| Introduction
Intracranial hypertension (ICH) is a condition which affects many patients
in intensive care units (ICU) and which has many different origins, both of the
central nervous system and of a systemic nature. Intracranial hypertension is
one of the most common causes of secondary cerebral lesions in children ().
The correlation between ICH and morbidity and mortality in pediatric patients
justifies the search for an improved understanding of the pathophysiology, leading,
consequentially, to more appropriate treatment ().
In order to correctly treat children with ICH, continuous monitoring of cerebral
function is necessary by means of clinical parameters and technological resources.
Clinical examinations do not always provide sufficient information to measure
the degree of ICH and some of the methods available for this evaluation require
the professional to exercise caution in their use ().
Intracranial pressure monitoring (ICP) is the only method which is accepted indiscriminately
as a safe form of increased intracranial pressure diagnosis, and also for the
treatment of ICH in certain clinical situations ().
Certain ICH treatment concepts are already very well defined while other
aspects remain controversial (). Pathophysiology
Primary cerebral lesions in the post-traumatic patient are the result of
direct impacts against the cerebral tissues. A primary cerebral lesion can also
occur when a patient is admitted to the ICU after a hypoxic-ischaemic event. This
damage can vary from minimal to the irreparable. Secondary cerebral lesions are
the result of the biochemical and cellular response to the initial insult. A chain
of events occurs within the brain which contributes to the appearance of diffuse
cerebral edema with lesions and cellular loss. This damage may include the loss
of cerebral blood-flow auto-regulation, rupture of the blood-brain barrier, intracellular
(cytotoxic) and extracellular (vasogenic) edema and ischaemic cerebral lesions.
Secondary cerebral lesions worsen with the passage of time reaching their peak
after around 3 to 5 days. The patient's prognosis depends upon the severity of
each phase of the injury ().
A "second insult" is different from a secondary cerebral lesion.
Second insults are events (e.g. hypotension, hypoxia) to which the patient may
be subjected after the primary lesion and which will determine the increase in
severity of the secondary cerebral lesion and be responsible for worsened prognosis
().
There are reports of the additional effects of hypotension and hypoxia almost
doubling the mortality rates in pediatric patients with Glasgow coma score of
3, after cranial-encephalic trauma (). Intracranial
pressure
The intracranial content consists of cerebral tissue
(80 %), cerebrospinal fluid (10 %) and blood (10 %) ().
Maintenance of ICP at normal values depends upon the preservation of intracranial
volume ().
Any event which provokes an increase in one of the intracranial components obliges
a reduction of the others for ICP not to increase. The compensation process frequently
occurs at the cost of a reduction in the volume of cerebrospinal fluid and blood,
since cerebral mass is less compressible. Around 30 % of the capacity to reduce
intracranial volume is provided by the cerebrospinal fluid which may be dislocated
to the spinal subarachnoid space or absorbed by arachnoid granulations. When compensation
mechanisms have been used to capacity, an increase in ICP occurs as a result ().
The increase in ICP, in turn, can provoke a reduction in tissue perfusion, leading
to aggravation of the cellular damage by ischaemia and resulting in brain death
().
One further ICP increase control mechanism in infants is cephalic perimeter growth,
which does not protect them from acute ICH development ().
Normal ICP upper limit values for children are still the subject of disagreements
within the literature, in contrast to those for adults which are well established.
Intracranial pressure varies with age and 8 to 10 mm Hg are considered normal
values for infants and ICP values below 15 mm Hg are considered normal for older
children and adults ().
Intracranial hypertension has been defined as ICP above 20 mm Hg persisting for
more than 20 minutes in adults (). Cerebral
blood flow
Alterations to cerebral blood flow (CBF) are significant
to the pathophysiology of ICH, fundamentally to brain damage due to head trauma
().
Cerebral blood flow is reduced soon after severe post-trauma brain damage and
provides a strategic focus for therapy ().
Cerebral blood flow maintains a relationship with cerebral perfusion pressure
and responds to variations in average arterial pressure (AAP), arterial carbon-dioxide
partial pressure (paCO2) and arterial oxygen partial pressure (paO2) ().
