1

Emergency Neurological Life Support:

Intracranial Hypertension and Herniation
Christopher Morrison, PharmD, BCCCP, FNCS1, Paulomi Bhalla, MD2, Christopher M.
Ruzas, MD3, Deborah S. Tran DNP, RN, CNRN, SCRN, NE-BC4,5, and Stephanie Qualls,
RN, BSN, CNRN7
1
Pharmacy & Drug Information Department, Grady Health System, Atlanta, GA
2
Department of Neuroscience, Kaiser Permanente, Redwood City, California
3
Department of Pediatrics, Section of Pediatric Critical Care Medicine, Children’s Hospital Colorado, University of
Colorado School of Medicine, Aurora, Colorado
4
Department of Neuroscience, Texas Health Dallas, Dallas, TX
5
College of Nursing and Healthcare Professions, Grand Canyon University, Phoenix, AZ
7
Neuroscience Intensive Care Unit, Massachusetts General Hospital, Boston, MA

Abstract
Sustained intracranial hypertension and acute brain herniation are “brain codes,” signifying
catastrophic neurological events that require immediate recognition and treatment to prevent
irreversible injury and death. As in cardiac arrest, a brain code mandates the organized
implementation of a stepwise management algorithm. The goal of this Emergency Neurological
Life Support (ENLS) protocol is to detail an evidence-based, standardized approach to the
evaluation and management of patients with intracranial hypertension and/or herniation.

Keywords
Intracranial hypertension, cerebral herniation, intracranial pressure management, elevated
intracranial pressure

1. Introduction
The ENLS suggested algorithm for the initial management of intracranial hypertension or cerebral
herniation is shown in Figure 1. In this version of ENLS, the algorithm articulates a tiered approach
to escalating therapy based on response to previous intervention(s). All patients at risk of having
elevation in intracranial pressure (ICP) or risk of herniation should have Tier Zero interventions.
Then based on the clinical course of the patient, escalation should follow the algorithm based on
evidence of intracranial hypertension or cerebral herniation. In some cases, a tier may be skipped
based on the etiology of the elevation in the ICP, or the speed with which the elevation occurs. For
example, if a patient has an extra-axial fluid collection, such as an epidural hematoma, surgical
evacuation would be a foundational intervention with other temporizing measures being performed
en route to the operating room.
According to the Monro Kellie doctrine, the sum of intracranial contents –– brain, blood, and
cerebrospinal fluid (CSF) –– represents a volume determined by the fixed nature of the cranial
vault.1,2 Relative volumes of these contents will change to accommodate an acutely developing,
space occupying mass; however, compensatory changes may be overwhelmed once a critical
volume change has occurred, as demonstrated by the inflection point of the pressure-volume
relationship (Figure 2). Intracranial hypertension and cerebral herniation occur when the adaptive
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intracranial compliance mechanisms are overwhelmed and unable to adapt to the developing space
occupying mass lesion.

Figure 1
ENLS Intracranial Hypertension and Herniation protocol
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Figure 2. Intracranial pressure-volume curve

The intracranial pressure-volume curve is biphasic and has a flat portion (a) in which compliance
(∆V/∆P) is high, and a steep portion (b) in which compliance is low. Under normal circumstances, when
compliance is high, a small change in ICV (∆V) results in only a small change in pressure (∆P1). Patients
with intracranial hypertension typically have low compliance, hence small changes in volume (∆V) result
in large changes in pressure (∆P2). Elastance, ∆P/∆V, is the reciprocal of compliance. ICP, intracranial
pressure; ICV, intracranial volume; ∆V, change in volume; ∆P, change in pressure

2. Management Protocol

The tiered approach to management of intracranial hypertension is shown in Figure 1. This

escalates from general critical care and nursing measures in Tier Zero, to cerebrospinal fluid
drainage, and increasing osmotic goal and hyperventilation in Tiers 1 and 2. Rescue decompressive
craniectomy may be used as a life saving measure in some cases. Tier Three involves deep sedation
and hypothermia - interventions that lower intracranial hypertension but have not been associated
with improved outcome.
Although frequently linked, elevations of ICP and brain herniation can occur independently.
Intracranial hypertension is defined as an acute sustained (>5 minutes) elevation of ICP to >22
mmHg.3 Measurement typically requires invasive monitoring, but certain clinical and
physiological signs may suggest increased ICP prior to instrumentation. Herniation syndromes
result from intracranial compartmental pressure gradients leading to parenchymal tissue shifts that
compress or displace the brainstem, cranial nerves, or cerebral vasculature. Ischemia or infarction
during such vascular compression may cause additional edema and worsening intracranial
hypertension.
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The etiologies of intracranial hypertension and herniation syndromes are classified anatomically
as extra-axial, focal, or diffuse intraparenchymal processes (Table 1). In the emergent setting of a
brain code, resuscitative measures are pursued even if the etiological mechanism has not been fully
characterized.

