Hoang Anh Thao Vy

Group 5
 Contents
 Introduction
 Physiology
 Pathophysiology
 Clinical manifestations
 Dianogsis
 Management
Introduction
 Elevated ICP is a potentially devastating complication of neurologic
injury
 Increased ICP is most often a complication of traumatic brain injury; it
may also occur in children who have hydrocephalus, brain tumors,
intracranial infections, hepatic encephalopathy, or impaired central
nervous system venous outflow
 Early recognition of elevated ICP can prevent neurologic sequelae and
death.
 Physiology

 Measured ICP >20 mmHg (27 cmH O) for longer than five minutes
with signs or symptoms is generally regarded as the threshold for
treatment
 Cerebral perfusion pressure (CPP) is a clinical surrogate for the
adequacy of cerebral perfusion. CPP is defined as mean arterial
pressure (MAP) minus mean ICP.

CPP = MAP – ICP

 Physiology

 Cerebral blood flow — When managing elevated ICP, the major goal is
to maintain CBF.
 The following factors significantly impact CBF:
 Partial pressure of arterial oxygen (PaO ) – PaO has its most significant
effects at levels below 50 mmHg, when it causes vasodilatation in an
attempt to maintain the oxygen supply to the brain
 Partial pressure of arterial carbon dioxide (PaCO ) – Hypercapnia causes
cerebral vasodilatation and increased CBF, whereas hypocapnia reduces
CBF
 Autoregulation
 CBF ≠ CPP?
 Pathophysiology

 Cerebral edema
Pathophysiology: Cerebral edema
 Cytotoxic or cellular edema – Cytotoxic or cellular edema is caused by
intracellular swelling secondary to direct cell injury. This form of edema
is common in patients who have severe cerebral injuries such as
traumatic brain injury, traumatic axonal injury, or hypoxic-ischemic
injury.
With these injuries, brain cells are often irreversibly injured, and
therapy has little effect on eventual outcome [18]. By contrast, reversible
edema can occur with water intoxication.
Pathophysiology : Cerebral edema
 Vasogenic edema – Vasogenic edema results when increased
permeability of capillary endothelial cells permits fluid to escape into
the extracellular space. Neurons are not primarily injured. Vasogenic
edema is seen with tumors, intracranial hematomas, infarcts, abscesses,
and central nervous system infections.
Therapy to decrease the edema may prevent secondary ischemic injury to
surrounding brain tissue because neurons are not primarily injured .
Steroid therapy may be beneficial for vasogenic edema that occurs in the
setting of mass lesions.
Pathophysiology : Cerebral edema
 Interstitial edema – Interstitial edema is characterized by increased
fluid in the periventricular white matter. Increased cerebrospinal fluid
(CSF) hydrostatic pressure, as occurs with hydrocephalus, is the most
common cause.
Interstitial edema responds to therapies to reduce CSF pressure.
Pathophysiology: Trauma
 After head trauma, a complex series of pathophysiologic changes may occur
and contribute to increased ICP :
1. Loss of autoregulation resulting in excessive cerebral blood flow (CBF)
2. Increased CSF production in response to cerebral hyperemia
3. Hypercapnia or hypoxia, which may cause vasodilation and increased CBF (see 'Cerebral
blood flow' above)
4. Cerebral vessel vasospasm, which may cause regional ischemia and swelling in a vascular
distribution [19]
5. Herniation, brain swelling, or subarachnoid hemorrhage, which may obstruct the flow of
CSF
6. Epidural or subdural hematomas, cerebral contusions, or cerebral edema, which increases
the volume of brain parenchyma with potential for decrease in blood and CSF volume
Pathophysiology: Brain herniation
syndromes
Herniation of brain tissue can cause injury by compression or traction on
neural and vascular structures. Herniation results when there is a
pressure differential between the intracranial compartments and can
occur in four areas of the cranial cavity

