Management of Intracranial Hypertension Symposium on Neurological Disorder–Advances in Management-II

Transcription

Symposium on Neurological Disorder–Advances in Management-II
Management of Intracranial Hypertension
Sunit C Singhi and Lokesh Tiwari
Pediatric Emergency and Intensive Care Units, Department of Pediatrics, Advanced Pediatrics Centre, Post
Graduate Institute of Medical Education and Research (PGIMER), Chandigarh, India
ABSTRACT
Raised intracranial pressure (ICP) is a life threatening condition that is common to many neurological and non-neurological
illnesses. Unless recognized and treated early it may cause secondary brain injury due to reduced cerebral perfusion
pressure (CPP), and progress to brain herniation and death. Management of raised ICP includes care of airway, ventilation
and oxygenation, adequate sedation and analgesia, neutral neck position, head end elevation by 200 -300, and short-term
hyperventilation (to achieve PCO2 32- 35 mm Hg) and hyperosmolar therapy (mannitol or hypertonic saline) in critically
raised ICP. Barbiturate coma, moderate hypothermia and surgical decompression may be helpful in refractory cases.
Therapies aimed directly at keeping ICP <20 mmHg have resulted in improved survival and neurological outcome.
Emerging evidence suggests that cerebral perfusion pressure targeted therapy may offer better outcome than ICP targeted
therapies. [Indian J Pediatr 2009; 76 (5) : 519-529] E-mail: [email protected]; [email protected]
Key words: Intracranial pressure; Children; Traumatic brain injury; Cerebral perfusion pressure; Hyperosmolar therapy.
Increased intracranial pressure (ICP) is a frequently
encountered life threatening syndrome caused by a
variety of neurologic and non neurological illnesses.
About 20% of all admissions to our PICU are because of
raised ICP. If unchecked it may lead to catastrophic
deterioration and death. Appropriate and timely
management of raised ICP is possible with proper
understanding of pathphysiology, and various
therapeutic modalities. We review here current
understanding and recent advances in management of
raised ICP. Most treatment modalities have evolved
from treating traumatic brain injury (TBI) and are
applied to treat raised ICP of other etiology.
PHYSIOLOGIC CONSIDERATIONS
atmospheric in newborns. 1 Usually normal limits are
taken as 5 to 15 mm Hg. Current pediatric data support
an ICP >20 mm Hg as threshold to define intracranial
hypertension requiring treatment. Sustained ICP values
of greater than 40mm Hg indicate severe, lifethreatening intracranial hypertension.2 There have been
some suggestions that lower threshold values for
younger children may be used, although there are no
data to support this. 3 A surge in ICP normally occurs
with activities such as suctioning, painful stimuli, and
coughing and does not warrant intervention unless it
does not return to baseline within about 5 minutes. It is
important to distinguish “normal” or expected
increases in ICP vs intracranial hypertension because
the latter requires immediate intervention.
CEREBRAL PRESSURE DYNAMICS
Intracranial pressure: Normal values
The normal range for ICP varies with age. Values for
children are not as well established as for adults.
Normal values are less than 10 to 15mmHg for adults
and older children, 3 to 7 mm Hg for young children,
and 1.5 to 6 mm Hg for term infants. ICP can be sub-
Correspondence and Reprint requests : Dr Prof. Sunit Singhi,
Head, Department of Pediatrics, Advanced Pediatric Centre,
Chandigarh, 160012, India. Phone No. Office: 91-172-275
5301and 5302; Residence: 91-172-2715619; Fax: 91172 2744401,
2745078
[Received March 17, 2009; Accepted March 17, 2009]
Indian Journal of Pediatrics, Volume 76—May, 2009
Monro-Kellie doctrine
Intracranial pressure is the sum total of pressure exerted
by the brain, blood, and cerebrospinal fluid (CSF) in the
non-compliant cranial vault. The Monro-Kellie doctrine
states that sum of intracranial volume of brain (» 80%),
blood (» 10%), and cerebrospinal fluid (» 10%) is
constant. An increase in any one of these components
must be offset by decrease in another to keep the total
volume constant or else the ICP will increase. In
response to increase in intracranial volume initial
compensation occurs by displacement of CSF from the
ventricles and the cerebral subarachnoid space to
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spinal subarachnoid space (vertebral canal), decreased
production, and increased absorption of CSF. Infants
and children with open fontanels and sutures may be
able to compensate better but will still be susceptible to
acute increases in ICP.
Compliance
Compliance is an indicator of the brain’s tolerance to
increases in ICP. Each patient has varying degrees of
compliance even with similar injuries. When the
patient’s compliance is exhausted, there is a dramatic
increase in the pressure/volume curve, leading to a
rapid elevation in ICP.