Table 1. Etiologies of Brain Code

3. Diagnosis

Clinically, symptoms of increased ICP include headache, nausea and vomiting, pupillary changes,
and/or altered mental status. Patients with increased ICP may demonstrate hypertension,
bradycardia, and irregular respirations or apnea (Cushing’s triad), although the concurrence of all
three signs is an uncommon and often late findings.4 Common sites for herniation are the cingulum
of the medial frontal lobe (subfalcine herniation), medial temporal lobe (uncal herniation), and
inferior cerebellum (tonsillar herniation) (Figure 3).
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Figure 3

The cardinal signs of transtentorial (uncal) herniation are an acute change in consciousness
associated with ipsilateral pupillary dilation and contralateral hemiparesis, resulting, respectively,
from compression or displacement of ascending arousal pathways, oculomotor nerve (III), and
corticospinal tract.5,6 In a subset of patients, herniation-associated shift of the midbrain compresses
the contralateral cerebral peduncle (crus cerebri) against the tentorium, resulting in hemiparesis
that is ipsilateral to the lesion (Kernohan’s false localizing sign).7 Transtentorial herniation may
cause ipsilateral cerebral infarction due to occlusion of the posterior cerebral artery. Brain
herniation is potentially reversible with appropriate and timely therapy. Reversal of transtentorial
herniation has been observed in 50-75% of adult patients with either traumatic brain injury (TBI)
or with supratentorial mass lesions.8,9

4. Prehospital Considerations
Recognition of herniation syndromes in the prehospital setting is important because life-saving
therapies can be initiated prior to the arrival in the Emergency Department (ED). It is important to
understand that not all patients with sudden onset of elevated ICP will have a traumatic injury.
Rapidly expanding blood volume from ruptured arteries (intracranial hemorrhage), sudden onset
decreased venous drainage (ischemic stroke), or the rapid cerebral spinal fluid accumulation
(hydrocephalus) may increase ICP without outward physical injury. Clinical signs of herniation
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include unilateral dilated pupil, loss of consciousness, posturing, limb weakness, loss of brainstem
reflexes, irregular respiratory patterns, as well as hypertension and bradycardia.10

Resuscitation begins with the management of airway, breathing, circulation, disability, and
exposure (ABCDEs). The head of the bed should be elevated when possible; head and neck should
be kept in midline position to facilitate cerebral venous drainage. If a cervical collar is in place,
assess to ensure it is not so tight that it might impede cerebral venous drainage, which may result
in venous congestion and greater difficulty controlling ICP. Although traumatically injured
patients are often transported on a backboard, it may be possible to place a rolled blanket or towel
beneath the board during transport to elevate the head. The head of the gurney can also be raised
to elevate the backboard, while ensuring that the patient is secure to prevent the body or board
sliding. Endotracheal intubation and/or supraglottic airway placement in the prehospital setting
will depend on the skill of the providers and local policies. A normal to slightly increased minute
ventilation should be used to decrease CO2. End tidal CO2 monitoring may be used for specific
targets. Assisted ventilation may be provided with a bag valve mask (BVM) in the absence of the
above devices. Hyperventilation can be initiated if clinical signs of herniation such as a unilateral
dilated pupil are present. This should be considered a temporizing measure till other higher tiered
therapies can be initiated. Hypertonic solutions should be administered if available. Prehospital
notification is also important so that necessary hospital resources are available upon arrival; a
sample communication is given in Table 2. Additional pre-hospital management improves
outcomes in patients with suspected traumatic brain injuries including avoiding hypoxia,
hypotension, and hyperventilation. See ENLS TBI module for more information.

Table 2. ICP/Herniation Standard Prehospital Notification

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5. Diagnosis

5.1 Neuroimaging
In the emergent setting of a brain code, a head computed tomography (CT) scan should be obtained
for diagnosis of etiology, measurement of severity, and possible identification of a process that
may require emergent surgical intervention. Initial resuscitative measures and stabilization,
including airway interventions, circulatory and ventilatory support, and initial hyperosmolar
therapy, must occur prior to and concurrently with diagnostic imaging. There is a statistically
significant increase in ICP when a patient’s head of bed is positioned at 0 degrees as compared to
30 degrees. The provider should expect that positioning the patient flat for the CT scan may put
the patient at risk for respiratory distress if they are unable to protect their airway or increase their
intracranial pressure and bring necessary emergency equipment and medication for transport to
imaging. Non-contrast head CT is preferred over magnetic resonance imaging (MRI) due to
immediate and broad availability and rapidity of image acquisition. In most cases, CT will identify
the underlying process (see Table 1), although MRI may subsequently be needed for further
characterization. MRI should only be sought once the imminent risk of an additional neuro-
worsening has been mitigated by medical and/or surgical intervention.

