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Clinical

DIMENSION

Management of Intracranial
Pressure: Part I
Pharmacologic Interventions
Tara L. Sacco, MS, RN, CCRN-K, AGCNS-BC, ACCNS-AG;
Samantha A. Delibert, PharmD, BCCCP

Dangerous, sustained elevation in intracranial pressure (ICP) is a risk for


any patient following severe brain injury. Intracranial pressure elevations
that do not respond to initial management are considered refractory to
treatment, or rICP. Patients are at significant risk of secondary brain
injury and permanent loss of function resulting from rICP. Both
nonpharmacologic and pharmacologic interventions are utilized to
intervene when a patient experiences either elevation in ICP or rICP. In
part 1 of this 2-part series, pharmacologic interventions are discussed.
Opioids, sedatives, osmotic diuretics, hypertonic saline solutions, and
barbiturates are drug classes that may be used in an attempt to
normalize ICP and prevent secondary injury. Nursing care of these
patients includes collaboration with an interprofessional team and is
directed toward patient and family comfort. The utilization of an
evidence-based guideline for the management of rICP is strongly
encouraged to improve patient outcomes.
Keywords: Intracranial pressure, Neurologic injury, Pharmacology
[DIMENS CRIT CARE NURS. 2018;37(3):120/129]

U.V. is a 31-year-old woman admitted to the neurologic with propofol and fentanyl infusions. U.V."s opening ICP
intensive care unit following a traumatic brain injury was 45 mm Hg and decreased to 18 mm Hg postopera-
(TBI) as the result of being struck by a car. U.V."s head tively; however, on postinjury day 1, her ICP has been
computed tomography scan revealed left-sided frontal- sustained at greater than 25 mm Hg. Her Glasgow Coma
parietal contusions, a subarachnoid hemorrhage, and Scale score has ranged from a 3 to 8, and she has not
a basilar skull fracture. At the scene, U.V."s Glasgow Coma followed commands. Her ICP has been managed with
Scale score was 3, and her left pupil was 7 mm and non- mannitol and 3% sodium chloride. However, her serum
reactive. She was intubated and brought to the trauma sodium and osmolality levels have risen to the point where
center. On evaluation, she received mannitol 100 g once she can no longer receive these mediations. A barbiturate
prior to surgical intervention. She arrived to the intensive coma is being discussed.
care unit status post a left hemicraniectomy and intracra- It is apparent from this case study that patients with
nial pressure (ICP) monitor placement. She is mechanically neurologic injuries are at high risk of elevated ICP. In
ventilated, with her pain and sedation needs being treated severe cases, elevated ICP becomes refractory to treatment.

120 Dimensions of Critical Care Nursing Vol. 37 / No. 3 DOI: 10.1097/DCC.0000000000000293

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Management of Intracranial Pressure