Cerebral blood flow
In an uninjured brain, cerebral blood flow (CBF) is
regulated to supply the brain with adequate oxygen
and substrates. Certain physiologic factors like
hypercarbia, acidosis and hypoxemia cause
vasodilatation, leading to increased CBF. Seizure
activity and fever will increase cerebral metabolic rate and
CBF. CBF in excess of tissue demand leads to hyperemia
and increased ICP. Methods to decrease the cerebral
metabolic rate, such as hypothermia and barbiturates,
will decrease CBF and thus the ICP.
Cerebral perfusion pressure
Cerebral perfusion pressure (CPP) is the pressure at
which brain is perfused. It is an important indicator of
cerebral blood flow. CPP provides an indirect
measurement of adequacy of CBF. It is calculated by
measuring the difference between the mean arterial
pressure (MAP) and the ICP (MAP – ICP), where MAP
= 1/3 systolic pressure plus 2/3 diastolic pressure. A
reduction in CPP can occur from an increase in ICP, a
decrease in blood pressure, or a combination of both
factors. Normal CPP values for children are not clearly
established, but the values that are generally accepted
as the minimal pressure necessary to prevent ischemia
are: adults >70 mm Hg; children >50–60 mm Hg;
infants/toddlers >40–50 mm Hg.4 CPP < 40 mm Hg is a
significant predictor of mortality in children with TBI.2
Autoregulation maintains a steady cerebral blood
flow (CBF) within a CPP range of 50-150 mmHg by
vasoconstriction and vasodilatation of the cerebral
vessels despite fluctuations in systemic blood pressure.
Autoregulation is lost at CPP values less than 50 mmHg.
Ability to pressure autoregulate may be impaired or lost
even with a normal CPP, CBF can passively follow
changes in CPP. Once autoregulation is lost, CBF and
cerebral blood volume (CBV) become dependent on
changes in systemic blood pressure.
CAUSES OF RAISED ICP
An increase in intracranial pressure is commonly
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caused by an increase in volume of brain (cerebral
edema), blood (intracranial bleeding), space occupying
lesion, or CSF (hydrocephalous). These mechanisms
could be operative singly or in various combinations.
Cerebral edema is the most important cause of raised
ICP in non-traumatic brain injuries such as central
nervous system (CNS) infections, and systemic and
metabolic encephalopathies. It can be vasogenic,
cytotoxic, or interstitial. Vasogenic cerebral edema is
due to injury to blood brain barrier and increased
capillary permeability around the area of injury or
inflammation particularly in CNS infections. It can be
local or diffuse and occurs around mass lesions and
inflammatory processes (e.g., meningitis, encephalitis).
Interstitial cerebral edema is due to an increase in the
hydrostatic pressure of CSF and is often seen in
patients with obstructive hydrocephalus or excessive
CSF production. Cytotoxic cerebral edema (Cellular
swelling) occurs following cerebral ischemia and
hypoxia causing irreversible cell damage and death.
Osmolar swelling may occur because of increased local
osmolar load around necrotic foci caused by infarction
or contusion, and possibly because of increased cerebral
blood volume (hyperemia) in CNS infections. Patients
with cerebral edema may have a combination of all 3
mechanisms operating.
The primary etiology could be intracranial or
extracranial (Table 1). When primary cause of
increased ICP is intracranial, normalization of ICP
depends on rapidly addressing the underlying brain
disorder. Intracranial hypertension due to an
extracranial or systemic process is often remediable.
Increased ICP can also occur after a neurosurgical
procedure.
TABLE 1. Causes of Intracranial Hypertension
Intracranial (primary)
• CNS infections – meningitis, encephalitis, brain abscess,
cerebral malaria, neurocysticercosis,
• Trauma (epidural and subdural hematoma, cerebral
contusions and edema)
• Brain tumor
• Intracranial bleed – intracerebral and intraventricular
hemorrhage
• Others – ischemic stroke, hydrocephalous, idiopathic or
benign intracranial hypertension.
• Status epilepticus.
Extracranial (secondary)
• Hypoxic Ischemic Injury - airway obstruction, hypoventilation, shock.
• Metabolic – hyperpyrexia, hepatic failure, lead intoxication.
• Drug (e.g., tetracycline, rofecoxib)
• Others – hypertensive encephalopathy
Postoperative
• Mass lesion (hematoma)
• Cerebral edema
• Increased cerebral blood volume (vasodilation)
• CSF obstruction.
Following traumatic brain injury (TBI), intracranial
hypertension is multifactorial:
• Trauma induced epidural or subdural hematomas,
hemorrhagic contusions, and depressed skull
fractures
• Cerebral edema (most important cause after
hematomas).5
• Hyperemia due to loss of autoregulation
• Hypoventilation leading to hypercarbia and
consequently cerebral vasodilation
• Hydrocephalus resulting from obstruction of the
CSF pathways or its absorption
• Increased intrathoracic or intra-abdominal pressure
as a result of mechanical ventilation, posturing,
agitation, or Valsalva maneuvers.