5.2 ICP Monitoring

There are several types of intracranial monitors including intraventricular catheters as well as
intraparenchymal, subdural, and epidural devices. Non-invasive monitoring is not yet as reliable
or available as traditionally invasive options. The decision to proceed with ICP monitoring
including the type of monitoring device used, is determined by availability of resources and the
underlying process and the likelihood of progression. In TBI, the Brain Trauma Foundation (BTF)
guidelines recommend placement of an ICP monitor for management of severe TBI patients.
Information from ICP monitoring is recommended to reduce in-hospital and 2-week post-injury
mortality.3 In patients who have suffered a TBI, ICP monitoring is recommended in those who
remain comatose after resuscitation (Glasgow Coma Scale [GCS] of 3-8) and have either (1)
abnormalities on cranial CT scan or (2) meet at least two of the following three criteria: age > 40
years; systolic blood pressure (SBP) < 90 mmHg; or abnormal posturing.3 While indications for
ICP monitoring have not been well established in non-traumatic coma, monitoring should be
considered an option when clinical suspicion of intracranial hypertension exists. The target ICP
for treatment is 22 mmHg and this is extrapolated from the TBI literature.3

Noninvasive methods for monitoring ICP continue to be evaluated as these tools would be
especially useful in the early management of critically ill patients before an invasive ICP monitor
can be placed. Most recently, there has been a growing line of inquiry on the validity of ultrasound
to measure optic nerve sheath diameter (ONSD) and using quantitative pupillometry. Despite
promising studies, finding reliable cut-offs ONSD when compared to invasive ICP monitoring has
been challenging, with studies showing ranges from 4.8mm to 5.9mm.10-12 Indeed, healthy
volunteers have had ONSD as high as 6.4mm reported in the literature. Meanwhile, quantitative
pupillometry remains promising as patients with abnormal light reactivity on quantitative
assessment have been found to have high ICP compared to those with normal reactivity.13,14 These
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studies have been limited to patients with known brain injury, and it remains unclear how
pupillometry would perform in the ED or prehospital environment.

Spinal fluid pressure obtained during a lumbar puncture may be an inaccurate representation of
ICP if the system does not communicate thus is not a recommended way to measure ICP.
Performing lumbar puncture with CSF removal in the setting of increased ICP is not recommended
as there is a possibility of inducing brain-stem compression and herniation.14
Cerebral perfusion pressure (CPP), used as a surrogate for global cerebral blood flow (CBF), is
approximated by the equation:

CPP = mean arterial pressure (MAP) – ICP

Guidelines for severe TBI management recommend target CPP values between 60-70 mmHg for
decreasing 2-week mortality and improving favorable outcomes.3 CPP targets for pediatric
patients are > 40 mmHg for infants and small children and CPP > 50 mmHg for older children.14
CPP targets for patients with non-traumatic intracranial hypertension have not been adequately
studied.

6. Management

6.1 Tiered Approach to Intracranial Hypertension Management

It is important to stress that any patient who is at risk for elevated ICP should have Tier Zero
interventions. Brain code resuscitation always begins with an assessment for airway patency,
oxygenation and ventilation, and adequate circulation. In the absence of an invasive intracranial
pressure monitor, optimizing hemodynamics to support adequate tissue oxygen delivery is advised.
When intracranial pressure recordings are available, targeting hemodynamics that provide goal
cerebral perfusion pressures is optimal.

Tier Zero
Resuscitation should begin with optimizing oxygenation and ventilation to normal values and
supporting hemodynamics to provide adequate tissue oxygen delivery and/or achieve adequate
CPP. The head of the bed should be elevated to >30 degrees and the head is kept in midline to
facilitate cerebral venous drainage.3,15 Stimuli such as tracheal suctioning, that may elevate ICP,
should be minimized. Hyperthermia, if present, may be treated with antipyretics and surface or
intravascular cooling devices with a target of normalizing body temperature to 36-37.4 degrees C.
Only iso- or hyperosmotic fluids should be used as intravenous (IV) solutions. If hyponatremia
(serum Na <135 mEq/L) is present, steps should be initiated for correction. High dose
corticosteroids are indicated for vasogenic edema resulting from brain tumors, abscesses, or non-
infectious neuroinflammatory conditions but should otherwise be avoided.15,16 If the brain has not
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yet been imaged, a non-contrast head CT scan should be performed when the patient can be
positioned safely for diagnostic imaging.