When this occurs, the patient requires complex management to compensate to maintain normal intracranial volume.
by an interprofessional team utilizing both nonpharmacologic This concept is known as the Monro-Kellie doctrine.1,2,9,10
and pharmacologic interventions. The prevention of second- Compensatory mechanisms include displacement or
ary brain injury related to elevated and refractory ICP (rICP) is reabsorption of CSF, compression of the venous system,
paramount in the care of the neurocritical care patient. The and shunting of blood out of the venous sinuses.2,3,7 When
goal of this article is to present the pharmacologic interven- these compensatory mechanisms begin to fail, ICP rises,
tions available for the treatment of elevated ICP and rICP. ultimately compromising tissue perfusion.9,10
In order to appropriately perfuse the brain with oxygen
NEUROLOGIC INJURIES and glucose, 15% to 20% of the body"s cardiac output is
Mass lesions, including brain tumors and abscesses,1-3 TBI dedicated to cerebral blood flow (CBF). Cerebral blood
from blunt or penetrating mechanisms,1-7 and both ischemic flow is measured indirectly by cerebral perfusion pressure
and hemorrhagic stroke can cause elevations in ICP.2,3,5,6 (CPP), calculated as mean arterial pressure minus ICP.9
Further, inflammatory conditions typically related to in- To meet metabolic demands, the size of the cerebral vas-
fections, such as meningitis or encephalitis, may cause cular bed is able to change. This function is referred to as
neurologic injury and raise ICP.1-3 Lastly, ICP elevation autoregulation.2,6,8 Vasodilation will increase CBF to meet
from anoxia and hepatic encephalopathy are considered increased demands, whereas vasoconstriction decreases
metabolic inuries.1,3 Hydrocephalus, which may result from CBF when demands are lessened. Vasodilation also allows
any of the aforementioned conditions, also contributes to for the removal of wastes that result from cellular me-
ICP elevation.1-3 Mass lesions, TBI, stroke, and inflam- tabolism.2 These compensatory mechanisms function well
matory and metabolic conditions can contribute to the in the uninjured brain; however, in the context of severe
development of cerebral edema, furthering the sequelae neurologic injury, they may be compromised.6 As ICP
of ICP elevation. rises, CBF decreases, causing vasodilation to meet metabolic
Cerebral edema is swelling within the brain, thus demands. Unfortunately, this compensatory mechanism
increasing the size of brain tissue. 2 There are generally increases arterial volume, which cannot be accommodated
3 types of cerebral edema: vasogenic, cytotoxic, and within the rigid skull, and further elevation in ICP can
interstitial. Each type can occur simultaneously, in both result.9 As this continues to occur, the brain becomes
a localized or diffuse manner.3 Disruption in the blood- ischemic, and autoregulation fails.2
brain barrier, often the result of vessel damage, increases A marker of how well the brain can accommodate ICP
capillary permeability and leads to vasogenic cerebral elevation is referred to as compliance or the ‘‘Ichange
edema,2,8 where fluid accumulates in the extracellular in pressure resulting from a change in volume.’’3(p213)
spaces within the brain. The most common causes of Because of compliance, the patient may be able to tolerate
vasogenic cerebral edema include TBI, surgical inter- increases in brain volume. Similar to the brain"s ability to
vention, mass lesions, and inflammatory mechanisms.2,3 autoregulate, the extent of compliance is limited. When
When a patient develops cytotoxic cerebral edema, fluid these mechanisms are depleted, further elevation in ICP
gathers in the intracellular space.2 Any cause of neuronal occurs.3 The patient may exhibit a multitude of symptoms
hypoxia and resultant anaerobic respiration can lead to related to ICP elevation, which can be found in Table 1.
cytotoxic cerebral edema.2,3,8 Alterations in cerebrospinal Significant patient complications result from compensatory
fluid (CSF) hydrostatic pressures, related to hydrocephalus, mechanism failure.
lead to interstitial cerebral edema. Regardless of the type
and cause, the processes resulting in cerebral edema occur Complications
immediately following neurologic injury and continue for Because health care providers are often unable to intervene
up to and beyond 72 hours postinsult.3 to prevent the primary brain injury, the focus of treatment
and management is to prevent secondary brain injury due
Pathophysiology to cerebral edema, elevation in ICP, hypoperfusion, and
Intracranial pressure is normally less than 15 mm Hg, with compensatory failure.9,11 Hypotension and hypertension,
an elevation considered anything sustained at greater than hypoxia, hypercapnia, fever, hypoglycemia and hypergly-
20 to 25 mm Hg.1,9,10 There are 3 components within the cemia, hyponatremia, seizure, vasospasm, excessive release
rigid skull: blood (arterial and venous), CSF, and brain of excitatory neurotransmitters, and ICP elevation are all
tissue. In order to maintain a normal ICP, these 3 compo- plausible causes of secondary brain injury.5,7,12,13 When
nents must be in balance; however, neurologic insults can CBF is affected, the inflammatory response is activated,
result in an increase in 1 or more component.2,3,8-10 Under leading to further metabolic derangements, ischemia, and
normal circumstances, the increase in one component cellular death.4 Neuronal cells are forced into anaerobic
will lead to a decrease in the others as the brain attempts respiration as a result of hypoxia, and normal cellular

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Management of Intracranial Pressure