A fall in paO2 provokes progressive vasodilation with an increase of up to 300
% in CBF being possible when paO2 reaches 25 mm Hg. Carbon-dioxide provokes cerebral
vasodilation. For each mm Hg that paCO2 reduces there is a corresponding reduction
of 3 % of CBF. Responses to alterations in paCO2 are rapid and equilibrium in
reached in a matter of minutes. Cerebral blood flow is also controlled by local
metabolism, with the local CBF being higher, the greater the metabolism of a specific
area (). Cerebral
perfusion pressure
Cerebral perfusion pressure (CPP) is equal
to the difference between AAP and ICP. The recommended CPP value to maintain an
adequate cerebral blood flow level is 50 mm Hg. Cerebral perfusion pressure values
below 50 mm Hg will lead to a proportional decrease in CBF ().
It is believed that young children can withstand CPP values below 50 mm HG
without developing ischaemia. Within certain limits it is possible to maintain
CBF independently of AAP; a phenomenon known as autoregulation ().
Cerebral insults can compromise CBF autoregulation mechanisms (). Traumatic
cerebral lesion mechanics
The forces involved in CET of adults
and children include contact and inertial forces. As the head-trunk ratio is much
greater in children, the angular biomechanical forces which cause accelerations
and decelerations are amplified in pediatric victims. As a result there is a greater
incidence of diffuse brain damage within this age group (). Clinical
status
During the initial physical examination the focus is on
a brief evaluation of neurological status, including level of consciousness and
an examination of pupils. There is always a suspicion of cervical trauma with
severe CET.
Clinical findings with ICH patients vary from situations
in which the neurological examination is normal to those in which there are unmistakable
signs of CNS compromise. In infants with ICH, a progressive increase in cephalic
perimeter may be the only finding. Clinical status depends upon the speed with
which hypertension builds up and the capacity to accommodate the intracranial
volume within the calvarium ().
With children who are conscious, complaints such as headaches, vomiting,
double vision, episodes of blindness and intermittent erratic movements may occur.
Cushing triage, characterized by bradycardia, bradypnea and arterial hypertension
may not be present with children ().
The Glasgow coma scale provides a guide for the assessment of such patients (Table
1). Table 1 -
Glasgow coma scale
 |
| Score |
Response | Modified
response for infants | |
| Eyes open |
| |
| 4 | Spontaneous | Spontaneous |
| 3 | To Speech | To
Speech | | 2 | To
Pain | To Pain | | 1 | Absent | Absent |
| | | |
| Best motor response
| | | | 6 | Obeys
commands | Moves spontaneously | |
5 | Localizing pain | Localizing pain (Withdraws
to touch) | | 4 | Withdrawal
from pain | Withdraws in response to pain |
| 3 | Flexion to pain (decorticate
posturing) | Flexion to pain (decorticate posturing) |
| 2 | Extension to pain (ecerebrate
posturing) | Extension to pain (decerebrate posturing) |
| 1 | Absent | Absent |
| | | |
| Best verbal response | | |
| 5 | Orientated
| Coos and babbles | | 4 | Confused | Irritable
cries | | 3 | Inappropriate
words | Cries to pain | | 2 | Incomprehensible
sounds | Moans to pain | |
1 | Absent | Absent |
| Severe CET (Glasgow score: 3-8); moderate
CET (Glasgow score: 9-12); mild CET (Glasgow score: 13-15). |
|
If there is an increase in pressure
in one of the hemispheres of the brain, uncal (transtentorial) herniation may
occur; if pressure increases in both hemispheres the consequence will be central
diencephalic herniation ().