Tier One

For acute elevations in ICP, hyperosmolar therapy with either mannitol or hypertonic saline (HTS)
have shown equivalent efficacy in lowering of ICP.17-20 Guidelines from the Neurocritical Care
Society (NCS) on medical management of cerebral edema with osmotherapy for various disease
states is now available on the NCS website and can be utilized as an additional reference
(https://www.neurocriticalcare.org/resources/guidelines). Recommendations from the NCS favor
use of HTS over mannitol for increased intracranial pressure related to intracerebral hemorrhage
and traumatic brain injury. For dosing of medications, reference should be made to the ENLS
Pharmacotherapy module for additional information. For hyperosmolar therapy to be effective, an
intact blood brain barrier and osmotic or sodium gradient between brain and serum are required to
have the diffusion vector of water from the parenchyma to the vasculature. Mannitol is
administered as 0.5-1 g/kg IV bolus over 5-15 minutes and may be repeated every 4-6 hours. A
peripheral IV may be used in a brain code.20 Repeat dosing of mannitol can be determined based
on the osmolar gap which is derived as the difference between measured and calculated osmolality.
No therapeutic benefit is appreciable with osmolar gap >20 mOsm/kg. HTS is available in
concentrations from 2% to 23.4% and can be administered as a bolus alone or in addition to
mannitol. Central venous catheter is the preferred method of administration of HTS but
administration via peripheral IV infusion with monitoring for infiltration has been demonstrated
to be safe in several clinical trials.20,21 Administration of HTS through intraosseous (IO) access
should be done with caution and only with concentrations of 7.5% or less due to uncertain risk of
myonecrosis. Bolus 23.4% NaCl has been associated with ICP reduction and reversal of
transtentorial herniation.9 Treatment with HTS requires serum sodium concentration levels to be
checked every 4-6 hours with serum sodium concentrations kept <160 mEq/L. Acute obstructive
hydrocephalus, as determined by neuroimaging, should be emergently managed with an external
ventricular drainage (EVD) system. If an EVD system is already in place, drain 5-10 ml of
cerebrospinal fluid for acute rise in ICP.22 Hyperventilation in the acute setting reduces ICP by
decreasing the arterial partial pressure of carbon dioxide. Consequent hypocapnia results in
cerebral vasoconstriction and reduction in cerebral blood flow, cerebral blood volume, and ICP.
Transient hyperventilation may be implemented by providing 18 – 20 breaths per minute (targeting
a PaC02 30-35 mmHg) as a temporizing measure while awaiting higher tiered interventions.
Prolonged hyperventilation should be avoided.23,24 If ICP is not controlled, and/or clinical signs of
herniation do not resolve with Tier One interventions, decompressive surgical options (e.g.,
evacuation of hemorrhagic contusion) should be considered.25,26 If surgery is not appropriate or
not undertaken, Tier Two interventions should be implemented. If ICP is not controlled with Tier
One interventions, consider repeating the head CT scan to rule out new processes.
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Tier Two

If Tier One interventions have failed to control ICP, Tier Two should be initiated. If hyperosmolar
therapy with HTS has been administered, serum sodium goals may be increased if they are not yet
at a maximal concentration. In practice, serum sodium concentration greater than160 mEq/L is
unlikely to provide significant additional benefit and may increase mortality. Once the ICP has
stabilized, sodium concentration should be maintained at the current concentration until the brain
edema has improved. This is often achieved with intermittent boluses of 3% NaCl during which
serum sodium levels are monitored every 6 hours. It is controversial whether continuous infusion
of 3% NaCl is beneficial for ICP control, although pediatric TBI guidelines suggest the use of
continuous infusions of 3% HTS to maintain ICP < 20 mmHg.27

Sedation may be increased to aid in ICP management. Propofol has been shown to reduce cerebral
metabolic demand (CMRO2) and CBV (cerebral blood volume) and, consequently, ICP.27 It is
administered as a bolus of 1-2 mg/kg and may be continued as an infusion (titrate to maximum
200 µg/kg/min) in ventilated patients. Propofol, especially when given as a bolus dose, is
associated with hypotension, which should be corrected with IV fluids and/or vasopressors to
maintain CPP goals. A small subset of patients receiving propofol may develop a propofol infusion
syndrome characterized by metabolic acidosis, cardiac dysfunction, rhabdomyolysis, and
hypertriglyceridemia, often with a fatal outcome.28 Propofol infusion syndrome is more likely to
develop at doses greater than >70 mcg/kg/min administered for >48 hours. If propofol is infused
at these extreme doses (200 µg/kg/min) it should only be done temporarily while other corrective
measures are executed. Other sedatives and analgesics can be used (e.g., benzodiazepines and
opiates) to aid in ICP management, with a preference towards short acting agents.