TABLE 1 Symptoms of Elevated Intracranial pressures of less than 50 mm Hg indicate decreased per-
Pressure fusion to the brain with potential ischemia and tissue death,2,8
Early Late
whereas CPP of greater than 70 mm Hg may be associated
with poor outcome and respiratory compromise.15 Both
Headache Further change in LOC (obtunded) ICP and CPP values should be utilized to direct therapy to
Emesis Further decrease in GCS score ensure adequate cerebral perfusion and decreased second-
Change in LOC Pupillary dilation (ipsilateral or bilateral) ary brain injury risk.4,8 To do so, multiple pharmacologic
interventions for ICP and rICP are available.
Decreased GCS score Compromised pupillary reaction
Irritability Hypertension ELEVATED ICP: INITIAL PHARMACOLOGIC
Pupillary changes Respiratory compromise MANAGEMENT
Cranial nerve dysfunction Cushing triad (ominous) Initial pharmacologic management for ICP elevation
includes interventions for pain and agitation and the use
Visual disturbance Bradycardia
of osmotic diuretics and hypertonic saline (HTS). Each
Seizure Systolic hypertension/wide pulse pressure therapy can effectively reduce ICP to normal ranges but is
Irregular respirations not without risk. Knowledge of each intervention, includ-
ing assessment parameters, mechanism of action, ap-
Abbreviations: GCS, Glasgow Coma Scale; LOC, level of consciousness.
propriate dosing, expected pharmacokinetics, and adverse
Sources: Inoue,1 2010; Marcoux,3 2005.
effects, is required for appropriate patient management.
Medication, mechanism of action, dosing/administration,
functions are no longer effective. Cell membranes break major adverse effects, and nursing considerations are found
down, resulting in alterations in intracellular and extracellu- in Table 2.
lar sodium, potassium, and calcium levels. The consequence
is furthered cerebral edema and thus worsening of ICP.2 Analgesia and Sedation
Uncontrolled elevation in ICP will cause cerebral Any noxious stimulus has the potential to increase ICP,1,2,10,15
hypoperfusion and hypoxia, leading to further tissue and therefore, treatment aimed at their reduction is
ischemia8,9 and worsening secondary injury. In severe warranted.7,14 Medications used to manage pain and
cases, this results in cerebral herniation and brain death.1,9 agitation in this population include intravenous opioids
When a patient"s ICP is sustained at greater than 25 mm (fentanyl, remifentanil) and intravenous anxiolytics (ben-
Hg despite initial interventions, it is considered rICP.9,12,14 zodiazepines, propofol).
The risk of death has been reported to be 4 to 5 times
higher in those who experience rICP compared with those OPIOIDS
who do not.14 Efforts to decrease ICP and the severity of Fentanyl and remifentanil are the 2 most commonly used
secondary neurologic injury are critical to the care of this continuous intravenous drips for the treatment of pain and
subset of patients.3,5,13 thus ICP. These medications act on opioid receptors in the
central nervous system and the gastrointestinal tract,13
NEUROLOGIC MONITORING producing pain relief.9 The onset of action for fentanyl
Not everyone who experiences a brain injury will require is immediate with a duration of action of 30 minutes to
invasive ICP monitoring. The Brain Trauma Foundation 1 hour and a half-life between 2 and 4 hours.16 Although
recommends that ICP and CPP monitoring be imple- it has been reported that opioids can increase CBF and
mented in patients following severe TBI to reduce inpatient potentially ICP,13 Colton et al17 reported that ICP decreased
mortality.15 Devices utilized to monitor ICP include in trauma patients after 2 hours with dose escalations of
subarachnoid, subdural, epidural, and intraparenchymal continuous fentanyl drips. The fentanyl dose reported in
bolts or external ventricular drains (ventriculostomies). this study ranged between 25 to 550 2g/h,17 although
These devices include a fiber-optic catheter and external typical doses do not exceed 300 2g/h. No dose adjustment
transducer that transmits the patient"s ICP to a monitoring is required for renal and hepatic impairment; however,
system. Intracranial pressure monitoring via a ventriculostomy elderly patients may be more sensitive to the effects of
has the additional ability to drain CSF and blood, which fentanyl.16 Remifentanil"s onset of action is 1 to 3 minutes,
in turn decreases ICP.1,6,8,10,14 Once the appropriate ICP with duration of 3 to 10 minutes and a half-life of 10 to
monitor is placed, both ICP and CPP can be monitored 20 minutes, allowing for this drug to be rapidly titrated.
continuously for abnormalities. When the ICP is elevated Dosages of remifentanil are recommended between 0.5
at greater than 20 to 25 mm Hg, CPP should be maintained to 15 2g/kg per hour. As with fentanyl, there are no dose
between 60 and 70 mm Hg.10,12,15 Cerebral perfusion adjustments required for renal or hepatic impairment.

122 Dimensions of Critical Care Nursing Vol. 37 / No. 3

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TABLE 2 Medication Information
Medication Mechanism of Action Dosing/Administration Adverse Effects Nursing Considerations

Opioids Bind to opioid receptors, providing pain Fentanyl: IV continuous drip 25-550 2g/h; Both: CNS depression Monitor: vital signs, ICP
Fentanyl relief and respiratory depression typically no greater than 300 2g/h Respiratory depression Neurologic exam
Remifentanil Remifentanil: IV continuous drip Hypotension Pain scores
0.5-15 2g/kg per hour Constipation Mechanical ventilation
Remifentanil: bradycardia Bowel regimen
Sedatives Benzodiazepines: bind to GABA receptors Benzodiazepines: midazolam IV loading dose Benzodiazepines: CNS depression Monitor: vital signs, ICP
Benzodiazepines producing anxiolysis, sedation, amnesia; 0.5-4 mg every 5-15 min until adequate Respiratory depression Neurologic exam
Midazolam also an antiepileptic sedation reached Delirium Sedation scores
Midazolam: metabolite accumulation Mechanical ventilation
Midazolam IV continuous infusion
Hypotension
0.02-0.1 mg/kg per hour