Transtentorial herniation is the most common type (figure 4). It results

from downward displacement of supratentorial brain tissue into the
Subfalcine herniation
Foramen magnum herniation
Pathophysiology: Brain herniation
syndromes
 CLINICAL MANIFESTATIONS
 Acutely elevated ICP — Acute elevation of ICP is an emergent
condition that requires prompt recognition and management.
Important findings include:
1. Headache
2. Vomiting
3. Altered mental status
4. Papilledema acute?
5. Hypertension with bradycardia or tachycardia
6. Transtentorial herniation – In addition to vital sign changes, the earliest
clinical signs of transtentorial herniation include ?
Papilledema
 CLINICAL MANIFESTATIONS
 Other findings – Less common findings of acute intracranial
hypertension consist of:
 A natural preference for the "knee-chest" position
 Seizures
 Spontaneous upper eyelid ecchymosis adjacent to the lid margin when an
abrupt increase in cerebral venous pressure is transmitted via the
cavernous sinus to the orbital venous system
 Transient (5 to 15 minutes) epidermal flushing involving the upper chest,
face, or arms during the period of deterioration
 DIAGNOSIS
 The diagnosis of elevated ICP is typically established by neuroimaging
or other noninvasive means in pediatric patients with suggestive
clinical findings . Papilledema, when present, is specific for intracranial
hypertension but has low sensitivity.
 Direct measurement of increased ICP >20 mmHg (27 cmH O) using an
external ventricular drain or intraparenchymal ICP monitor is the
definitive way to confirm the presence of intracranial hypertension.
 DIAGNOSIS
 In awake patients with findings that indicate subacute or chronic
elevation of ICP (eg, headache, peripheral vision loss, and papilledema)
but a nonfocal neurologic examination and normal neuroimaging,
elevated opening pressure on lumbar puncture (>27 cmH O) can
establish the diagnosis of idiopathic intracranial hypertension
(pseudotumor cerebri).

 Acute ≠ subacute and chronic?

Noninvasive detection of elevated ICP
 In children, neuroimaging is the primary means of noninvasively
detecting elevated ICP :
Computed tomography . The goal of the emergency CT is to assess for a
surgical cause of raised ICP that necessitates immediate neurosurgery
(eg, epidural hematoma or acute, obstructive hydrocephal.Findings
consistent with elevated ICP on head CT include :Midline shift,
Effacement of the basilar cisterns , Effacement of the sulci ,
Thumbprinting referring to increased gyral markings on the inner table
of the skull in patients with chronically elevated ICP
Evidence of contusions with surrounding edema (top arrow),
effacement of cisterns (middle arrow), and effacement of sulci
(lowest arrow).
This large temporal epidural hematoma is associated with midline shift and compression of the ventricular system. The dark
swirls within the hematoma represent rapid arterial bleeding.
An infant presented in coma with pupillary dilatation. There was no significant trauma history. Computed tomography (image
A) reveals a large right, concave subdural hematoma and significant brain shift. After urgent craniotomy, the patient had
malignant brain swelling due to the underlying traumatic and hypoxic-ischemic injury on follow-up computed tomography
(image B) and did not survive. Bilateral retinal hemorrhages and skeletal fractures were also detected.
Noninvasive detection of elevated ICP
 Magnetic resonance imaging — MRI of the brain is more accurate for
detecting elevation of ICP than CT but is less accurate than invasive
measurement of ICP.
 MRI does have greater sensitivity for detecting conditions that can cause cerebral edema than
computed tomography of the head. In clinical practice, these different forms of edema can be
differentiated by comparing images from T2-weighting (T2-W), diffusion-weighting (DW), and
apparent diffusion coefficient (ADC) sequences
T1 (Panel A) and T2 (Panel B)-weighted MRI images show enlargement of the subarachnoid spaces, establishing
the diagnosis of benign extra-axial fluid of infancy. Follow-up T1 (Panel C) and T2 (Panel D)-weighted images
reveal chronic subdural hematoma within the enlarged spaces. The child was completely asymptomatic from
this and required no treatment. The areas of hematoma resolved spontaneously.
Noninvasive detection of elevated ICP
 Detection of papilledema — Papilledema on funduscopy has low
sensitivity for intracranial hypertension as demonstrated in small
studies of children with shunt failure or idiopathic intracranial
hypertension (pseudotumor cerebri) . Furthermore, papilledema takes
time to develop and is typically not present in patients with increased
ICP caused by acute head injury or hemorrhage.
Invasive detection of elevated ICP
 Intracranial monitoring with an external ventricular drain or
intraparenchymal ICP monitor should be strongly considered in pediatric
patients with a GCS ≤8 (table 10) after head trauma or who are diagnosed
with a condition that warrants aggressive medical or surgical treatment to
manage ICP based upon clinical findings and results of neuroimaging
Laboratory studies
 Serum electrolytes, calcium, magnesium
 Blood urea nitrogen, creatinine
 Arterial blood gas or pulse oximetry with measurement of venous blood gas
 Complete blood count
 Additional studies in febrile patients with possible central nervous system
infection
 Additional studies in pediatric patients in whom intoxication is suspected
based upon history or physical findings
 In young infants in whom metabolic disease is suspected, evaluation
according to presenting features
 Management
 INITIAL STABILIZATION :
1. Ensuring normal oxygenation and ventilation prevents vasodilation caused
by hypoxemia and hypercapnia which, in turn, can increase ICP.
2. Maintenance of blood pressure is necessary to prevent cerebral ischemia by
promoting adequate cerebral perfusion pressure (CPP) which is calculated
as the difference between mean arterial pressure (MAP) and ICP.
During stabilization, elevation of the head from 15 to 30 degrees while maintaining a midline position,
avoidance of fever, and providing adequate pain control are supplementary measures to treat elevated ICP
Whenever, possible consultation with a neurosurgeon with pediatric expertise should occur before
administration of hyperosmolar therapy or therapeutic hyperventilation. For what?
Management: Airway
 Indications for endotracheal intubation in children with elevated ICP include:
Refractory hypoxia, Hypoventilation, Glasgow coma score (GCS) of ≤8 or
GCS <12 and rapidly declining, Loss of airway protective reflexes, Acute
herniation requiring controlled hyperventilation
 Cervical spine stabilization must be maintained in patients with potential
cervical spine injury.
 Rapid sequence intubation :
 Hemodynamically unstable patients – For hemodynamically unstable patients we use
etomidate and rocuronium (initial dose 1.2 mg/kg to facilitate rapid onset of paralysis).
 Hemodynamically stable or hypertensive patients – Propofol (1 to 3 mg/kg/dose IV),
fentanyl (1 mcg/kg/dose IV), and rocuronium, (initial dose 1.2 mg/kg to facilitate rapid
onset of paralysis); etomidate may be used instead of propofol.
 Midazolam , diazepam , fenanyl for rapid sequence intubation?
Management: Breathing
 Hyperventilation (PaCO <35 mmHg) decreases cerebral blood flow and may
cause cerebral ischemia.
 Consequently, PaCO should be maintained between 35 and 40 mmHg unless
there are signs of acute or impending herniation that require emergency
measures prior to a more definitive intervention.
 Temporary therapeutic hyperventilation (PaCO 30 to 35 mmHg for up to two
hours) may be initiated under direction by a neurosurgeon in patients with
signs of impending herniation in whom surgical intervention is planned.?
Management: Circulation
 Cerebral perfusion must be maintained to prevent secondary ischemic
injuries.
 Hypovolemia should be avoided because it decreases cerebral perfusion.
When present, hypovolemia should be treated with isotonic fluids (eg,
normal saline) with a goal of attaining a state of normal, rather than excess,
volume. Excess intravascular volume may exacerbate the development of
cerebral edema.
 The administration of hypotonic fluids, such as D5W, should be avoided because they deliver too
much free water, which may exacerbate cerebral edema and cellular destruction.
Management: Circulation
 In patients with distributive shock caused by central nervous system or spinal
cord injury, appropriate mean arterial pressure for age ? should be
maintained using intravenous fluids and pharmacologic vasopressors with
alpha adrenergic effects (eg, norepinephrine or phenylephrine) as needed.