History is an important part of the initial assessment of the severity of
head traumas in children. The age of the patient, determination of the height
of a fall, the mechanics of impact and also the evolution since the incident of
symptoms such as level of consciousness (somnolence, lethargy, coma), the presence
of focal neurological symptoms, the occurrence of convulsive crises and headaches
are of help in the determination of the risk of CET. Loss of consciousness, in
isolation, is a poor indication of prognosis (). Imaging
exams
Any child with a suspicion of ICH and who presents an altered
level of consciousness, focal neurological deficit or physical signs of head trauma
should undergo computerized tomography (CT) of the cranium for etiologic and topographic
diagnosis of the resulting lesions ()
(Figure 1). Figure 1 -
CT of the cranium showing ICP monitoring through ventricular drainage catheter
coupled to an external transducer in its tip, in patient with severe CET, multiple
head injuries and frontal contusions. 
The presence of increased encephalic volume, indicated by compression or obliteration
of the mesencephalic cisterns, is strongly associated with subsequent development
of ICH. Other findings which are suggestive of cerebral edema are; staining of
white and gray cerebral matter, loss of the subarachnoid space and ventricular
compression.
Studies have demonstrated that children less than 2 years
old, and particularly less than twelve months, may present normal clinical neurological
examinations even when there are tomographic alterations which require surgery
().
Cerebral magnetic resonance imaging (MR) does not provide further information
to indicate surgery; however it does provide significant correlation between the
extent of lesions and cognitive prognosis, and, is frequently indicated to assess
the extent of cerebral and brain stem lesions (). Invasive
intracranial pressure monitoring
Monitoring allows for the correct
assessment of ICP and cerebral perfusion pressure, permitting customization of
therapy. Continuous monitoring of intracranial pressure is indicated for patients
at Glasgow < 8, since increases in intracranial pressure and reductions
in cerebral perfusion pressure contribute to secondary lesions. This is performed
by means of the insertion of an intraventricular catheter that permits monitoring
and drainage of cerebrospinal fluid (when this becomes necessary). Cerebral perfusion
pressure should be maintained within normal limits, guaranteeing sufficient oxygen
supply to the brain. The observed survival rate from severe CET is 94% when ICP
is maintained below 20 mmHg ().
Intracranial pressure monitoring has been most widely studied and its indication
most fully established for patients with severe cranial-encephalic trauma. There
is a significant reduction in mortality, from 50 % to 36 %, as result of the employment
of intensive care protocols including ICP monitoring ().
Notwithstanding, ICP monitoring can be useful in other situations, despite the
absence of standardized indications, such as, for example, during the post-operative
period of spontaneous hematomas and tumors and in patients with encephalitis and
ischaemic vascular accidents.
The indications for ICP monitoring of patients
with cranial-encephalic trauma, according to the recommendations of the Brain
Trauma Foundation (2000) are: patients with severe CET and abnormal Computerized
Tomography (CT) of the cranium Severe CET is defined as a Glasgow scale score
of 3 to 8 after cardiopulmonary resuscitation and CT abnormalities include hematoma,
contusions, edema or compromised basal cisterns ().
With adults ICP monitoring is also indicated in the presence of normal cranium
CT results when two of the following factors are present: age over 40, systolic
arterial pressure < 90 mmHg and abnormal motor posture (decerebrate or decorticate).
For children there are no specific recommendations in cases of severe CET when
cranium CT results are normal. Types of monitoring systems
Recommendations exist for the choice of intracranial pressure monitoring system.
The ideal monitoring apparatus is that which is reliable, precise, of low cost
and which causes minimum morbidity to the patient ().
Currently available monitors permit pressure to be recorded by means of a
ventricular drain coupled to an external transducer (e.g. any invasive pressure
monitor), a transducer at the tip of an electrode (e.g. CODMAN®)
or by means of fiber optic technology (e.g. CAMINO®) (Figure 2). Figure
2-
Intracranial pressure monitoring. 
1.
Ventricular drain (catheter) coupled to an external transducer - These are invasive
pressure transducers coupled to the external ventricular drain, and in contact
with the liquid column (cerebrospinal fluid). They can be recalibrated at any
time. An obstruction of the drain makes measurement imprecise or impossible. An
external transducer must be maintained in a fixed position in relation to the
patient's head to avoid measurement errors.