Nonbenzodiazepine Propofol: binds to GABA receptors; sedative Propofol: begin IV continuous drip at Propofol: propofol-related Propofol: monitor vital signs, ICP
Propofol hypnotic effects with CNS depression 5 2g/kg per minute infusion syndrome Neurologic exam
Rapidly titrate by 5-10 2g/kg per minute until Hypotension Pain scores
adequate sedation reached Bradycardia Labs: triglycerides, lactate, CK, myoglobin
Maintenance continuous drip dose Respiratory depression Mechanical ventilation
5-50 2g/kg per minute Change IV tubing every 12 h

Osmotic diuretics Osmotic effects: decreases water in brain IV bolus dosing 0.25-1 g/kg every 4-6 h Hypotension Monitor: vital signs, ICP
Mannitol tissue, intracellular, and interstitial space AKI Neurologic exam
to decrease ICP Hyperkalemia I & O electrolytes every 4-6 h
Rheologic effects: plasma expansion, decreased Rebound ICP elevation Serum osmolarity every 4-6 h;
hematocrit, increased RBC deformability, goal e320 mOsm/L

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decreased blood viscosity to increase CBF Administer through an inline filter
Diuretic effects: Changes the osmotic gradient
in the kidney to decrease water reabsorption,
leading to excretion in urine

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(continues)
Management of Intracranial Pressure

123
124
TABLE 2 Medication Information, Continued
Medication Mechanism of Action Dosing/Administration Adverse Effects Nursing Considerations

Dimensions of Critical Care Nursing


Hypertonic saline Change the osmotic gradient by increasing sodium G23.4%: Bolus infusions volume varies by AKI Monitor: vital signs, ICP
Concentrations: and osmolarity concentration, give over 30 min or more
Management of Intracranial Pressure

Pulmonary edema Neurologic exam


G23.4% Decreases water in brain tissue, intracellular, and 23.4%: 30-60 mL over 20 min
Hypernatremia I & O electrolytes every 4-6 h; sodium goal
23.4% interstitial space to decrease ICP Hypokalemia 155-160 mEq/L
Rheologic effects: plasma expansion and RBC Acidosis Serum osmolarity every 4-6 h, goal

Vol. 37 / No. 3
deformability to increase CBF Phlebitis/necrosis 350-360 mOsm/L
Rebound ICP Central line preferred
23.4% Concentration may be administered only
by a provider, check nursing practice act

Barbiturates Sedative/hypnotic that decreases metabolic IV loading dose 10 mg/kg over 1 h, Hypotension Monitor: vital signs, ICP
Pentobarbital demand, CBF, and ICP followed by 5 mg/kg per hour  3 h, Decreased peristalsis EEG for burst suppression
followed by an IV continuous drip CNS depression Pentobarbital levels: 3%-4% target
1-4 mg/kg per hour
Respiratory depression Mechanical ventilation
Do not infuse faster than 50 mg/min Will be unable to perform neurologic and
pupillary examinations

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Abbreviations: AKI, acute kidney injury; CBF, cerebral blood flow; CK, creatinine kinase; CNS, central nervous system; GABA, +-aminobutyric acid; I & O, intake and output; ICP, intracranial pressure; IV, intravenous; RBC, red blood cell.
Management of Intracranial Pressure