Head CT

If brain imaging has not yet been performed despite completion of Tier One and Two interventions,
a head CT scan should be obtained to further elucidate the cause of herniation or intracranial
hypertension. The CT is also used to monitor for any interval worsening (e.g., blossoming of
contusion or increase in cytotoxic edema of a middle cerebral artery infarct). If ICP is not
responsive to Tier Two interventions, rescue decompressive surgery should be considered as a life-
saving intervention. If the patient is ineligible for surgery, Tier Three (below) should be engaged.

Decompressive Surgery

Surgical interventions for the management of intracranial hypertension include (a) placement of
an external ventricular drain, (b) evacuation of extra-axial lesion, (c) removal of intracerebral mass
lesion, (d) removal of brain parenchyma, and (d) uni- or bilateral large decompressive
craniectomies. Patients may benefit from removal of focal space-occupying lesions including those
with brain tumors, brain abscesses, or parenchymal hemorrhages, particularly when the
hemorrhages are lobar or cerebellar in location.29-31 Decompressive craniectomy may also be
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considered in patients with diffuse brain swelling associated with TBI, meningoencephalitis, or
non-infectious neuroinflammatory conditions (e.g., acute demyelinating encephalomyelitis), and
stroke with brain edema, the process in which hemicraniectomy has been most extensively
studied.32-37

Tier Three

Tier Three measures represent the most aggressive level of management and carry the highest risk
of adverse effects. Rigorous randomized prospective studies are lacking, and recommendations are
driven by consensus. This tier includes administration of barbiturates titrated to ICP goal or burst
suppression of 5-20 seconds or at least 50% on continuous electroencephalogram (EEG).
Pentobarbital (bolus 5-15 mg/kg over 30 min - 2 hours, then maintenance infusion of 1-4 mg/kg/hr)
is frequently used. Some patients may not tolerate these doses as pentobarbital is associated with
respiratory depression, cardiovascular instability, immune suppression, and paralytic ileus.38-40
Vasopressors are often necessary for hemodynamic support, thus invasive arterial blood pressure
monitoring, and central venous access should be strongly considered in patients receiving
infusions. During treatment, the neurological examination is limited by sedation. High dose
pentobarbital can mimic signs of brain death including unreactive pupils even by pupillometry and
caution is to be exercised in prognostication, as pentobarbital plasma clearance may take days after
discontinuation of infusion.

Targeted temperature management (TTM) to target a core temperature of 32-34°C may be

associated with a reduction in ICP but has not been shown to result in improved outcomes, and in
the case of TBI may worsen outcomes.41 In the Eurotherm3235 trial, hypothermia plus standard of
care was compared to standard of care alone for patients with TBI and intracranial hypertension.
This trial was stopped early due to harm with increased risk of death and unfavorable functional
outcomes in the hypothermia group, but treatment did decrease the measured intracranial pressure.
Early prophylactic hypothermia in severe TBI did not improve neurological outcomes in the
POLAR trial. When using TTM for mild hypothermia, external surface cooling devices or
intravascular or esophageal cooling devices may be used.42-47 Hypothermia may be associated with
shivering, cardiac arrhythmias, sepsis, and electrolyte disturbances and protocols for induction,
maintenance and rewarming should be used to prevent or treat these complications.

6.2 Consider Additional Monitoring

Patients who have had or are at risk for intracranial hypertension may benefit from additional
neuromonitoring, including jugular venous oximetry, brain tissue oxygenation, cerebral perfusion
and cerebral microdialysis. Treatment based on ICP and CPP overlooks significant information on
the physiologic and metabolic state of the injured brain. Impairment of cerebral autoregulation
may limit the effectiveness of management strategies focused only on brain perfusion.
Complementary neuromonitoring techniques should be considered to optimize medical
management in selected patients with severe brain injury. However, thus far, none of these invasive
monitoring strategies have been definitively shown to be associated with improved outcome.
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The BOOST-II study supports the hypothesis that PbtO2 directed therapy may reduce the risk of
secondary brain injury following severe TBI.48 A clinical trial evaluating PbtO2 directed treatment
in TBI (BOOST-III) is ongoing. When PbtO2 monitoring is used, the best available data suggest
treating PbtO2 when less than 20mmHg. Studies using brain tissue oxygen sensors indicate that
significant parenchymal hypoxia may occur when ICP and CPP are normal.49,50