2. Transducer or fiber optic
catheter at the tip of an electrode - The transducer is positioned inside the
cranium. They are calibrated before insertion and cannot be recalibrated (without
an associated ventricular catheter). As a consequence there is a risk of measurement
errors occurring (drift), particularly if monitoring is continued for a
number of days. Both systems may present measurement errors, however it appears
that the electrode with a transducer at the tip is less likely to suffer from
this problem over a 5 day period. The precision of these gauges can be verified
by using the transducer electrode or fiber optic catheter together with a ventricular
drain. Ideal intracranial location for monitoring
The measurement
of intraventricular pressure is the reference standard for ICP monitoring.
The measurement of ICP with an intraparenchymal or subdural transducer electrode
with a catheter coupled to a liquid column is considered to be similar to intraventricular
pressure.
The values obtained for pressure using a fiber optic catheter
placed within the parenchyma or in a subdural position does not always correlate
with intraventricular pressure On the other hand, measurements taken with transducers
at the tips of electrodes placed within the subdural space present large differences
to those taken from the interior of the parenchyma.
Measurement by means
of an epidural catheter coupled to a liquid column or with a subarachnoid bolt
is less precise than intraventricular monitoring. Monitoring complications
Clinically significant intracranial infection associated with ICP monitoring
systems is rare. Colonization of systems increases significantly 5 days after
implantation and when this is detected the removal of the system is indicated.
Irrigation of systems coupled to liquid columns increases the risk of infection
(from 6 % to 19 %). Reductions in infection rates have been reported in observational
studies through the use of modified insertion techniques or prophylactic antibiotics
().
Hemorrhage occurs in around 1.4 % of cases, with only 0.5 % requiring surgery
to drain the hematoma ().
Replacement of ventricular catheters due to malfunction or obstruction occurs
in only 3 % of cases. In cases where ICP > 50 mmHg there is an increased risk
of obstruction or loss of signal. With fiber optic catheters in ventricular or
intraparenchymal positions, cases in which replacement due to malfunction is necessary
vary from 9 % to 40 % ().
Systems with catheters coupled to liquid columns and external transducers
are the least expensive.
In conclusion, the external ventricular drainage
catheter coupled to a pressure transducer is the most precise, reliable and low
cost method of monitoring ICP. It offers the treatment option of cerebrospinal
fluid drainage. The use of fiber optic catheters (e.g. CAMINO®)
or of electrodes with pressure transducers at the tip (e.g. CODMAN®)
positioned inside the ventricular drain offers similar benefits, but at an increased
cost.
Intracranial pressure monitoring with fiber optic catheters or
with electrodes with pressure transducers at the tip located within the parenchyma
(intraparenchymal) is similar to intraventricular monitoring, however there is
a possibility of measurement errors (drift). Epidural, subdural or subarachnoid
monitoring are all less precise. - Intracranial pressure monitoring technology
rankings.
- Ventricular catheter coupled to an external transducer or
to an electrode with a transducer at the tip or to a fiber optic catheter.
- Intraparenchymal transducers (electrode or fiber optical).
- Subdural:
catheter coupled to a liquid column and external transducer or an electrode with
a transducer at the tip.
- Subarachnoid: Bolt coupled to a liquid column
and an external transducer.
- Epidural Currently available studies
do not provide for standardized recommendations with respect of the use of prophylactic
antibiotics, surgical technique and time of removal of ICP monitoring. Nevertheless
it is the practice of the authors to use antibiotics throughout the monitoring
period. Removal of monitoring equipment is performed between 24 and 48 hours after
ICP has normalized. Electrophysiological monitoring
Neurophysiological monitoring is a significant additional method for monitoring
the neurological function of patients with CET.
Continuous or serial
monitoring of somatosensory evoked potential and of electroencephalogram are still
controversial, but have been used for early detection of sudden changes in cerebral
function (e.g. the evolution of a hematoma).
Electroencephalographic
studies show that a subtle slowing of the trace may be associated with a good
prognosis and that the absence of variations and reactivity correlate with poor
evolution ().