However, doses for elderly patients should be decreased system depression,21,23 amnesia, anxiolysis, muscle relax-
by 50% compared with younger adults.18 ation, and antiepileptic effects.21 Typical propofol dosing
The precautions and adverse effects for fentanyl and regimens begin at 5 2g/kg per minute, with rapid titration
remifentanil are similar. Both can cause central nervous of 5 to 10 2g/kg per minute until the patient is adequately
system and respiratory depression, gastrointestinal effects sedated. Maintenance doses of 5 to 50 2g/kg per minute
(nausea, vomiting, constipation), and hypotension.16,18 are recommended.23 Similar to the effects of opioids, Colton
Additional adverse effects of remifentanil include bradycardia et al17 reported that dose escalations of propofol led to
and heart block,18 whereas prolonged use of fentanyl can ICP decreases for 2 hours following administration. An
lead to drug dependence.16 added benefit of propofol use is a decrease in vascular
There are many nursing considerations related to the resistance, which can be neuroprotective13 and decreases
administration of opioid analgesics. Patients with ICP intracranial metabolism.10 This medication has a very rapid
elevations and those receiving continuous opioid drips onset and short duration of action, 9 to 51 seconds and 3 to
require appropriate airway management with mechanical 10 minutes respectively,23 allowing for rapid titration and
ventilation. Continuous monitoring of vital signs, includ- frequent neurologic evaluation.
ing ICP and CPP, is warranted. By nature of their disease There are major adverse effects to both benzodiaze-
states, these patients already display central nervous system pine and propofol use. The metabolites of benzodiazepines
dysfunction, and therefore astute neurologic assessments can accumulate, leading to ongoing sedation and impeded
are required. Further, a bowel regimen should be in place to neurologic examination.2 Metabolite accumulation oc-
prevent gastrointestinal complications. The 2013 Society of curs more commonly following long infusion duration
Critical Care Medicine (SCCM) Pain, Agitation, and and in patients with renal or hepatic impairment; drug
Delirium guideline outlines specific recommendations for tolerance may be a problem.21 High doses of midazolam
pain management in critically ill patients. According to the can also lead to hypotension and subsequent reduction in
SCCM, pain should be routinely monitored with a valid and CPP.13 Respiratory depression and central nervous
reliable tool.19 In addition, an analgesia-first methodology system depression are both common with benzodiazepine
should be incorporated, meaning that pain is treated prior to use.21 Lastly, benzodiazepine use has been linked to the
agitation, as this may be a symptom of underlying pain.20 development of delirium in critical care patients.20,21
Communication with the patient and family is an important The most concerning adverse effect of propofol is
component of care and can reduce noxious stimuli and stress.10 propofol-related infusion syndrome (PRIS), which oc-
curs when the medication is infused at high doses and is
BENZODIAZEPINES AND PROPOFOL manifested by metabolic acidosis, rhabdomyolysis, dys-
Similarly to analgesia, sedation decreases ICP and the rhythmias, and cardiac arrest.13,23 Patients at higher risk
stress response triggered after brain injury.9 Intracranial of PRIS are those with sepsis, respiratory compromise,
metabolism can also be decreased using sedative agents. and severe brain injury.23 To facilitate early detection of
Benzodiazepines are commonly used for sedation in this PRIS, triglyceride, lactate, creatinine kinase, and myoglobin
patient population,2 with midazolam being the most levels should be monitored.21 Hypotension, bradycardia,
commonly used benzodiazepine for continuous sedation. and respiratory depression are other common adverse
This medication is protein bound and lipid soluble, allowing effects associated with propofol use. Another disadvantage
it to cross the blood-brain barrier.13,21 Midazolam binds of propofol infusion is that vials and intravenous tubing
to +-aminobutyric acid (GABA) receptor sites, leading to need to be discarded after 12 hours,21,23 because of the
anxiolysis at lower doses and sedation, amnesia, and anti- risk of bacterial contamination.21
epileptic properties at higher doses.21 Midazolam doses The nursing considerations related to the administra-
are recommended to be an initial bolus dose of 0.5 to 4 mg, tion of sedatives are similar to those related to opioids and
repeated every 5 to 15 minutes until the patient is adequately include reduction of noxious stimuli, airway management,
sedated. An infusion is then started at a rate of 0.02 to continuous vital sign monitoring, and close neurologic
0.1 mg/kg per hour.22 Further, this medication can be rapidly assessment. According to the Pain, Agitation, and Delir-
titrated because of a short onset of action (2-5 minutes) ium guideline, patient agitation levels should be monitored
and duration of action (2-4 hours),21 allowing for expe- using a valid and reliable tool. A nonbenzodiazepine sedative,
dited patient comfort and neurologic examination.2 such as propofol, is preferred over benzodiazepines because
Propofol is an alternative option to benzodiazepine of the risk of delirium.19 Although the SCCM recommends
use for patients with intracranial injury. This medication light sedation,19 in patients with elevated ICP and those
is a sedative/hypnotic that also crosses the blood-brain likely to develop rICP, deeper sedation may be necessary.
barrier with a rapid onset of action.2 It is thought that Ongoing communication with the patient and family is
propofol works on GABA receptors, causing central nervous supported to reduce noxious stimuli and stress.10

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Management of Intracranial Pressure