Cerebral microdialysis measures brain interstitial lactate, pyruvate, glucose, and glutamate,
indicators of cerebral metabolic activity whose levels may be altered independently of ICP and
CPP.51 Cerebral autoregulation allows for consistent cerebral perfusion over a wide range of
systemic perimeters. Failure of this protective system risks hypo- or hyper-perfusion injuries.
Measurement of dynamic changes of cerebral autoregulation can correlate a systemic
hemodynamic parameter such as arterial blood pressure and an intracranial physiological
parameter such as ICP, transcranial Doppler-derived CBF velocity, or brain tissue PO2. High
degrees of correlation suggest dysregulation and an increased risk of secondary injury.52 Ideally,
each patient’s unique autoregulation curve could be derived from these measurements, and
optimized CPP and optimized arterial blood pressure can be individualized specifically for the
needs of the patient in real time. The COGiTATE study is underway testing feasibility and safety
of this approach.

6.3 Revise ICP/MAP goals

Depending on the clinical circumstances and availability of patient specific brain monitoring data,
the standard goals of MAP and ICP may be adjusted to best match patient need. For example, a
patient who is awake and without symptoms in whom ICP is more than 22 mmHg, or a CPP below
50 mmHg, may not require any intervention.

6.4 Pediatric Considerations

Monitoring and management of intracranial hypertension in the pediatric population follows

analogous tiers as in adults. Importantly, the presence of an open fontanel in infants does not
preclude the development of intracranial hypertension and cerebral herniation.54 Recent updates
to the Brain Trauma Foundation guidelines for the management of pediatric severe TBI direct
clinicians to obtain a non-contrast head CT and place an ICP monitor if post resuscitation GCS
remains ≤8. Subsequent management follows Tier Zero of the above recommendations for adults.
Additional recommendations include strategies to ensure adequate tissue oxygen delivery such as
maintaining normal PaO2, restoring intravascular volume if low, targeting Hgb >7.0 g/dL and
treating coagulopathy to prevent further intracranial or extracranial hemorrhage.55,56

Thresholds for treatment of elevated ICP and decreased CPP are similar for pediatric patients, with
a goal of maintaining ICP < 20 mmHg and CPP > 40 mmHg in infants and small children and CPP
> 50 mmHg in older children and adolescents.55,56 Establishment of optimal CPP for individual
patients may require advanced neuromonitoring (i.e., Pbt02) due to the lack of well-defined, age
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dependent CPP thresholds and the risk of abnormal cerebrovascular autoregulation.57 In small
infants sub-galeal hematomas can cause blood loss sufficient to cause hypotension and be life-
threatening. Hypotension in children is defined as systolic blood pressure (SBP) below the 5th
percentile for age or by clinical signs of shock. Age-specific percentiles curves for pediatric
patients in acute care have been recently published.57

Tier One measures to control elevated ICP are also comparable. It is recommended to start with
CSF drainage if a ventriculostomy is present. Hyperosmolar therapy with HTS (recommended
dose: 2-10 ml/kg 3% HTS) is preferred in pediatrics due to more available evidence supporting its
use over mannitol.57 If mannitol is used (recommended dose: 0.5-1 g/kg), significant diuresis
should be anticipated and isotonic IV fluid boluses should be provided to prevent/treat systemic
hypotension. Continuous infusions of HTS can be utilized. Avoidance of persistently (≥72 hours)
elevated serum sodium values greater than 160 mEq/L is recommended to minimize complications
as there is no evidence to support improved outcomes with higher serum concentrations.57

Within Tier Two of the above guidelines, optimization of sedation/analgesia with midazolam and
fentanyl is recommended. Treatment of elevated ICP with bolus fentanyl or midazolam, in the
setting of adequate sedation/analgesia, is not recommended. Propofol should be used with caution
in pediatric patients due increased mortality in young patients, as well as patients with TBI, who
develop propofol infusion syndrome. An alternative sedative to be considered within Tier Two is
pentobarbital.57

Tier Three recommendations are analogous in pediatric and adult patients. Barbiturate infusion
guided by ICP and cEEG, mild hypothermia with controlled rewarming and mild/moderate
hypocapnia (PaCO2 28-34 mmHg) are consistent with current recommendations.57

