Drug Update Management of Intracranial Hypertension: Focus on Pharmacologic Strategies

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AACN Advanced Critical Care
Volume 22, Number 3, pp.177–182
© 2011, AACN
Drug
Update
Earnest Alexander, PharmD, and
Gregory M. Susla, PharmD
Department Editors
Management of Intracranial Hypertension:
Focus on Pharmacologic Strategies
Kelly M. Ennis, PharmD
Gretchen M. Brophy, PharmD, BCPS
hypertension is a medical emergency requiring prompt attention
Ithentracranial
and intervention to prevent devastating neurologic outcomes. Approaches to
management of elevated intracranial pressure (ICP) include pharmacologic
and nonpharmacologic strategies, both of which are relevant to the critical care
nurse practitioner. The aim of this column is to briefly familiarize the reader
with the normal physiology and principles of ICP as well as provide a focused
review of pharmacologic strategies to reduce elevated ICP. Mannitol (Osmitrol)
and hypertonic saline will be reviewed in detail, including dosing, administration, potential adverse effects, and monitoring issues for each. The role of analgesia and sedation in managing elevated ICP also will be discussed. Finally, the
use of barbiturates as well as nonpharmacologic measures will be reviewed
briefly.
Physiology and Principles of ICP
Understanding the basic anatomy and physiology of the central nervous system
is paramount to understanding the pathophysiology of intracranial hypertension. The skull is a fixed compartment containing approximately 80% brain tissue, 10% cerebrospinal fluid (CSF), and 10% blood volume.1 The key to
understanding the strategies in the management of elevated ICP, both pharmacologic and nonpharmacologic, is the Monroe-Kellie principle. This theory
states that the total volume in this system is fixed, and the individual components must compensate if a pathologic process affects the normal quantities of
any one of these components; that is, an increase in brain size, blood volume, or
CSF must be accompanied by an equal decrease in 1 of these components or an
elevation in ICP will occur.1,2 Therefore, reducing ICP may be achieved by 1 or
more of the following approaches: reducing brain size (edema) through the use
of hyperosmolar therapies, reducing CSF via physical drainage, reducing blood
volume by inducing hyperventilation and vasoconstriction, or surgical removal
of a space-occupying lesion such as a tumor or hematoma.1
Normal ICP ranges from 5 to 15 mm Hg for adults. Severe intracranial
hypertension is considered present at pressures greater than 20 to 25 mm Hg
and typically requires some form of treatment.3 Elevated ICP leads to a decrease
in cerebral perfusion pressure (CPP) and decreased flow, resulting in cerebral
Kelly M. Ennis is PGY2 Critical Care Pharmacy Resident, Department of Pharmacy Services, Virginia
Commonwealth University Health System, 401 N 12th St, PO Box 980042, Richmond, VA 23298
(kennis2@mcvh-vcu.edu).
Gretchen M. Brophy is Professor of Pharmacotherapy & Outcomes Science and Neurosurgery, Virginia
Commonwealth University, Medical College of Virginia Campus, Richmond, VA.
DOI: 10.1097/NCI.0b013e318214564b
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Drug Update
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ischemia. Intracranial pressure values consistently greater than 40 mm Hg represent lifethreatening intracranial hypertension because
of the risk for brain herniation.
Autoregulation allows the brain to maintain adequate cerebral blood flow (CBF) when
CPP is in a normal range (50–150 mm Hg).2 In
patients with elevated ICP, it may be necessary
to maintain a higher MAP as a method to keep
CPP approximately 50 to 70 mm Hg. Cerebral
perfusion pressure values less than 50 mm Hg
have been associated with cerebral ischemia
and poor outcomes.1,3
Elevated ICP
Elevated ICP or intracranial hypertension may
have a variety of etiologies, including a primary
or intracranial process, an extracranial process,
or it may be a complication of a neurosurgical
procedure. Primary or intracranial processes may
be a result of a brain lesion (malignant or infectious in nature), neurotrauma, intracerebral
hemorrhage, ischemic stroke, or hydrocephalus.