Osmotic Diuretics Hypertonic Saline


Osmotic diuretics, namely, mannitol, have been widely Hypertonic saline is used to manage both elevated ICP and
used for the management of elevated ICP. This medica- rICP. Also used for its osmotic effects, HTS increases serum
tion works by pulling water out of the brain tissue and sodium levels and serum osmolarity, which pulls water
the intracellular and interstitial spaces. The medication from the brain tissue and intercellular and interstitial spaces
crosses the blood-brain barrier, enters the vasculature, and across the blood-brain barrier.7,8,11-13,27 Hypertonic saline
is removed from the cranial vault, decreasing ICP.8,12 As administration also causes a rheologic effect.8,15,27 An
fluid enters the vasculature, plasma expands. Subsequently, additional benefit of HTS is an increase in intravascular
rheologic effects occur: hematocrit and blood viscosity volume and cardiac function.3,8,11,27 Although changes in
decrease, and red blood cells become more deformable. osmolarity can cause diuresis; the mechanism is much
Each of these effects increases CBF and oxygenation.2,3,7,8,15,24 different than that of mannitol. Hypertonic saline stimulates
The diuretic effects of mannitol occur in the kidney; an atrial natriuretic peptide release, leading to both diuresis
osmotic gradient develops, decreasing water reabsorption and natriuresis.8 Concentrations vary from 2% to 23.4%
and leading to water excretion in urine.8,24 This diuretic saline8,11,12; the higher the concentration, the greater the
effect may continue for hours after the mannitol dose.7 The osmotic effect.8 The lower concentrations of HTS are more
onset of action of mannitol is 15 to 20 minutes with duration frequently given by intravenous bolus for ICP elevation.11
of 1 to 5 hours12; however, reduction in ICP may occur for Hypertonic saline administration has caused renal
1.5 to 6 hours.24 Mannitol should be administered as an failure, pulmonary edema, hypernatremia, hypokalemia,
intravenous bolus, through an in-line filter; recommended acidosis, phlebitis/tissue necrosis, and rebound ICP eleva-
doses are between 0.25 and 1 g/kg8 every 4 to 6 hours.3 tion.12 Similarly to mannitol, HTS increases serum osmo-
Related to the osmotic and diuretic effects of mannitol; larity, which can lead to AKI. When HTS is administered,
hypotension, acute kidney injury (AKI), hyperkalemia, hypokalemia and acidosis transiently occur, often lasting
and rebound elevation in ICP are noted to be adverse 1 hour following administration. As fluid moves from the
effects. The mechanism behind rebound elevation in ICP is brain and into the intravascular space, pulmonary edema
unclear,12 although this may occur when the blood-brain may result.12 Patients with underlying cardiac or pulmonary
barrier has been compromised because of neurologic injury, conditions are at higher risk of experiencing pulmonary
changing the normal osmotic gradient, and allowing for edema with HTS administration.12 Elevation of sodium and
mannitol accumulation within the brain.8,12,13 The other subsequently chloride may result in hyperchloremic acidosis
potential cause is related to the diuretic effects of mannitol, following administration.8 The risk of phlebitis and tissue
which may lead to hypovolemia,12 intravascular dehydra- necrosis is higher with HTS than with isotonic solutions;
tion, hypotension, and a reduction in CPP.4 Because of historically, this medication has been administered via
adverse renal effects, mannitol is contraindicated in those central line.8,11,12,28 However, a recent retrospective cohort
with preexisting renal dysfunction24; use of mannitol for study indicated that administration of 3% HTS via
ICP management in this population is cautioned and a peripheral intravenous line can be done safely, and a central
risk-versus-benefit discussion is warranted. line may not be required at rates up to 75 mL/h.28 Lastly,
Nursing considerations related to mannitol administra- rebound ICP elevation can occur when serum sodium
tion include monitoring intake and output, electrolytes and levels return to baseline12 or if an accumulation of sodium
serum osmolarity and osmolar gap, and hemodynamics.12,25 in extracellular spaces alters the osmotic gradient.8 If the
Strict monitoring of intake and output is important, with patient experiences a rebound ICP elevation, repeating a
euvolemia being the target when a patient requires mannitol dose of HTS may be necessary.12
for ICP reduction.2 To avoid hypovolemia, fluid replace- Monitoring intake and output, serum osmolarity, blood
ment may be necessary.8 Alterations in potassium, sodium, chemistries, and vital signs is essential when administering
and chloride can occur, and therefore blood chemistries HTS. As with mannitol, the goal is to maintain euvolemia.3
must be monitored frequently. Serum osmolarity and os- In order to prevent AKI, the maximum recommended serum
molar gap must also be monitored closely. Serum osmolarity osmolarity level for HTS is 350 to 360 mOsm/L. Hypertonic
is determined by the concentrations of solutes in serum, saline administration may also cause hypernatremia; the
whereas osmolar gap is the difference between measured and maximum recommended serum sodium level in this patient
calculated osmolarity.26 Mannitol doses should be withheld population is 155 to 160 mEq/L.12 Vital signs, including ICP
if the patient"s osmolarity reaches 320 mOsm/L or higher and CPP, should be monitored continuously.
or an osmolar gap greater than 20 in order to prevent
AKI.3,8,12,24,25 Laboratory monitoring is recommended Patient Evaluation
every 4 to 6 hours.2 Ongoing monitoring of hemodynamics The patient"s physiologic parameters will indicate the ef-
is essential, as hypovolemia can lead to hypotension.10 fectiveness of initial interventions implemented to decrease

