation,
auscultation of breath sounds, and measurement
of oxygen saturation. Another high priority is the
maintenance of a patients airway during a seizure.
Alteration in Neurologic Function
A rapid neurologic assessment is completed with
the admission assessment by the Phase I PACU
nurse. A baseline neurologic assessment should in-
clude level of consciousness, pupillary reaction
and responsiveness to stimuli using the GCS score.
As appropriate, TT should have deep tendon
reflexes, gross motor function, and screening for
posturing completed.4 Assessment of head dress-
ing and location and appearance of the intracranial
monitor should be completed, and an admission
ICP obtained and reported. Sedation and paralytic
orders should be received and administered to
decrease cerebral metabolism and facilitate me-
chanical ventilation. Seizures should be prevented
because they will rapidly deplete intracranial nutri-
tion, increasing the use of ATP by 250% and oxy-
gen consumption by 60%.5 Seizures also lead to
an increase of blood flow to the brain by 250%5
and can lead to a catastrophic outcome for patients
with increased ICP. TT should receive ordered
prophylactic antiseizure medications.
Alteration in Cardiovascular Function
Frequent assessment of vital signs and continuous
cardiac monitoring are used for any patient recov-
ering from general anesthesia. Hypotension should
be treated rapidly because MAP is the major con-
tributor to CPP. Maintenance of a CPP less than
70 mm Hg may reduce mortality and can usually
be achieved with a MAP more than 90 mm Hg.4 In-
vasive arterial line insertion or the insertion of cen-
tral venous catheters should be incorporated into
TTs care if needed for assessment and treatment
of hypotension.1 Neurovascular assessment of ex-
tremities is important given TTs orthopedic in-
juries and surgical correction. Elevation and deep
vein thrombosis prophylaxis should be incorpo-
rated as ordered.
INCREASED ICP
Alteration in Fluid and Electrolyte Balance
The availability of a running intravenous line is re-
quired for the rapid administration of needed med-
ications. Osmotic diuretics such as mannitol may
be required to manage intracranial hypertension
and may lead to a decrease in circulating blood vol-
ume and blood pressure. Continuous assessment
of intake and output and the administration of
crystalloids or blood products as indicated should
be used to maintain MAP in a normal range to
ensure adequate CPP. Communication of current
status to the anesthesia care provider is always im-
portant, because it is the receipt and delivery of re-
ceived physician orders.
Alteration in Musculoskeletal Function
As with any orthopedic surgical patient, careful
assessment and ongoing monitoring of TTs left
References
1. Cowley NJ, da Silva EJ. Prevention of secondary brain
injury following head trauma. Trauma. 2008;10:35-42.
2. Grathwohl KW, Black IH, Spinella PC, et al. Total intrave-
nous anesthesia including ketamine versus volatile gas anesthe-
sia for combat-related operative traumatic brain injury.
Anesthesiology. 2008;109:44-53.
3. Maerz LL, Davis KA, Rosenbaum SH. Trauma. From the
section on trauma, surgical critical care and surgical emergen-
cies and section of perioperative and adult anesthesia. Int
Anesthesiol Clin. 2009;47:25-36.
4. Hebb MO, Clarke DB, Tallon JM. Development of a provin-
cial guideline for the acute assessment and management of adult
247
arm is important especially if immobilization is
maintained due to TTs fractured clavicle. Monitor-
ing for digit refill, sensation, and color is part of the
ongoing assessment. The application of ice and
use of elevation should be guided by patient condi-
tion and physician order.
Conclusion
In conclusion, the patient with a TBI presents with a
multitude of perianesthesia nursing care priorities.
Admission and ongoing assessment can assist the
nurse to anticipate and prevent a secondary brain
injury. A comprehensive review of intracranial
physiology and an updated review of possible treat-
ment strategies can prepare the perianesthesia
nurse for new treatment modalities for the neuro-
surgical patient with increased ICP.
and pediatric patients with head injuries. Can J Surg. 2007;50:
187-194.
5. Porth CM, Matfin G. Pathophysiology: Concepts of Altered
Health States, 8th ed. Philadelphia: Lippincott Williams &
Wilkins; 2009.
6. Barazangi N, Hemphil C. Advanced cerebral monitoring
in neurocritical care. Neurology (India). 2008;56:405-
414.
7. Drain CB, Odom-Forren J. PeriAnesthesia Nursing: A
Critical Care Approach, 5th ed. St Louis, MO: Saunders; 2009.
248 KIM A. NOBLE