Extracranial processes may include airway
obstruction, hypoventilation, dysregulation of
blood pressure, posture, fever, seizure activity,
hepatic failure, or drug toxicity.4 Elevated ICP
may also occur after neurosurgical procedures
because of hematoma, residual edema, excess
vasodilation, or disturbances in CSF.2
Pharmacologic Treatment of
Elevated ICP
The pharmacologic management of elevated ICP
centers mostly around the use of hyperosmolar
agents, including mannitol and hypertonic saline.
For many years, the mainstay of hyperosmotic
therapy for elevated ICP was mannitol, with the
use of hypertonic saline becoming more prevalent recently. Several comparative studies have
been done with these 2 agents with inconclusive
results; no evidence supports one therapy over
the other.5–9 Each patient’s clinical scenario
should be taken into account when choosing
between these hyperosmolar therapies.
Mannitol
Mannitol is an osmotic diuretic that is most
commonly used in the reduction of ICP. Mannitol reduces ICP in 2 ways. First, it expands
plasma volume, leading to decreased blood
viscosity and increased CBF and oxygen delivery. It also increases serum osmolality, resulting in the creation of an osmotic gradient
between the intravascular space and extracel-
lular space in the brain. This gradient allows
fluid from the cerebral parenchyma to be
drawn into the serum, resulting in a reduction
in cerebral edema, subsequently reducing ICP.
In cases of intracranial hypertension, mannitol
is administered via intravenous (IV) bolus over
20 to 30 minutes. The dose ranges from 0.25
to 1.5 g/kg IV as a 20% solution. Doses of
1 g/kg or more are used when an urgent reduction of ICP is necessary. Administration as an
IV bolus results in a reduction in ICP in less
than 5 minutes, with the peak effect occurring
between 15 and 30 minutes after administration. The duration of the reduction in ICP may
last from 1.5 to 6 hours, depending on the
clinical condition. For patients requiring
prolonged reduction in ICP, doses of 0.25 to
1 g/kg may be repeated every 2 to 6 hours.2,3
Although the administration of mannitol
may be lifesaving, there are concerns related to
the administration and potential adverse effects
of this drug. Mannitol is a vesicant or an agent
that may cause tissue blistering; therefore, care
should be taken to avoid extravasation; administration via central IV access is preferable.
This product should be inspected for crystal
formation before administration. If crystals are
present, the product should be redissolved by
warming the solution. Because of the potential
for crystal formation, mannitol must be administered through a 5-micron, in-line filter set.
Mannitol may not be administered with blood
products because of the risk of agglutination or
clumping of red blood cells.
It is important to monitor patients for
adverse effects that may result from the administration of mannitol. Although mannitol draws
fluid from the cerebral parenchyma into the
intravascular space, it also induces profound
diuresis. Intravascular volume depletion as well
as electrolyte loss may be induced after administration. Intake and output should be monitored
closely, and fluid lost during this process should
be replaced. Because of its diuretic effect, mannitol is relatively contraindicated in hypovolemic patients. Other adverse effects that may
occur include nephrotoxicity, rebound increases
in ICP upon discontinuation, as well as respiratory distress resulting from fluid overload in
patients with cardiovascular disease. Mannitol
is primarily eliminated in the urine as an
unchanged drug; therefore, adverse effects are
most likely to be seen in patients with reduced
renal function or after repeated administration
of high doses. Nephrotoxicity may be prevented
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VO L U M E 2 2 • N U M B E R 3 • J U LY – S E P T E M B E R 2 011
by avoiding the use of mannitol in patients with
preexisting renal disease or sepsis, by targeting
serum osmolality less than 320 mOsm/L, and
by avoiding the use of other nephrotoxic
medications.3,10,11
Hypertonic Saline
Human and animal studies have shown that
hypertonic saline possesses the ability to reduce
ICP through administration both as a bolus
and as a continuous infusion.3,12 Similar to the
mechanism of action of mannitol, hypertonic
saline reduces ICP through its osmotic effects.