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Management of Intracranial Pressure

ICP. Ideally, patient response will include a decrease in ICP, 23.4% saline may also cause immediate, but transient,
maintenance or increase in CPP, and hemodynamic stability. hypotension and decreased hemoglobin levels.30 Decreased
Further, the patient should be maintained euvolemic, with systemic vascular resistance or a vagal effect likely accounts
laboratory values within normal limits or within the for the drop in blood pressure. Increased blood pressure
parameters of treatment, and free of pain and agitation. In and cardiac contractility often follow this adverse effect.33
the event that the patient"s ICP remains elevated despite initial The changes in serum osmolarity following adminis-
interventions or meets the criteria described in Table 3, tration are likely to disrupt red blood cell membranes,
management of rICP begins. resulting in decreased serum hemoglobin levels.30 Nursing
care and monitoring following administration of
ELEVATED ICP: REFRACTORY 23.4% saline are similar to those described for lower
PHARMACOLOGIC MANAGEMENT saline concentrations.

Hypertonic Saline Barbiturates


Hypertonic saline in concentrations of 23.4% is used in A barbiturate coma may be induced for the management
the management of rICP and impending cerebral hernia- of rICP. Working in the reticular formation, barbiturates
tion. This concentration is delivered in bolus doses of 30 are sedative/hypnotics and inhibit nerve impulses from
to 60 mL30,31 and is administered over 20 minutes,30 as reaching the cortex,2 reducing cerebral metabolic demand
compared with other concentrations of HTS, which may and CBF.2,9,13,34 When CBF decreases, ICP also decreases.2,34
be administered over 30 minutes to multiple hours11,32; The most commonly used barbiturate is pentobarbital,
23.4% saline is administered by a provider because of the with an onset of action within 5 minutes and duration of
significant risks of rapid administration30 and must be 15 to 45 minutes.34 Administration includes a loading
given via central line.11,32 Institutional policy should guide dose followed by a continuous infusion.12 The typical dosing
provider administration of 23.4% saline, and providers regimen is 10 mg/kg over 1 hour followed by 5 mg/kg per
may be considered attending physicians, fellows, or ad- hour for 3 hours, then initiating a continuous drip at 1 to
vanced practice providers. In some cases, the administration 4 mg/kg per hour.14,34 Doses should not be administered
of 23.4% saline has been noted to reverse transtentorial faster than 50 mg/min.34 The medication is then rebolused
herniation.30 The successful reduction in ICP and impact and titrated based on ICP and physiologic parameters.
on herniation is related to the same mechanisms of HTS Adverse effects of pentobarbital include hypotension,
described previously: changes in the osmotic gradient pulling myocardial depression, vasodilation,9,12 decreased peri-
fluid from the brain tissue. stalsis, and respiratory effects.12 Hypotension may result
Because this concentration is given by a rapid intra- in reduction of CPP; vasopressors may be indicated to
venous bolus, there is a risk that sodium levels will rise too counter this effect.12,14,34 Barbiturates are respiratory
quickly, resulting in central pontine myelinolysis.3,8,12,32 depressants. As such, induction of a barbiturate coma
This syndrome most frequently occurs if underlying requires the patient to be mechanically ventilated.14
hyponatremia is corrected too rapidly8 or as a result of Nursing care for the patient in a barbiturate coma
precipitous changes in serum osmolarity.3 When this occurs, includes monitoring vital signs and electroencephalogram
the nerves within the pons demyelinate,8,12 resulting (EEG) waveform.9 Pentobarbital levels may be monitored,9
in lethargy,8 quadriplegia,8,12 and long-term ventilator with the appropriate laboratory capabilities. Blood pres-
dependence.8 Fortunately, central pontine myelinolysis sure, heart rate, ICP, and CPP should be monitored con-
has rarely been reported after the administration of HTS tinuously. Invasive or minimally invasive hemodynamic
for the management of elevated ICP.30 Administration of monitoring may be considered. Burst suppression (Figure),
as noted on the EEG waveform, indicates that the dose of
barbiturate is effective.9 Pentobarbital doses should be
TABLE 3 Refractory Intracranial Pressure titrated based on both EEG waveform and ICP; it may be
(ICP) Criteria reasonable to titrate to pentobarbital levels.9 Burst sup-
ICP Sustained at 925 mm Hg Despite Initial Interventions or pression and serum levels do not always correlate,12 and
therefore serum levels may not be a reasonable parameter
Closed Skull Open Skull
for titration. It is important to note that inducing a barbi-
ICP 925 mm Hg for 30 min ICP 915 mm Hg for 15 min turate coma will result in the inability to perform neuro-
ICP 930 mm Hg for 15 min ICP 920 mm Hg for 10 min logic assessments as the patient will be unresponsive and
unable to move. Pupillary dilation may also occur because
ICP 940 mm Hg for 1 min ICP 930 mm Hg for 1 min
of the barbiturate infusion; thus, pupil size and reactivity
Sources: Bader et al, 2005; Censullo and Sebastian,14 2003; Eisenberg et al,29 1998.
9
cannot be considered a reliable assessment tool.7,12 Because