A secondary increase in the ICP is often observed 3
to 10 days after the trauma, mainly as a result of a
delayed formation of epidural or acute subdural
hematoma, or traumatic hemorrhagic contusions with
surrounding edema, sometimes requiring evacuation.
Other potential causes of delayed increases in ICP are
hypoventilation,
and
cerebral
vasospasm, 6
hyponatremia.
INTRACRANIAL PRESSURE MONITORING
Acute raised ICP is an important cause of secondary
brain injury hence at–risk patients should have close
monitoring of systemic parameters, including
temperature,
heart
rate,
blood
pressure,
electrocardiogram, blood glucose, ventilation,
oxygenation, and fluid intake and output. They should
be on continuous monitoring with pulse oximetry and
capnography to avoid unrecognized hypoxemia and
hypoventilation or hyperventilation. A central venous
catheter should be placed to evaluate volume status,
and a Foley catheter for accurate urine output. Patients
with suspected intracranial hypertension should have
monitoring of ICP. Monitoring of cerebral oxygen
extraction with jugular bulb oximetry is desirable, if
available.
Indications
Clinical symptoms of increased ICP, such as headache,
nausea, and vomiting, are impossible to elicit in
comatose patients. Papilledema, though a reliable sign
of intracranial hypertension, is uncommon after acute
events, even in patients with documented elevated ICP.
On the other hand, signs such as pupillary dilation and
decerebrate posturing can occur in the absence of
intracranial hypertension. CT scan signs of brain
swelling, such as midline shift and compressed basal
cisterns, are predictive of increased ICP, but intracranial
hypertension can sometimes occur without those
findings. 7
Monitoring of ICP is an invasive technique and has
some associated risks. The aim of monitoring is
prevention of cerebral ischemia and secondary brain
injury. For a favorable risk-to-benefit ratio, therefore, ICP
monitoring is indicated only in selected at-risk
patients. 8 These include patients with Glasgow Coma
Scale of 8 or less and patients with TBI who have an
abnormal admission head CT scan. 9 Patients who are
able to follow commands have a low risk for developing
raised ICP and can be followed with serial neurologic
examinations. Patients with a Glasgow Coma Scale
score greater than 8 also might be considered for ICP
monitoring if they require a treatment that might
increase ICP, such as positive end-expiratory pressure
(PEEP). Other, less common indications include
patients with multiple systemic injuries with altered
level of consciousness and subsequent to removal of an
intracranial mass (e.g., hematoma, tumor). ICP
monitoring also must be considered in nontraumatic
conditions in which an intracranial mass lesion is
present (e.g., cerebral infarction) and has a likelihood of
expansion leading to intracranial hypertension and
clinical deterioration. The duration of monitoring is
until ICP has been normal for 24 to 48 hours without a
need for therapy to reduce ICP. Although ICP
monitoring has never been subjected to randomized
controlled studies to evaluate its effectiveness, its use
has been associated with decreased morbidity and
mortality, and improved outcome in patients with TBI,
intracerebral hemorrhages, and CNS infections.8,10-12 ICP
monitoring is crucial to identify rapidly increasing
pressure and to institute appropriate therapy to prevent
cerebral herniation and preserve cerebral perfusion. It is
also necessary to monitor ICP in order to calculate the
CPP.
Sites for ICP monitoring
The most common sites used for ICP monitoring are
intraventricular and intra-parenchymal. Intraventicular
catheter remained the preferred device for monitoring
ICP and the standard against which all newer monitors
are compared.13 These days the use of intraventricular
catheter placement, preferably with an implantable
micro-transducer (fiberoptic or strain-gauge) 14 allows
simultaneous monitoring of ICP and management of
increased ICP by CSF drainage.The advantages of the
ventriculostomy are its relatively low cost, the option to
use it for therapeutic CSF drainage, and its ability to
recalibrate to minimize errors owing to measurement
drift. Disadvantages are difficulties with insertion into
compressed or displaced ventricles, risk of infection,
inaccuracies of the pressure measurements because of
obstruction of the fluid column, and the need to
maintain the transducer at a fixed reference point
relative to the patient’s head. The system should be
checked for proper functioning at least every 2 to 4
hours, and any time there is a change in the ICP,
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neurologic examination, and CSF output. This check
should include assessing for the presence of an
adequate waveform, which should have respiratory
variations and transmitted pulse pressure. When the
ventricle cannot be cannulated, intraparenchymal site
can be used. Other alternatives for monitoring ICP
include subdural, subarachnoid, and epidural catheter
placement using microsensor transducer and fiberoptic
transducer tipped catheters. The main advantages of
micro-transducers are the ease of insertion, especially in
patients with compressed ventricles. However, none of
the micro-transducer- tipped catheters can be
recalibrated after they are inserted into the skull. They
also exhibit measurement drift over time15 and must be
replaced if monitoring is in excess of several days.