Sodium chloride administered in hypertonic
concentrations ranging from 3% to 23.4% creates an osmotic gradient that forces fluid (cerebral edema) to the intravascular space, thereby
reducing ICP. Bolus doses are usually administered in response to a measured ICP and may
be repeated as needed until either the ICP is in
an acceptable range or serum sodium concentrations have risen above normal (greater than
145–155 mEq/L).12 Table 1 summarizes various
regimens of hypertonic saline that have been
studied and may be seen in practice.6,13–16
Limited data also suggest that hypertonic
saline administered as a continuous infusion
may result in a reduction in ICP. Continuous
infusions of 3% hypertonic saline may be titrated
to treatment goals including serum sodium of
145 to 155 mEq/L and serum osmolality of 310
to 320 mOsm/L.17,18
Hypertonic saline in concentrations of 3% or
more must be administered through central IV
access because of its high osmolarity and tonicity.
A 3% sodium chloride solution has an osmolarity of 1027 mOsm/L and contains 513 mEq/L of
sodium, compared with 0.9% sodium chloride,
which has an osmolarity of 308 mOsm/L and
contains 154 mEq/L of sodium. The Institute
for Safe Medication Practices includes this medication among its list of drugs that may cause
significant patient harm when used in error at
concentrations greater than 0.9%. The Joint
Commission recommends that concentrated
electrolyte solutions such as hypertonic saline be
obtained from pharmacy services and not be
readily available in patient care areas. For this
reason, mannitol may be a more convenient
option in an urgent clinical situation.
Table 1: Evidence-Based Hypertonic Saline Regimens
Trial
Study Design
Regimen
ICP Threshold*
(mm Hg)
Outcome
Kerwin et al13
Retrospective
review, single
center, N ⫽ 22
23.4% sodium chloride
solution: 30 mL
administered IV
over ⱖ30 min
⬎20
HS: ↓ ICP more
than mannitol
Huang et al14
Prospective,
observational,
single center,
N ⫽ 18
3% sodium chloride
solution: 300 mL
administered IV
over 20 min
⬎20
Rapid infusion of
HS is safe to
↓ ICP
Ware et al15
Retrospective
review, single
center, N ⫽ 13
23.4% sodium chloride
solution: 30 mL
administered IV
(Patients included had
become tolerant to
mannitol.)
⬎20
HS: ↓ ICP
comparable
to mannitol
Vialet et al6
Prospective,
randomized,
single center,
N ⫽ 20
7.5% sodium chloride
solution: 2 mL/kg
administered IV
over 20 min
⬎25
HS: ↓ no. of
elevated ICP
episodes
Munar et al16
Prospective,
nonrandomized,
single center,
N ⫽ 14
7.2% sodium chloride
solution: 1.5 mL/kg
administered IV
over 15 min
⬎15
HS: sig.↓ ICP
without sig.
change in CBF
Abbreviations: CBF, cerebral blood flow; HS, hypertonic saline; ICP, intracranial pressure; IV, intravenous.
*ICP Threshold ⫽ ICP at which hypertonic saline was administered in patients included.
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Hypertonic saline may be the osmotic therapy
of choice in hypovolemic or hypotensive patients
because it remains in the intravascular space,
thereby expanding intravascular volume and
increasing mean arterial pressure. Despite these
positive effects, potentially deleterious effects may
result from administering high concentrations of
sodium chloride. Hypertonic saline administration
has been shown to cause natriuresis secondary to
increased renal perfusion pressure and associated
diuresis. Despite this natriuretic response, serum
sodium increases after the administration of
hypertonic saline. Prolonged hypernatremia may
result in hypokalemia because of sodium and
potassium exchange at the distal tubule of the
kidney, as well as nonspecific symptoms such as
lethargy, weakness, and in more severe instances
seizure or coma. These more severe symptoms
may result from abrupt changes in sodium concentrations, such as an increase of greater than
10 to 12 mEq/L in a 24-hour period.