Some studies have shown that a bilateral absence of cortical peaks in somatosensory
evoked potential reading is a strong predictor of poor functional evolution in
children (). Treatment
Treatment objectives with children with ICH are aimed at the prevention of
a second insult which would exacerbate neural damage and accentuate secondary
cerebral lesions. The effort to achieve these objectives consists of interventions
aimed at reducing intracranial pressure and at maximizing cerebral perfusion pressure
and the oxygen supply to the brain. Cerebral perfusion pressure and oxygen supply
depend upon adequate ventilation, cardiac function and systemic perfusion.
Immediate care resulting in a correct diagnosis and stabilization of the
patient is essential. The treatment routine should include measures to achieve
global stabilization of the patient and also specific measures for the control
of intracranial pressure. General Measures
Head
positioning
The head should be maintained in a neutral position,
elevated by thirty degrees in order to optimize venous return. When it becomes
necessary to move the patient, the head should be maintained aligned with the
spine. Rotational movements to the right may increase ICP more than those to the
left. Prone positioning should be avoided as it increases intra-abdominal and
intrathoracic pressures with increased ICP as a consequence. Body temperature
The objective in terms of temperature is to maintain the patient at normal
body temperature, aggressively avoiding hyperthermia, since this can increase
cerebral metabolism ().
Prolonged hypothermia may reduce leukocytes increasing the risk of infection and
does not improve morbidity or mortality from many neural insults. Furthermore
it may cause disturbances to ventricular conduction and the coagulation cascade
().
There are other issues related to this subject which will be further discussed
below. Hemodynamic monitoring
The installation of an arterial
catheter is recommended to continuously measure AAP and of a central catheter
to monitor central venous pressure (CVP). Hypotension should be aggressively treated
with vasoactive drugs. Mild systemic arterial hypertension (SAH) should be tolerated,
since this can be a compensating factor maintaining CPP. In situations where cerebral
autoregulation has been lost, any change in pressure can be transmitted directly
to the cerebral veins, with an increased risk of edema or ischaemia. In such cases
sodium nitroprusside or beta-blockers can be employed. Respiratory management
Intubation is recommended when the patient shows clinical signs of ICH, Glasgow
score less than or equal to 8, respiratory suffering, hypercapnia or refractory
hypoxemia ().
The rapid-sequence intubation technique (preparation, pre-oxygenation, sedation,
cricoid pressure, neuromuscular blockade and oral endotracheal intubation) has
proved to be safer than nasotracheal intubation or oral endotracheal intubation
without neuromuscular blocking ().
Patient saturation levels should be maintained above 92 %. PaCO2
should be maintained at around 35mm Hg (avoiding PaCO2 levels
> 38mm Hg). Prophylactic hyperventilation should not be employed due
to the risk of arterial vasoconstriction and the resultant cerebral ischaemia.
A low respiratory frequency is recommended for assisted ventilation, since
the increased expiratory period facilitates venous return. The use of
positive end-expiratory pressure (PEEP) is not contra-indicated, however
its potential for hemodynamic interference should not be ignored ().
Hemoglobin and hematocrit should be maintained above 10 mg/dL and 30%
respectively ().
Sedation/Analgesia
The patient should be maintained without pain or agitation, avoiding
stimulation whenever possible. Before aspiration or intubation, the use of intravenous
lidocaine 1 mg/Kg is recommended with the objective of avoiding PIC increase ().
Commonly used drugs are midazolam, morphine or fentanyl. Propofol infusion should
be limited to 12 hours because of the risk of hypertension and metabolic acidosis.
The use of ketamine should be avoided as it increases ICP. Sometimes it is necessary
to induce muscular paralysis with agents derived from curare. Once paralyzed,
the patient requires adequate attention to all corporal pressure points. Patients
who have been treated with curare should be monitored continuously with electroencephalography
because of the risk of a convulsive crises. Prophylaxis for venous thrombosis
should be considered for older children and those requiring high doses of barbiturates
or prolonged paralysis (). Control
of convulsive crises
Convulsive crises may lead to hypoxemia
and hypercapnia with increases in ICP and CBF. Studies with adults have shown
phenytoin to be an effective prophylactic during the first week post-trauma, reducing
the number of convulsive crises. For children, the use of anticonvulsants is indicated
in cases of: repeated convulsive crises, a history of epilepsy, evidence of severe
cortical contusions or evidence of laceration at surgery (). Nutritional
support
Patient nutrition should be started early, preferably
enteral. Administration should be around 30 to 60 % of the basic metabolic usage.