Intracranial pressure waveforms
Tidal
(redbound)
P2
Complications of ICP monitoring(13)
The most common complication of ventricular catheter
placement is infection (incidence of 5% to 14%);
colonization of the device is more common than clinical
infection. 17 There was a nonlinear increase of risk
during 10 to 12 days, after which the risk diminished.17
Use of antibiotic-coated ventricular catheters has been
shown to reduce the risk of infection from 9.4% to
1.3%.18 Other complications of ventricular catheters are
hemorrhage (incidence 1.4%), malfunction, obstruction,
and malposition.
MANAGEMENT OF INCREASED ICP
The normal ICP waveform contains three phases (Fig.
1A)
• P1 (percussion wave) represents arterial pulsations.
• P2 (rebound wave) reflects intracranial compliance.
• P3 (dichrotic wave) represents venous pulsations.
Percussion
(arterial)
P1
waveform, but high amplitude. C waves may be
superimposed on plateau waves.16
Low pressure wave,
non-compliant cranium
Dichrotic
P3 (venous)
Fig. 1A. Normal ICP wave forms
As the ICP increases, cerebral compliance decreases,
arterial pulses become more pronounced, and venous
components disappear. Pathologic waveforms include
Lundberg A, B, and C types (Fig. 1B). Lundberg A
waves or plateau waves are ICP elevations to more than
50 mm Hg lasting 5 to 20 minutes. These waves are
accompanied by a simultaneous increase in MAP, but it
is not clearly understood if the change in MAP is a
cause or effect. Lundberg B waves or pressure pulses
have amplitude of 50 mm Hg and occur every 30
seconds to 2 minutes. Lundberg C waves have
amplitude of 20 mmHg and more and a frequency of 4
to 8 per minute; they are seen in the normal ICP
High pressure wave,
non-compliant cranium
In patient with raised ICP in addition to treatment of
primary cause-whether intracranial or extracranial, the
main focus of treatment is to prevent and minimize
secondary injury. Secondary brain injury refers to the
processes that occur within hours to days after the
primary injury that can be prevented or minimized—
such as cerebral ischemia, cerebral edema, and
neurochemical alterations including excitatory
neurotransmitters, the formation of free radicals, and
increased levels of intracellular calcium and
potassium. 19 Factors that are known to worsen
secondary injury are hypoxia and hypotension.20 The
neurological devastation caused by the secondary
injury is often worse than the underlying primary
disorder. Most of the current treatment recommendations
are based on consensus and clinical
experience. Few specific treatment options have been
subjected to randomized trials.
Since there are limited outcome studies to support
the current management of children with increased ICP
from etiologies other than TBI it is the knowledge
gained from treating TBI that is often applied to treat
raised ICP of other etiologies also.
Goals of therapy
• Maintain ICP less than 20 to 25 mm Hg.
• Maintain adequate CPP usually greater than 60 mm
Hg, by maintaining adequate MAP.
• Avoid factors that aggravate or precipitate elevated
ICP.
An overall approach to the management of
intracranial hypertension is presented in fig. 2.
Airway, Breathing, and Circulation
Fig. 1B. High ICP wave forms
522
The initial management of the child with suspected
increased ICP includes assessment of airway, breathing, and circulation. Even prior to a thorough
Head midline
elevated 20-30o
Fig. 2. Approach to the management of intracranial hypertension
Abbreviations : ICP – Intracranial Pressure, GCS – Glargow coma score, HTS – Hypertonic saline
neurological exam, if the patient is unarousable, has a
GCS<8 or has difficulty maintaining a patent airway,
rapid sequence intubation should be done immediately.
Endotracheal intubation should also be considered if
the child has a neurological injury at risk for
decompensation, chest wall instability, abnormal
respiratory pattern, loss of protective airway reflexes, or
upper airway obstruction. Medications that facilitate
intubation without increasing the ICP such as
thiopental,
lidocaine,
and
a
short-acting,
nondepolarizing neuromuscular blockade agent (e.g.,
vecuronium, atracurium) should be used just before the
523
procedure. Adequate oxygenation is necessary to
prevent sequelae of secondary insults and should be
maintained with a PaO 2 > 60 mm Hg, an oxygen
saturation > 92%, and physiologic positive end
expiratory pressure (PEEP) of 5 cm H2O. Blood pressure
must be maintained at levels appropriate for age or
restored to ensure adequate CPP and prevent further
ischemia. Fluid boluses should be given to the
hypotensive neurologically injured child in the same
way as any other child presenting in shock.
Vasopressor support is initiated if the child remains
hypotensive despite appropriate fluid resuscitation.