Rapid changes in serum sodium concentrations
may result in osmotic demyelination syndrome.
This syndrome results from a rapid decrease in
brain volume in response to a rapid increase in
serum sodium. Resulting neurologic changes
range from mild confusion that is reversible to
severe irreversible disability including seizure or
coma.19 Other adverse effects that may result from
the administration of hypertonic sodium chloride
include hyperchloremic acidosis resulting from
excess chloride administration. One strategy to
avoid hyperchloremic acidosis is to administer a
sodium acetate infusion rather than sodium chloride or a combination of the 2.15,17,20
Other potential complications are cardiovascular and/or respiratory compromise resulting
from intravascular fluid overload as well as
bleeding. The bleeding risk results from prolongation of prothrombin and activated partial
thromboplastin times and decreased platelet
aggregation due to an unknown mechanism.21
Further research is necessary to fully understand
the process by which this adverse effect occurs.
As with mannitol, the risk of rebound intracranial hypertension exists after discontinuation.
Important monitoring parameters include strict
recording of intake and output, and judicious
monitoring of serum electrolytes, and neurologic, cardiovascular, and respiratory status.
Analgesia, Sedation, and
Neuromuscular Blockade
In addition to the methods listed earlier, ICP elevations may be reduced by providing the patient
with adequate analgesia, sedation/anxiolysis, and,
in some cases, paralysis via neuromuscular
blockade. Although there are no randomized
controlled trials showing a beneficial effect of
these strategies on mortality or Glasgow Outcome Score, it has been shown that controlling
pain and agitation significantly reduces ICP
and resistance to mechanical ventilation.3,13,22
The neurologic examination may be compromised when patients are under the influence of
analgesics and sedatives; therefore, agents with
a quick onset and short duration of action are
viewed more favorably. Agents commonly chosen for these patients include fentanyl, which
has an immediate onset and duration of effect
of approximately 30 minutes to 1 hour, and
propofol, which has an onset of 1 to 2 minutes
and duration of effect of approximately 3 to
10 minutes.23
Barbiturates
In addition to the usual sedation and analgesia
provided in the intensive care unit environment
for a patient with elevated ICP, a barbiturateinduced coma may be considered. Barbiturate
coma is typically used only for patients with
elevated ICP refractory to other treatment
options because of the risks associated with
high-dose barbiturates as well as the inability
to perform a neurologic assessment on a comatose patient. The mechanism of action of barbiturate coma is severalfold, including reducing
the CBF and cerebral metabolic rate of oxygen
consumption, resulting in a decreased cerebral
blood volume and subsequently reduced ICP.2,3
To date, there is no evidence supporting a beneficial effect of barbiturate coma on outcomes in
head injury.3 The most recent comment from
the Brain Trauma Foundation regarding the
use of barbiturates to control elevated ICP recommends barbiturate therapy in hemodynamically stable patients with severe traumatic
brain injury and associated elevation in ICP
refractory to maximum medical and surgical
treatment.3
The most commonly used barbiturate in this
setting is pentobarbital administered IV in a
loading dose of 10 mg/kg over 1 to 2 hours followed by additional 5 mg/kg bolus doses as
needed with a goal of achieving burst suppression on electroencephalogram. The maintenance
dose is then initiated at 1 to 2 mg/kg/h and may
be titrated up to a maximum of 4 mg/kg/h in the
setting of continuous electroencephalographic
technology. Complications related to pentobarbital
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administration include hypotension, hypokalemia,
respiratory depression, infections, and hepatic
and renal dysfunction. Barbiturates as a pharmacologic class cause widespread suppression of all
excitable tissue, including the central nervous
system. This central nervous system depression
may range from calmness and sleep to unconsciousness and coma, which may progress in a
dose-dependent fashion to respiratory and cardiovascular depression if left unmonitored. For
this reason, patients receiving continuous barbiturate therapy must be mechanically ventilated
and undergo continuous cardiac monitoring.