Patients treated with high doses of barbiturates may require parenteral nutrition
because of gastroparesis or protracted ileum ().
Rigorous glycemia control should be promoted, avoiding the infusion of glucose
during the first 48 hours, unless there is hypoglycemia (<75mg/dl), in consideration
of the potential risk of lactic acidosis (). Fluid
management
Restriction of water intake is indicated in patients
with dilutional hyponatremia ().
Furthermore electrolytes and osmolarity should be regularly monitored, taking
into account the current tendency to maintain patient serum sodium content at
higher levels ().
maintain rigorous urinary output control with special attention to patients who
have used/are using diuretics to avoid dehydration (). Specific
treatment for increased intracranial pressure
Specific treatment
for increased intracranial pressure aims at keeping cerebral perfusion pressure
at 40-45 mm Hg with infants and young children and at 50-55 mm Hg with older children
and adolescents. Treatment for ICH should be started if ICP: > 15mmHg
with infants, > 18 mmHg with children younger than 8 and >20 mmHg
for older children and adolescents (). Cerebrospinal
fluid Drainage
This strategy is employed to reduce ICP when the
patient has an intraventricular catheter. The removal of quantities of between
3 and 5 ml of cerebrospinal fluid at a time with reevaluation of PIC each time
is recommended (). Diuretic
and osmotic Agents
The use of osmotics and diuretic agents presupposes
that the patient is maintained in euvolemia with hyperosmolarity.
Mannitol:
Mannitol will initially cause plasma expansion reducing hematocrit and blood viscosity,
increasing blood flow and the provision of oxygen to the brain, reducing ICP within
a few minutes. During a second phase, serum osmolarity increases, dehydrating
the cerebral parenchyma ().
When administered in bolus, mannitol will reduce ICP in between 1 and 5 minutes,
peaking after between 20 and 60 minutes. However, when an urgent reduction is
necessary, the initial dose should be 1mg/Kg should be administered in approximately
20 minutes ().
Mannitol is dramatically effective, reversing signs of transtentorial herniation
().
Continuing the treatment, 0.25 to 0.5 mg/Kg should be administered every 2 to
4 hours, monitoring plasma osmolarity because of the risk of renal insufficiency.
Plasma osmolarity should be maintained at around 320 mOsm/L ().
Mannitol penetrates the blood-brain barrier and, if used for prolonged periods,
can cause an increase in ICP. Furthermore, doses should be reduced gradually as
mannitol can cause ICH rebound ().
Furosemide: Can be used at doses of 1 mg/Kg up to every six hours
in order to reduce cerebrospinal fluid production, primarily when ICP remains
elevated in spite of Mannitol use ().
It should not be used if serum osmolarity is above 320mOsml/L ().
Some authors consider its use unnecessary (). Barbiturates
Used to control refractory ICH in hemodynamically stable patients. They reduce
ICP by reducing cerebral metabolism with reduced CBF as a consequence. The factor
limiting barbiturate use is related to the decrease in sympathetic tone, leading
to peripheral vasodilation which occurs in up to 50 % of patients ().
The short action barbiturate, for intravenous use, which is available in
our locale is thiopental. We begin with an attack dose of 5mg/Kg over 10 minutes.
Continuous infusion is then maintained at a level of between 1 and 5mg/Kg/hour,
with boost doses of 2.5mg/Kg, if and when necessary. Therapeutic serum levels
should be maintained between 6 and 8.5mg/dl ().