General measures
Prevention or treatment of factors that may aggravate or
precipitate intracranial hypertension should be
undertaken. Specific factors that may aggravate
intracranial hypertension include obstruction of venous
return (head position, agitation), respiratory problems
(airway obstruction, hypoxia, hypercapnia), fever,
severe hypertension, hyponatremia, anemia, and
seizures.
Head elevation and position
Elevation of the head-end of the bed and keeping the
head in a neutral position are standard recommendations to minimize resistance to venous outflow and
promote displacement of CSF from the intracranial
compartment to the spinal compartment. Elevation of
the head up to 30o reduces ICP and increases CPP, but
does not change brain tissue oxygenation. 21 The
reduction in ICP resulting from 15 o to 30 o of head
elevation is probably advantageous and safe for most
patients. The child must be euvolemic prior to placing
in this position to avoid orthostatic hypotension. When
head elevation is used, the pressure transducers for
blood pressure and ICP must be zeroed at the same level
(at the level of the foramen of Monro) to assess CPP
accurately.
Management of Respiratory failure
Comatose patients often have respiratory dysfunction
requiring mechanical ventilation, pneumonia and
pulmonary insufficiency, or periodic episodes of
hypoventilation. Resultant hypoxia and hypercapnia
can increase ICP dramatically, and mechanical
ventilation can alter cerebral hemodynamics. Controlled
ventilation may be needed for optimal management
and to maintain normal carbon dioxide . During
mechanical ventilation high PEEP can increase ICP by
impeding venous return and increasing cerebral venous
pressure, and by decreasing blood pressure leading to a
reflex increase of cerebral blood volume. The effects of
PEEP on ICP also depend on lung compliance; minimal
effect is seen when lung compliance is low.22
524
Sedation and analgesia
Children with acute brain injury, especially those who
are mechanically ventilated, should be appropriately
sedated and given adequate analgesia to prevent pain
and anxiety, both of which increase the cerebral
metabolic rate and ICP. There are no randomized
controlled studies comparing sedation methods in
children with acute neurological injury. In general,
benzodiazepines have no effect on ICP, whereas the
opiates have been reported to increase ICP in adult
patients with TBI. 23 One consideration in the choice of
sedative should be to minimize effects on blood
pressure because most available agents can decrease
blood pressure. Hypovolemia predisposes to
hypotensive side effects and should therefore be
corrected before administering sedatives. Selection of a
shorter acting agent (midazolam) may have the
advantage of allowing brief interruption of sedation to
examine neurologic status. Propofol is not approved for
sedation in PICU as its safety is not established by US
FDA and UK committee on safety of Medicine.
Fever
Fever increases metabolic rate by 10% to 13% per degree
Celsius and is a potent vasodilator. Fever-induced
dilation of cerebral vessels can increase CBF and may
increase ICP. In patients at risk of intracranial
hypertension, fever should be controlled with
antipyretics and hydrotherapy. Etiology of fever must
be sought and treated appropriately. A significant
relationship has been seen between fever and a poor
neurologic outcome in head injury patients.24
Hypertension
Elevated blood pressure is seen commonly in patients
with raised ICP. Characteristically systolic blood
pressure increase is greater than diastolic increase. It is
unwise to reduce elevated blood pressure associated
with untreated raised ICP, especially in patients with
intracranial mass lesion, because the high blood
pressure maintains cerebral perfusion. In the absence
of an intracranial mass lesion, the decision to treat
elevated blood pressure has to be individualized. When
autoregulation is impaired, which is common after TBI,
systemic hypertension may increase CBF and ICP, may
exacerbate cerebral edema and increase the risk of
postoperative intracranial hemorrhage. Systemic
hypertension may resolve with sedation. If the decision
is made to treat systemic hypertension, vasodilating
drugs, such as nitroprusside, nitroglycerin, and
nifedipine, should be avoided; these increase ICP,
which may be deleterious to the marginally perfused
injured brain. Sympathomimetic-blocking antihypertensive drugs, such as beta-blocking drugs (labetalol,
esmolol) or central acting alfa-receptor agonists
(clonidine), are preferred because they reduce blood
pressure without affecting the ICP. Agents with a short
half-life have an advantage when the blood pressure is
labile.
Treatment of anemia
Patients with severe anemia have been reported to
present with symptoms of increased ICP and signs of
papilledema, which resolve with treatment of the
anemia.25 The mechanism is thought to be related to the
marked increase in CBF that is required to maintain
cerebral oxygen delivery when anemia is severe.
Although anemia has not been clearly shown to
exacerbate ICP after TBI, a common practice is to
maintain hemoglobin concentration around 10 g/dL. A
large randomized trial of critically ill patients showed
better outcome with a more restrictive transfusion
threshold of 7 g/dL.26. The issue of optimal hemoglobin
concentration in patients with raised ICP needs further
study.