The risk for rebound intracranial hypertension
exists after discontinuation of pentobarbital;
therefore, the weaning process should take
place slowly, with the rate of administration
decreased by one-half over each 24-hour period
until discontinued.2,3
Nonpharmacologic Management of
Elevated ICP
Nonpharmacologic measures may be used to
assist in reducing ICP in addition to drug therapy. These include positional strategies, airway
and ventilation manipulation, surgical management, and potentially hypothermia. To maximize outflow of CSF from the intracranial
compartment to the spinal compartment minimizing ICP, keep the head of the patient’s bed
elevated at 30⬚.2 After the airway has been
secured, if ICP ⬍20 mm Hg, ventilator settings
should allow a slight hyperventilation with a
target PaCO2 of approximately 35 mm Hg.
This reduction in PaCO2 increases the serum
pH and, in turn, the pH of the CSF. This produces arterial vasoconstriction, which increases
cerebral vascular resistance resulting in reduced
CBF, cerebral blood volume, and ICP.1 Hyperventilation may become more aggressive, with a
target PaCO2 between 30 and 35 mm Hg if elevated ICP persists despite other interventions.
An additional option for patients with
refractory intracranial hypertension is the use
of decompressive craniectomy to relieve ICP.1–3
The use of therapeutic hypothermia (goal core
body temperature of 33°C) in the management
of elevated ICP is somewhat controversial.
Although hypothermia has been shown to be
effective in reducing ICP, it is unclear whether
these patients have improved neurologic outcomes after rewarming.3 Therapeutic hypothermia is not a benign process and has an effect on
the body’s metabolic processes, including drug
metabolism.24 It is important to understand
that the metabolism of drugs may be impaired
in these patients, resulting in elevated circulating drug concentrations. This is especially true
of medications whose primary route of metabolism is hepatic (eg, fentanyl, midazolam,
phenytoin, propofol). Limited data exist surrounding the specific pharmacokinetic profiles
of drugs used in the hypothermic patient; therefore, specific recommendations for dose adjustments are not available.
Discussion
Prolonged intracranial hypertension results in
compromised CPP and subsequent cerebral
ischemia. Health care providers must understand the various strategies used to manage elevated ICP, including hyperosmolar therapy,
sedatives, and analgesics, as well as barbiturate
coma. The agents used for hyperosmotic therapy
are mannitol and hypertonic saline, which both
act by creating an osmotic gradient between the
intracranial and intravascular spaces. Mannitol
is limited by its potential for nephrotoxicity
when administered to a patient with serum
osmolality more than 320 mOsm/L. Administration of hypertonic saline is limited by both
serum sodium and serum chloride levels after
repeated doses. Both agents carry a risk of
rebound intracranial hypertension upon discontinuation. Adequate analgesia and sedation have
been shown to be beneficial in assisting with
reduction of ICP. Barbiturate comas are typically
reserved for patients with intracranial hypertension refractory to all other available medical and
surgical management. Nonpharmacologic measures are also used in the management of elevated
ICP, including elevation of the head of bed, hyperventilation, surgical intervention, and potentially
hypothermia. Understanding the benefits and risks
of these therapies is imperative to optimally manage the patient with elevated ICP.
REFERENCES
181
1. Vincent JL, Berré J. Primer on medical management of
severe brain injury. Crit Care Med. 2005;33:1392–1399.
2. Rangel-Castillo L, Robertson C. Management of intracranial hypertension. Crit Care Clin. 2007;22:713–732.
3. Brain Trauma Foundation. Guidelines for the management of severe traumatic brain injury, 3rd ed. J Neurotrauma. 2007;24(suppl 1):S1–S106.