Treatment lasts for a minimum of 48 hours after ICP is controlled, and is reduced
gradually. If ICP remains elevated despite adequate serum levels of the medication,
or if hypotension ensues, the infusion should be suspended. Hyperventilation
Hyperventilation should only be employed in situations in which transtentorial
herniation is imminent (with transient dilation of pupils, abnormal posture, inexplicable
hypertension or bradycardia) or in cases of refractory ICH, because of the risk
of cerebral ischaemia. Reducing PaCO2 to below 30mmHg may lead to loss
of cerebral autoregulation. When hyperventilation is indicated, the objective
should be to maintain PaCO2 between 30 and 35mmHg initially and between
25 and 30mmHg during a second phase. It is important to aggressively avoid PaCO2
< 25mmHg and, if control over ICP is achieved, the patient should be
slowly returned to normal breathing, because of the risk of rebound ICH ().
Corticosteroids
No studies exist which show that
any advantage is gained through their use. They are not recommended in clinical
practice. Other ICH treatment strategies
Sodium
Chloride at 3 %
Recent studies have returned to look at the use of
a hypertonic sodium chloride solution (NaCl 3 %) which increases osmolarity, reducing
ICP and maintaining intravascular volume. It acts by creating an osmotic gradient
at the intact blood-brain barrier, reducing cerebral volume. Research on animals
and n children have shown that both Mannitol and NaCl 3 % are effective in reducing
ICP, but that the effect achieved with a hypertonic saline solution infusion is
more accentuated and lasts longer. The use of NaCl 3 % is recommended when ICP
continues elevated (> 25 mmHg) despite maximum therapy including controlled
hyperventilation and barbiturate coma ().
The objective is to raise sodium levels to 160 mEq/L and maintain osmolarity
at around 330mosm/L. The administration of NaCl 3% should be performed by continuous
infusion, with serum sodium control every six hours, respecting a maximum sodium
increase of around 15 mEq/L/day. Peterson et al. suggest a continuous infusion
of NaCl 3% varying from 0.1 to 1 ml/Kg/h, depending upon the sodium concentration
and fluid ration desired. In order that rebound cerebral edema does not occur,
a rapid decrease in osmolarity should be avoided. During withdrawal, a maximum
decrease in serum sodium concentration of 10 mEq/L/day is recommended. In this
way, there is little risk of the patient developing pontine myelinolisis, cerebral
hemorrhage or renal insufficiency (). Decompressive
craniectomy
While there is work extant which proposes decompressive
craniectomy in cases of refractory ICH, there is no standardized recommendation
for its use. Studies reveal better results when it is employed at an early stage
(< 48 hours), in selected cases (). Mild
hypothermia
Mild hypothermia (32-34 oC) has been shown
to be neuroprotective in experiments on animals. It reduces excitatory amino acid
levels in the peri-trauma region.
Research performed on adult patients
reveal conflicting results ().
While some published work does not show this therapy to be of advantage, other,
more recent, studies suggest benefits from its use. Work is underway with the
objective of demonstrating the beneficial potential of this therapeutic method
(). Dexanabinol
This is a non-psychotropic, synthetic cannabinoid which is non-competitive
NMDA receptor antagonist (N-methyl-d-aspartate), which also acts as a toxic radical
remover and inhibits the production of tumor necrosis factor. Reductions in ICH
and systemic hypotension are observed which, when added to its anti- excitatory,
antioxidant and anti-inflammatory properties make dexanabinol a promising drug
for the treatment of ICH. It is indicated during the first six hours of severe
CET. It is currently at the clinical trial phase ().
Figure 3 presents the algorithm of management of intracranial hypertension. Figure
3 -
Algorithm of management of intracranial hypertension. 
Morbidity
and mortality
During the last twenty years there has been a significant
reduction in morbidity and mortality associated with head trauma in children.
However, they remain at higher levels than with adults, peaking among infants
(). Conclusions
The objectives of intracranial hypertension management of children include:
criteria based monitoring of intracranial pressure, permitting attempts to normalize
intracranial pressure, optimize cerebral blood flow and cerebral perfusion pressure,
prevent imbalances which exacerbate secondary lesions and avoid complications
associated with treatments employed. Despite significant advances in understanding
of the mechanisms which cause secondary lesions, long-term prognosis for infants
and children who have suffered CET remains poor. | 