Prevention of seizures
Seizures occur commonly in association with raised
ICP irrespective of etiology, be it meningitis,
encephalitis or severe head injury. Seizures increase
cerebral metabolic rate and lead to a dramatic rise in
ICP, but there is no clear relationship between the
occurrence of early seizures and a worse neurologic
outcome. In patients with severe TBI as well as in those
with nontraumatic coma, seizures may be subclinical
and can be detected only with continuous
electroencephalographic monitoring. Prophylactic
anti-seizure therapy may be considered for prevention
of early posttraumatic seizures (PTS) in children at high
risk of seizure following TBI. However, prophylactic
use of anti-seizure therapy is not recommended for
children for prevention of late post-traumatic seizure.27
If a late PTS occurs, the patient should be managed in
accordance with standard approaches to patients with
new-onset seizures.27
MEASURES FOR REFRACTORY INTRACRANIAL
HYPERTENSION
For patients with sustained ICP elevations of greater
than 20 to 25 mm Hg, additional measures are needed
to control the ICP.
Hyperosmolar therapy
Mannitol is the most commonly used hyperosmolar
agent for the treatment of intracranial hypertension.28
More recently, hypertonic saline has also been used. A
few studies have compared the relative effectiveness of
these two hyperosmotic agents, but more work is
needed.
Intravenous bolus administration of mannitol lowers
the ICP in 1 to 5 minutes with a peak effect at 20 to 60
minutes. The effect of mannitol on ICP lasts 1.5 to 6
hours, depending on the clinical condition.29 Mannitol
is usually given as a bolus of 0.25 to 0.5g/kg; when
urgent reduction of ICP is needed, an initial dose of 1 g/
kg may be given. Two prospective clinical trials in
adults, one in patients with subdural hematoma and
the other in patients with herniation secondary to
diffuse brain swelling, have suggested that a higher
dose of mannitol (1.4 g/kg) may give significantly better
results than a lower dose in these extremely critical
situations. 30 When long-term reduction of ICP is
needed, 0.25 to 0.5 g/kg can be repeated every 2 to 6
hours. Attention should be paid to replacing fluid that
is lost because of mannitol-induced diuresis, or else
intravascular volume depletion would result.
Mannitol has rheologic and osmotic effects. 31
Infusion of mannitol increases serum osmolarity, which
draws edema fluid from cerebral parenchyma. This
process takes 15 to 30 minutes until gradients are
established. Immediately after infusion of mannitol,
therefore there is an expansion of plasma volume and a
reduction in hematocrit and in blood viscosity, which
may increase CBF and oxygen delivery to the brain.31 In
patients with intact pressure autoregulation, infusion
of mannitol induces cerebral vasoconstriction, which
maintains constant CBF and causes a considerable
decrease in ICP. In patients with absent pressure
autoregulation, infusion of mannitol increases CBF,
and hence the decrease in ICP is less pronounced.
Mannitol opens the blood-brain barrier, and may
cross it. Mannitol that has crossed the blood-brain
barrier may draw fluid into the central nervous system,
which can aggravate vasogenic edema. For this reason,
when it is time to stop mannitol, it should be tapered to
prevent ICP rebound.31 For optimal effect of mannitol,
serum osmolality should be between 300-320 mOsm.
Keeping osmolality less than 320 mOsm also helps to
prevent complications such as hypovolemia,
hyperosmolarity, and renal failure. The adverse effects
of mannitol are more likely when it is present in the
circulation for extended periods, such as in slow or
continuous infusions or with repeated administration
of high doses.
Hypertonic saline administration appears to be a
promising therapy for control of cerebral edema. Given
in concentrations ranging from 3% to 23.4%, it creates
an osmotic force to draw water from the interstitial
space of the brain parenchyma into the intravascular
compartment in the presence of an intact blood-brain
barrier, reducing intracranial volume and ICP. In some
studies in adults, hypertonic saline has been more
effective in reducing ICP in TBI than mannitol. 32
However, variations in hypertonic solution prepara525
tions and dosing regimens, difference in inclusion and
exclusion criteria, and small numbers of patients make
these studies difficult to compare. Hypertonic saline is
said to have advantage over mannitol in hypovolemic
and hypotensive patients as it augments intravascular
volume and may increase blood pressure in addition to
decreasing ICP. However, use of hypertonic saline as
prehospital bolus to hypotensive patients with severe
TBI was not associated with improved neurologic
outcomes.33
Adverse effects of hypertonic saline administration
include hematologic and electrolyte abnormalities, such
as bleeding secondary to decreased platelet aggregation
and prolonged coagulation, hypokalemia, and
hyperchloremic acidosis. Available data show only
level II evidence supporting the use of continuous
infusion of 3% saline for treatment of elevated ICP in
pediatric TBI. 34 An effective minimum dose on a
sliding scale (0.1 – 1.0 ml/kg/hour) to keep ICP <20
mm/kg should be used.28 Infusion can be continued if
serum osmolality is below 360 mOsm/L.