Traumatic Brain Injury and Increased Intracranial Pressure

1.41 Contact Hours

Purpose of the Journal of PeriAnesthesia Nursing: To facilitate communication about and deliver
education specific to the body of knowledge unique to the practice of perianesthesia nursing.
Purpose/Goal: The purpose of this article is to focus on the special issues of patients with traumatic brain
injuries and present strategies to nurses for optimization of perianesthesia care.
Target Audience: The primary audience for JOPAN includes nurses in perianesthesia settings: ambulatory
surgery, preadmission testing, postanesthesia (Phases I, II, III), and pain management. Additionally, the Jour-
nal provides information of interest to professionals practicing in office-based settings, operating rooms,
medical/surgical and critical care nursing, and all areas where sedation/analgesia is utilized. Facilities and
settings of care delivery vary and therefore it is the practice, not the location that determines the focus.
Article Objectives: (1) Describe the alterations in neurologic function found in the patient with a TBI. (2)
Discuss new technological forms of intracranial monitoring that are available. (3) Describe assessment and
patient care priorities for the perianesthetic patient with a TBI.
Accreditation: American Society of Perianesthesia Nurses is accredited as a provider of continuing nursing
education by the American Nurses Credentialing Centers Commission on Accreditation.
Accreditation does not imply that ASPAN or ANCC-COA approves or endorses any product included in the
activity. Additional provider numbers: Alabama #ABNP0074, California #CEP5197, Florida 50e114.
Registered nurse participants can receive 1.41 contact hours for this activity.
Non-endorsement of products: Accreditation refers to recognition of continuing nursing education ac-
tivities only and does not imply Commission on Accreditation approval or endorsement of any commercial
product.
Disclosure: All authors and planning committee members of nursing continuing education activities are
required to disclose (1) any significant financial relationships with the manufacturer(s) of any commercial
products, goods or services and (2) any unlabeled/unapproved uses of drugs or devices discussed in the
educational activity. Such disclosures will be printed in the educational activity. Any conflicts of interest
must be resolved prior to the development of the educational activity.
The members of the planning committee for this continuing nursing education activity do not have financial
arrangements, interests or affiliations related to the subject matter of this continuing education article.
The author for this continuing nursing education activity does not have financial arrangements, interests or
affiliations related to the subject matter of this continuing education article.
Off-label use of a Commercial Product: The author will not be discussing any off-label use equipment,
products, etc. in this nursing continuing education activity.
Verification of Participation: Verification of your participation in this educational activity is done by
having you complete the registration form and submit the form along with the post test and evaluation
form to the ASPAN national office.
Requirements for Successful Completion: To receive contact hours for this nursing continuing educa-
tion article a minimum grade of 80% must be achieved on the post test.
Directions: The multiple-choice examination below is designed to test your understanding of Traumatic
Brain Injury and Increased Intracranial Pressure according to the objectives listed. To earn contact
hours from the American Society of PeriAnesthesia Nurses (ASPAN) Continuing Education Provider Program:
(1) read the article, (2) complete the posttest by indicating the answers in the test grid provided, and (3) tear
out the page (or photocopy) and submit postmarked before August 31, 2012, with check payable to ASPAN
(ASPAN member, $12.00 per test; nonmember, $15.00 per test) and return to ASPAN, 90 Frontage Road,
Cherry Hill, NJ 08034-1424. Notification of contact hours awarded will be sent to you in 4 to 6 weeks.
INCREASED ICP
Posttest Questions
1. The brain receives what percentage of the
total cardiac output?
a. 10%
b. 15%
c. 20%
d. 25%
2. Which of the following is the most important
regulator of cerebral blood flow?
a. Mean arterial blood pressure
b. Sympathetic nervous system
c. Intracranial pressure
d. Carbon dioxide
3. Which of the following is the final intracra-
nial consequence of ischemia?
a. Seizure activity
b. Decreased neurotransmitters
c. Cerebral edema
d. Impaired motor activity
4. Which of the following monitoring capabil-
ities has the most research data to support
its clinical use?
a. Cerebral blood flow monitoring
b. Cerebral microdialysis
c. Brain tissue oxygen tension
d. Jugular bulb venous oxygen saturation
5. Which of the following physiologic parame-
ters is a desirable outcome for the selection
of anesthetic agent(s)?
a. Decreased cerebral metabolic rate for
oxygen
b. Increased cerebral perfusion pressure
c. Increased cerebral blood flow
d. Increased intracranial pressure
6. Which of the following is a true statement
described by the Monro-Kellie hypothesis?
a. Increases in the volume of intracranial pres-
sure are easily accommodated with the
downward movement of cranial tissue.
b. The skull is a rigid container and pressure
increases are not tolerated in brain tissue.
c. There are three components contained
within the skull; early increases in one
are compensated by the other two.
249
d. The skull is a rigid container and pressure
fluctuations are commonly seen with sys-
temic blood pressure changes.
7. Ischemia would have which of the following
ultimate outcomes?
a. Increased intracranial blood volume from
increased carbon dioxide
b. Decreased cerebral contents from
dehydration
c. Increased cerebral perfusion pressure
caused by decreased ICP
d. Limited impact on the Monro-Kellie hy-
pothesis
8. Which is the best indicator of neurologic
function?
a. Pupillary reaction
b. Respiratory pattern changes
c. Abnormal posturing
d. Decreased level of consciousness
9. What is the cerebral perfusion pressure for
a patient with a blood pressure of 84/38
mm Hg (mean arterial pressure 54) and an
intracranial pressure of 21 mm Hg? Is this
normal?
a. 75 mm Hg; yes, the cerebral perfusion
pressure is normal
b. 33 mm Hg; no, the cerebral perfusion
pressure is severely decreased
c. 33 mm Hg; the cerebral perfusion pres-
sure is low but not dangerous
d. 54 mm Hg; the cerebral perfusion pres-
sure is adequate
10. What is the rationale for continuing the ad-
ministration of propofol in TT?
a. To decrease the work of breathing and
prevent CO2 retention
b. To keep TT pain free in the immediate
postoperative period
c. To reduce the release of catecholamines
and prevent hypertension
d. To reduce cerebral metabolism, preserve
cerebral blood flow and reduce intracra-
nial pressure
250 KIM A. NOBLE