A special category of children at risk for non-traumatic increased ICP and brain herniation are
children with diabetic ketoacidosis (DKA). Approximately 0.5-1% of children with DKA will have
severe cerebral edema, which carries a mortality rate of 20-25%.58,59 Factors thought to be
associated with increased risk of neurologic complications in pediatric DKA are young age,
duration, and severity of symptoms, low pCO2, overly aggressive fluid resuscitation,
administration of hypotonic fluids, administration of sodium bicarbonate, and decreases in serum
glucose > 100 mg/dL/hour.59,60 Hence, initial resuscitation should be administered with caution, in
small aliquots, and be directed at supporting hemodynamics rather than correcting calculated
dehydration. Boluses of sodium bicarbonate and/or insulin should be avoided. Mental status should
be checked at least hourly. Children with DKA will often become somnolent with initiation of
treatment, possibly due to progressive cerebral edema, but they should remain arousable with
stimulation. Children who are unarousable, those with papilledema, and those with warning signs
of cerebral herniation (Cushing’s triad) should receive hyperosmolar therapy. HTS may be
preferred to mannitol since osmolality is already high in DKA due to elevated glucose
concentrations. Hyperventilation could also be considered as a means of reducing ICP in this
patient population, but due to the typical Kussmal breathing pattern of patients with DKA, they
likely already have a low PaCO2. If intubation is required due to depressed mental status, it will
be necessary to utilize a high minute ventilation to mimic the natural respiratory compensation for
the metabolic acidosis associated with DKA.
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6.5 Nursing Considerations

The patient who is at high risk for elevated ICP and/or herniation should be assessed frequently
(i.e., hourly). A decline in neurological exam or clinical signs of increased ICP should be addressed
with the critical care provider. Assessments should be performed with the lowest amount of
stimulation necessary to prevent any further increase in ICP.

Patients at risk for increased ICP can often have many procedures occurring sequentially such as
placement of an external ventricular catheter, central venous catheter and/or arterial line making it
difficult to perform frequent neurologic assessments. If possible, perform focused neurologic
assessment such as pupil checks in between procedures or during procedures. Patient care such as
hygiene measures, suctioning and turning as well as procedures and imaging can increase ICP
especially if the patient’s head of bed must be lowered.61-64 Consider performing these activities
when ICP is low such as after treatment with a hyperosmolar medication if possible. Do not use
Trendelenburg positioning to aid in positioning patients in the presence of increased ICP. A critical
care nurse with training in care of acute neurologically injured patients should be part of a
multidisciplinary team engaged in creating and implementing brain code protocols.65,66

Nursing will accompany the patient within the facility (e.g., ED to ICU and/or radiology) and
perform continued physiologic monitoring including monitoring and ICP during transport. Any
handoff between nurses should include both RNs completing a neurological assessment
concurrently to ensure consistency of future exams. The nurse assisting with placement of an
intracranial pressure monitoring device and will need to prime and zero the drainage system upon
insertion and re-zeroed each shift. Newer intracranial catheters are zeroed to atmospheric pressure
just once upon insertion making them easier during times of movement/transport. Document and
trend ICP, CSF appearance and CSF output as frequently as ordered or by hospital policy, often
hourly. Notify responding clinician if there is a perceived change in CSF appearance or amount as
intervention may be required.

Ensure EVD is closed and closely monitored while repositioning a patient or transferring a
patient to ensure there is no over drainage of CSF or dislodgement of the catheter. Re-level the
EVD before opening. Changes to this level can result in under and over drainage. Education
should be performed with the patient and/or family regarding calling for assistance to reposition,
change the level of the head of the bed and ambulate to avoid under or over draining. If
available, consider locking the position of the head of the bed.

6.6 ICP waveform interpretation

The waveform analysis of the ICP monitor, calculation of CPP, and neurological assessments
should be performed and documented per hospital guidelines, but generally every hour at a
minimum, and more frequently when the patient is unstable or undergoing active therapeutic
intervention (e.g., to gauge the response after administration of osmotic therapy for raised ICP)
(Figure 4). A normal ICP waveform will look like a mountain (P1) and two progressive hills (P2
& P3) immediately following. As ICP rises, the center wave (P2) becomes closer to the height of
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the P1, this represents an increase of ICP, but the patient can compensate for the change. When
the pressure becomes too high to compensate, P2 becomes greater than P1 and P3, making it
difficult to see distinct waves. Waveforms that flatten out or plateau can be a sign of brain
ischemia/infarction.66,67

6.7 Positioning

Ensure the heigh of bed (HOB) is >30. Keep the neck and head midline to allow for optimal venous
outflow, consider using towels or pillows to keep this position. If turning a patient is associated
with increased ICP, decrease the frequency of turning and document the rationale. Assess the fit
of cervical collar if present, if the collar is too tight it could impede venous outflow.