Heavy sedation and paralysis
Routine paralysis of patients with severe raised ICP is
not indicated; however, intracranial hypertension
caused by agitation, posturing, or coughing can be
prevented by deep sedation and nondepolarizing
muscle relaxants that do not alter cerebrovascular
resistance.35,36 A commonly used regimen is morphine
and lorazepam for analgesia/sedation and cisatracurium or vecuronium as a muscle relaxant, with the
dose titrated by twitch response to stimulation. The
disadvantage of this therapy is that the neurologic
examination cannot be monitored closely. The sedatives
and muscle relaxants can be interrupted once a day,
usually before morning rounds, to allow neurologic
assessments. Since the use of neuromuscular block will
eliminate motor activity associated with seizures, but
not brain epileptiform activity, children at high risk for
seizures should have continuous electroencephalograph (EEG) monitoring.36
Hyperventilation
Hyperventilation decreases PaCO 2 , which induces
constriction of cerebral arteries; the resulting reduction
in cerebral blood volume decreases ICP. 37,38 Acute
hyperventilation decreases global CBF. Sometimes this
reduction in flow could be sufficient to induce ischemia
in injured brain.39,40 Hyperventilation has limited use in
the management of intracranial hypertension, because
its effect on ICP is time limited. The vasoconstrictive
effect on cerebral arterioles lasts only 11 to 20 hours
because the pH of the CSF rapidly equilibrates to the
new PaCO2 level. As the CSF pH equilibrates, the
cerebral arterioles redilate, possibly to a larger caliber
than at baseline, and a possible rebound phase of
526
increased ICP. 38 The precise relationship between
hyperventilation and outcome has not been studied in
children with raised ICP of any etiology. Based on
current evidence, following suggestions can be made:
• Prophylactic hyperventilation should be avoided.
• Mild hyperventilation (PaCO 2 30–35 mm Hg) may
be considered for longer periods for intracranial
hypertension refractory to sedation and analgesia,
neuromuscular blockade, cerebrospinal fluid
drainage, and hyperosmolar therapy.
• Aggressive hyperventilation (PaCO2 <30 mm Hg)
titrated to clinical effect may be considered as a
second tier option in the setting of refractory
hypertension and for brief periods in cases of
cerebral herniation or acute neurologic
deterioration.37
Barbiturate coma
Small studies of high-dose barbiturate therapy suggest
that barbiturates are effective in lowering ICP in selected
cases of refractory intracranial hypertension in children
with severe head injury. However, studies on the effect
of barbiturate therapy for uncontrolled ICP have not
evaluated neurologic outcome.41 Thiopental is given in
a loading dose of 5mg/kg over 30 minutes,(monitor for
hypotension) followed by infusion of 1-5 mg/kg hour
until the electroencephalogram shows a burst
suppression pattern. The mechanism of ICP reduction
by barbiturates is unclear. It probably reflects a coupled
reduction in CBF and cerebral metabolic rate with an
immediate effect on ICP. 42 Complications of barbiturate
coma include hypotension, hypokalemia, respiratory
depression, infections, and hepatic and renal
dysfunction. Hypotension caused by barbiturate should
be treated first with volume replacement and then with
dopamine, if necessary. Dopamine infusion increases
cerebral metabolic requirements and may partially
offset the beneficial effects of barbiturates on cerebral
metabolic rate. There is no evidence to support use of
barbiturates for the prophylactic neuroprotective effects
or prevention of the development of intracranial
hypertension in children with severe TBI.43
Induced Hypothermia
A phase II trial to test safety and efficacy of hypothermia
in children with TBI did not show a beneficial effect on
neurologic outcome, however, a reduction in ICP was
evident during the hypothermia treatment.44 There were
no significant differences between the hypothermia and
no-hypothermia patients with respect to complications
viz. arrhythmia, coagulopathy or infection. However,
the early hypothermia group had a trend toward better
neurological outcome at 3 and 6 months. 44 A recently
completed multicentre trial by Hypothermia Pediatric
Head injury Trial investigators, Canadian Critical Care
Groups that included 225 children, found a detrimental
trend with hypothermia.45 Currently therefore, routine
induction of hypothermia is not indicated. However,
hypothermia may be an effective adjunctive treatment
for increased ICP refractory to other medical
management.
Corticosteroids
Steroids are commonly used for primary and
metastastic brain tumors, to decrease the vasogenic
cerebral edema. Focal neurologic signs and decreased
mental status secondary to surrounding edema
typically begin to improve within hours. 46 Increased
ICP, when present, decreases over the following 2 to 5
days, in some cases to normal. The most commonly
used regimen is intravenous dexamethasone, 4 mg
every 6 hours. For other neurosurgical disorders, such
as TBI or spontaneous intracerebral hemorrhage in
adults, corticosteroids are not useful. Use of
methylprednisolone for 48 hours in CRASH trial
resulted in a significant increase in the risk of death
from 22.3% to 25.7% (relative risk 1.15, 95% confidence
interval 1.07–1.24). 47 This trial confirmed previous
studies and guidelines that routine administration of
steroids is not indicated for patients with TBI.