TRAUMATIC BRAIN INJURY AND INCREASED INTRACRANIAL PRESSURE

ANSWERS

W010812 Please circle the correct answer

1. a. 2. a. 3. a. 4. a. 5. a.
b. b. b. b. b.
c. c. c. c. c.
d. d. d. d. d.

6. a. 7. a. 8. a. 9. a. 10. a.
b. b. b. b. b.
c. c. c. c. c.
d. d. d. d. d.
________________________________________________________________________________________

Please Print

Name__________________________________Nursing License No./State____________________________

Address__________________________________________________________________________________

City_______________________________State_______________________Zip_________________________

ASPAN Member #__________________________________________________________________________

EVALUATION: Traumatic Brain Injury and Increased Intracranial Pressure

(SD, strongly disagree; D, disagree; ?, uncertain; A, agree; SA, strongly agree) SD D ? A SA

1. To what degree did the content meet the objectives? 1 2 3 4 5
a. Objective # 1 was met 1 2 3 4 5
b. Objective # 2 was met 1 2 3 4 5
c. Objective # 3 was met 1 2 3 4 5
2. The program content was pertinent, comprehensive, and useful to me. 1 2 3 4 5
3. The program content was relevant to my nursing practice. 1 2 3 4 5
4. Self-study/home study was an appropriate format for the content. 1 2 3 4 5
5. Identify the amount of time required to read the article and take the test.
Under 30 min 30-60 min 61-90 min 91-120 min over 120 min

Test answers must be submitted before August 31, 2012, to receive contact hours.