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Management of Intracranial Pressure

Figure. Electroencephalogram (EEG) with demonstration of burst suppression. Electroencephalogram demonstrates barbiturate-induced burst
suppression pattern. The 27-second EEG epoch demonstrates 2 periods of bursts separated by a 10-second period of cerebral inactivity.

of a long half-life elimination and accumulation of the require several, if not all, of the interventions described
medication, once a pentobarbital coma is stopped, it can previously. In addition to the pharmacologic management
take days for the medication to be completely removed described, each patient requires astute nursing care. Patient
from the patient"s system.14 care activities should be clustered to decrease stimuli.14
Many patients will require surgical intervention, ventilator
Patient Evaluation support, and other nonpharmacologic therapies, which
Ideally, when these interventions are implemented, the will be discussed in part 2 of this series. Elevated ICP may
patient"s physiologic parameters will improve. Once a lead to very subtle changes that the bedside nurse should
barbiturate coma has been induced, if the patient"s ICP is be equipped to recognize and address with the interprofes-
sustained at less than 20 mm Hg for at least 48 hours, sional team.1 Regardless of the type of interventions
and if the interprofessional team determines it is appro- performed, the goals of care are to maintain oxygenation
priate, pentobarbital may be weaned.14 The half-life of and perfusion to the injured brain.8 Experiencing a brain
pentobarbital can range from 15 to 50 hours14,34; thus, injury is a life-altering event for both the patient and the
the weaning process is slow. The risk during this time is family. Nursing care directed to the patient"s condition and
that the patient may exhibit rebound ICP or seizure activity. well-being and that to the family are important consid-
In the event this occurs, the coma may be reinduced.14 erations.7 Use of an evidence-based protocol for the
These measures are intended to be lifesaving immediately management of rICP is strongly recommended to provide
after the injury. Patient functional outcomes will vary on structure to the complex management of these critically
a case-by-case basis, and unfortunately ongoing neurologic ill patients.
deficits and patient death are still possibilities, despite
aggressive rICP management. Acknowledgments
The authors thank Dr Olga Selioutski, DO, assistant pro-
CONCLUSION fessor of neurology and associate director, Critical Care
The management of rICP is complex. It is likely that the Neurophysiology Monitoring, Strong Epilepsy Center,
most critical and unstable patients with brain injuries will University of Rochester Medical Center, New York.

128 Dimensions of Critical Care Nursing Vol. 37 / No. 3

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Management of Intracranial Pressure

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Tara L. Sacco, MS, RN, CCRN-K, AGCNS-BC, ACCNS-AG, is visiting
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uptodate.com/contents/sedative-analgesic-medications-in- Address correspondence and reprint requests to: Tara L. Sacco, MS,
critically-ill-adults-properties-dosage-regimens-and-adverse- RN, CCRN-K, AGCNS-BC, ACCNS-AG, Wegmans School of Nursing,
effects?source=search_result&search=benzodiazepines&selected St John Fisher College, 3690 East Ave, Rochester, NY14620 (tsacco@sjfc.edu).
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