Resection of mass lesions
Intracranial masses producing elevated ICP should be
removed when possible. Acute epidural and subdural
hematomas are hyperacute surgical emergencies. Brain
abscess must be drained, and pneumocephalus must be
evacuated if it is under sufficient tension to increase
ICP. Surgical management of spontaneous intracerebral
bleeding is controversial.48
Cerebrospinal fluid drainage
CSF drainage lowers ICP immediately by reducing
intracranial volume and more long-term by allowing
edema fluid to drain into the ventricular system.
Drainage of even a small volume of CSF can lower ICP
significantly, especially when intracranial compliance
is reduced by injury. If the brain is diffusely swollen, the
ventricles may collapse, this modality then has limited
utility. CSF drainage is generally done intermittently
whenever ICP spikes above a threshold—such as 20
mmHg, but can also be done continuously using
gravity, often to a level set at 5-10 cm above the center of
the head. In a recent two-center study, in pediatric TBI,
continuous CSF drainage was associated with higher
CSF volume drainage and lower ICP, as compared to
intermittent drainage.49
Decompressive craniectomy
This involves surgical removal of part of the calvaria to
create a window in the cranial vault, which allows for
herniation of swollen brain through the bone window
to relieve pressure. Decompressive craniectomy has
been used to treat uncontrolled intracranial
hypertension of various origins, including cerebral
infarction, trauma, subarachnoid hemorrhage, and
spontaneous hemorrhage.50 Patient selection, timing of
operation, type of surgery, and severity of clinical and
radiologic brain injury are factors that determine the
outcome of this procedure. A small randomized clinical
trial in 27 children with TBI found a reduced risk ratio
for death and vegetative status, or severe disability 6 to
12 months after injury. 51 Ruf et al 52 and Figaji et al53
collectively reported no mortality and favorable
outcome in 7 of the 11 pediatric cases where very early
application of either unilateral or bilateral
decompression was used. In a retrospective study of 23
children (mean admission GCS score of 4.6) who
underwent decompressive craniectomy if ICP remained
above 20mm Hg, even after medical management, 16 of
the 23 patients survived and 13 of the 16 had a
favorable outcome. 54 Reported complications of
decompressive craniectomy include hydrocephalus,
hemorrhagic swelling ipsilateral to the craniectomy site,
and subdural hygroma.
CPP targeted protocols
The conventional approach in management of raised
ICP aims at reducing ICP below 20 mmHg. Emerging
evidence however favours CPP targeted therapy
wherein the paradigm is shifting to target optimum
CPP. It is believed that a certain minimum CPP is
needed to maintain adequate supply of O2 and essential
nutrients to brain. What should this minimum be and
whether this minimum should be adjusted according to
a child’s age remains unclear. A review of available
studies in pediatric TBI suggests that a CPP between 4065 mmHg represents an optimum threshold; a CPP <40
mmHg is associated with high risk of death.55
In a prospective observational study at Chandigarh,
in children 3 months – 12 years old with raised
intracranial pressure caused by central nervous system
infection, we were able to achieve a CPP greater than 50
mm Hg in first 24 hours mainly by increasing the blood
pressure, and after 24 hours by using measures to
reduce ICP. All 4 patients with mean CPP less than 50
mm Hg died. In contrast, only 3 of 16 patients with
mean cerebral perfusion pressure more than 50 mm Hg
died.56
CONCLUSION
Effective treatment of intracranial hypertension
involves meticulous avoidance of factors that
precipitate or aggravate increased ICP. When ICP
becomes elevated, it is important to rule out surgically
treatable lesions. Medical management of increased ICP
should include sedation, and osmotherapy with either
527
mannitol or hypertonic saline and controlled short term
hyperventilation if needed. For intracranial
hypertension refractory to initial medical management,
barbiturate coma, hypothermia, or decompressive
craniectomy should be considered. Steroids have a very
limited role and are not indicated routinely in
intracranial hypertension resulting from TBI. Studies
with rather large sample size are needed to evaluate
various established doctrine and therapies—to improve
the current standard of care. Few recent outcome
studies suggest that optimum values of CPP in children
lie between 50-65 mm Hg, depending of their age.
Pediatric Intensivity Level of Therapy (PILOT) scale
may be a useful tool to monitor intensity of treatment
used for ICP control and optimize the therapies.57
14.
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Management of Intracranial Hypertension Symposium on Neurological Disorder–Advances in Management-II

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