6.8 Pain and sedation

Pain and agitation can increase intracranial pressure. Frequent assessment of pain and agitation
using validated assessment tools is recommended and treated as ordered.68 Short acting drugs with
the least amount of effect on the blood pressure are preferred. Use the lowest amount of pain and
sedative medication as possible to preserve neurologic exam. Medications such as propofol should
be stopped and the patient should be allowed to wake up prior to a neurologic assessment.
Education with family about minimizing stimulation to prevent agitation is advised. Instruct the
family to provide reassurance and reorientation and to talk to their loved in a calm manner which
may decrease ICP.69

6.9 TTM and Shivering

If TTM is being used frequently, assess the patient for shivering. Uncontrolled shivering has been
shown to counteract neuroprotective benefits of TTM in animal studies. Shivering has been
associated with decreased brain tissue oxygenation. Follow shivering protocols to ensure shivering
is controlled. Methods to control shivering include counter warming with a forced air warming
system and various pharmacologic options.70

Figure 4. ICP Wave Form [68]

ICP curve showing normal brain compliance (left panel, P1 > P2) vs. impaired brain compliance (right
panel, P2 > P1) [68]. Not only is the absolute value of ICP important, but so is the configuration of the
ICP waveform. In the right panel, the increase in the second component of the invasive ICP curve
 16

(P2=cerebral venous return) is a warning sign that the brain has poor compliance. This should prompt
aggressive therapy of intracranial hypertension.

6.7 Family

Nursing is also invaluable in establishing key contact information for family/caregiver, performing
education with the patient and/or family, facilitating spiritual care, social services and participating
in family conferences. Finally, for the patient who progresses to irreversible brain herniation or
brain death, nurses can alert the local organ procurement agency that can engage with the family
in organ donation conversations.

7. Communication Checklist

When communicating transfer of care of a patient that was treated for intracranial hypertension or
herniation, consider including the key elements listed in Table 3.
 17

Table 3. ICP/Herniation Standard Communication during Transfer of Care

 18

Clinical Pearls
• Sustained intracranial hypertension (ICP > 22mmHg for > 5min)
and acute brain herniation are “brain codes,” that are potentially
reversible with appropriate and timely therapy.
• Clinical symptoms of increased ICP include headache, nausea and
vomiting, pupillary changes, and/or altered mental status.
• Hypertension, bradycardia, and irregular respirations or apnea
(Cushing’s triad) may be present but the concurrence of all three
signs is uncommon and often are late findings.
• Obtain emergent non-contrast head CT for patients that are
perceived to have new symptoms of intracranial hypertension or
brain herniation as soon as clinically reasonable.
• ICP monitoring should be used if a patient has clinical or
radiographic evidence of elevated ICP and might benefit from ICP
or CPP targeted intervention.
• All patients at risk of elevations in ICP should receive Tier 0
interventions including: optimized hemodynamics, elevate the
head, maintain normal PCO2, PaO2, sodium concentration, and
temperature.
• For acute ICP elevations, utilize hyperosmolar therapy with either
HTS or Mannitol, and sedation optimization.
• Selected patients with rapid neurological deterioration from focal
space-occupying lesions may benefit from surgical decompression.
• Tier 3 therapies including pentobarbital and/or TTM (32–34°C)
may be used for ICP that is refractory to prior therapies. Tier 3
treatments are the most aggressive and carry the greatest risk of
complication.
 19

Starred References
** Landmark paper
* Important paper

**3 (Carney N et al.): TBI guidelines from Brain Trauma Foundation

*20 (Francony G., et al.): Comparative study of hyperosmotic agents for ICP management
**37 (Hutchinson PJ, et al.): RESCUE-ICP for decompressive craniectomy for refractory ICP in
head trauma
*48 (Chang JJ, et al.): BOOST-2 trial for Pbt02 monitoring
**55 (Kochanek PM, et al.): Pediatric TBI guidelines
*56 (Allen BB, et al.): Age-specific CPP thresholds for pediatric TBI

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Acknowledgements
The authors are grateful for the contributions and insight provided by the following
reviewers: Aaron Raleigh, BA, EMT-P; Amina George, PharmD, BCCCP; and Christi
DeLemos, MSN, CNRN, ACNP-BC.