4. Stravitz RT. Critical management decisions in patients
with acute liver failure. Chest. 2008;134(5):1092–1102.
5. Battison C, Andrew PJD, Graham C, et al. Randomized,
controlled trial on the effect of a 20% mannitol solution
and a 7.5% saline/6% dextran solution on increased
intracranial pressure after brain injury. Crit Care Med.
2005;33:196–202.
6. Vialet R, Albanese J, Thomachot L, et al. Isovolume hypertonic solutes (sodium chloride or mannitol) in the treatment
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of posttraumatic intracranial hypertension: 2 mL/kg 7.5%
saline is more effective than 2 mL/kg 20% mannitol. Crit
Care Med. 2003;31:1683–1687.
Cooper DJ, Myles PS, Mcdermott FT, et al. Prehospital
hypertonic saline resuscitation of patients with hypotension and severe traumatic brain injury: a randomized
controlled trial. JAMA. 2004;291:1350–1357.
White H, Cook D, Venkatesh B. The use of hypertonic
saline for treating intracranial hypertension after traumatic brain injury. Anesth Analg. 2006;102:1836–1846.
De Vivo O, Del Gaudio A, Ciritella P, et al. Hypertonic
saline solution: a safe alternative to mannitol 18% in
neurosurgery. Minerva Anesthesiol. 2001;67:603–611.
Gondim FA, Aiyagari V, Shackleford A. Osmolality not
predictive of mannitol-induced acute renal insufficiency.
J Neurosurg. 2005;103:444–447.
Rabetoy GM, Fredericks MR, Hostettler CF. Where the
kidney is concerned, how much mannitol is too much?
Ann Pharmacother. 1993;27:25–28.
Doyle JA, Davis DP, Hoyt DB. The use of hypertonic saline
in the treatment of traumatic brain injury. J Trauma.
2001;50:367–383.
Kerwin AJ, Schinco MA, Tepas JJ III, et al. The use of
23.4% hypertonic saline for the management of elevated
intracranial pressure in patients with severe traumatic
brain injury: a pilot study. J Trauma. 2009;67:277–282.
Huang SJ, Chang L, Han Y, et al. Efficacy and safety of
hypertonic saline solutions in the treatment of severe
head injury. Surg Neurol. 2006;65:539–546.
Ware ML, Nemani VM, Meeker M, et al. Effects of 23.4%
sodium chloride solution in reducing intracranial pressure
in patients with traumatic brain injury: a preliminary study.
Neurosurgery. 2005;57:727–736.
16. Munar F, Ferrer AM, de Nadal M, et al. Cerebral hemodynamic effects of 7.2% hypertonic saline in patients with
head injury and raised intracranial pressure. J Neurotrauma. 2000;17:41–51.
17. Qureshi AI, Suarez JI, Castro A, et al. Use of hypertonic
saline/acetate infusion in treatment of cerebral edema in
patients with head trauma: experience at a single center.
J Trauma. 1999;47:659–665.
18. Qureshi AI, Suarez JI, Bhardwaj A, et al. Use of hypertonic (3%) hypertonic saline/acetate infusion in the treatment of cerebral edema: effect on intracranial pressure
and lateral displacement of the brain. Crit Care Med.
1999;26:440–446.
19. Sterns RH, Riggs JE, Schochet SS, et al. Osmotic demyelination syndrome following correction of hyponatremia.
N Engl J Med. 1986;314:1535–1542.
20. Qureshi AI, Suarez JI. Use of hypertonic saline solutions
in treatment of cerebral edema and intracranial hypertension. Crit Care Med. 2000;28:3301–3313.
21. Reed RL II, Johnston TD, Chen Y, et al. Hypertonic saline
alters plasma clotting times and platelet aggregation.
J Trauma. 1991;31:8–14.
22. Kelly PF, Goodale DB, Williams J, et al. Propofol in the
treatment of moderate and severe head injury: a randomized, prospective double-blinded pilot trial. J Neurosurg.
1999;90:1042–1057.
23. Jacobi J, Fraser GL, Coursin DB, et al. Clinical practice
guidelines for the sustained use of sedatives and analgesics
in the critically ill adult. Crit Care Med. 2002;30:119–141.
24. Henderson WR, Dhingra VK, Chittock DR, et al. Hypothermia in the management of traumatic brain injury: a systematic review and meta-analysis. Intensive Care Med.
2003;29:1637–1644.
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CE Test Questions
Management of Intracranial Hypertension: Focus on
Pharmacologic Strategies
Objectives:
1. Review physiology and principles of intracranial pressure (ICP).
2. Examine pharmacologic treatment of elevated ICP.
3. Describe 3 nonpharmacologic treatment modes for elevated ICP.
1. Which statement correctly outlines the Monroe-Kellie
principle?
a. Increase of brain size must be accompanied by decrease in
cerebrospinal fluid (CSF) or blood volume to prevent
increased ICP.
b. Increase of brain size must be accompanied by decrease in
CSF or blood volume to cause increased ICP.
c. Increase of blood volume must be accompanied by increase
in CSF or brain size to prevent increased ICP.
d. Increase of CSF must be accompanied by decrease in brain
size or blood volume to cause increased ICP.
7. Which statement is true?
a. Mannitol reduces ICP by increasing serum osmolarity and
expanding plasma volume.
b. To reduce ICP, mannitol is administered as a continuous IV
drip.
c. Mannitol is safest given through peripheral IV lines.
d. Crystal formation from mannitol can be resolved by refrigerating the solution.
8. What are two adverse effects of mannitol administration?
a. Hepatotoxicity and extravascular volume depletion
b. Nephrotoxicity and respiratory distress
c. Intravascular volume depletion and gastroparesis
d. Cardiotoxicity and sepsis
2. Which ICP reading could cause a decrease in cerebral
perfusion pressure (CPP)?
a. 4 mm Hg
b. 9 mm Hg
c. 14 mm Hg
d. 24 mm Hg
9. What is the advantage of using hypertonic saline over
mannitol?
a. Mannitol can only be given as an IV infusion.
b. Hypertonic saline solution of 3% can be given peripherally.
c. Mannitol’s effect lasts only 30 minutes.
d. Hypertonic saline possesses the ability of lowering ICP
through bolus and continuous IV infusion.
3. What is the normal range of CPP?
a. 25-50 mm Hg
b. 50-150 mm Hg
c. 150-200 mm Hg
d. 200-300 mm Hg
4. What CPP level is associated with cerebral ischemia?
a. 25-50 mm Hg
b. 50-150 mm Hg
c. 150-200 mm Hg
d. 200-300 mm Hg
10. What syndrome results from rapid decrease in brain
volume in response to rapid increase in serum sodium?
a. Decreasing ICP syndrome
b. Hypertonic saline syndrome
c. Osmotic demyelination syndrome
d. Displacement syndrome
5. Which of the following is not a potential cause of
elevated ICP?
a. Brain lesion
b. Intracerebral hemorrhage
c. Airway obstruction
d. Myocardial infarction
11. Which medications are used to provide adequate analgesia and sedation of short duration?
a. Pentobarbital and valium
b. Mannitol and fentanyl
c. Hypertonic saline and valium
d. Fentanyl and propofol
6. Which statement is true?
a. Primary processes that increase ICP are hypoventilation
and fever.
b. Extracranial processes that increase ICP include ischemic
stroke and hydrocephalus.
c. Neurosurgical procedures can increase ICP if hematoma or
excess vasodilation occurs.
d. Hepatitis C is a major cause of increased ICP.
12. Which of the following nonpharmacologic measures
will increase ICP?
a. Hyperthermia
b. Decompressive craniectomy
c. Head of bed at 30 degrees
d. Hyperventilation with target PaCO2 of 30 mm Hg
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