 Bradycardia caused by cervical spinal cord or high thoracic spinal cord

disruption may require external pacing or administration of atropine.
 CPP for ages?
Management: Temperature control
 Children with increased intracranial pressure (ICP) should be prevented from
becoming febrile through the use of antipyretics, and if necessary, cooling
blankets.

 Most centers do not use hypothermia early in treatment. However, some

centers still reserve the use of hypothermia therapy for control of refractory
intracranial hypertension.

 Gastric lavage?
Medical treatment of sustained intracranial
hypertension or impending herniation
 We suggest an approach to patients with sustained (>5 minutes) and
symptomatic intracranial hypertension (ICP >20 mmHg [27 cmH ]) or
impending herniation that is based upon the principles of Emergency
Neurologic Life Support
 Whenever possible, a neurosurgeon with pediatric expertise should be
involved with the decision to administer osmolar therapy with hypertonic
saline or mannitol or the initiation of hyperventilation and to determine the
need for surgical intervention.
Medical treatment of sustained intracranial
hypertension or impending herniation
 The goals of therapy are to minimize ICP elevation and maintain adequate
cerebral perfusion pressure (CPP). Limited observational evidence suggests
that target CPP in children should be age-specific as follows
1. 0 to 5 years of age – 40 to 50 mmHg
2. 6 to 17 years of age – 50 to 60 mmHg
Medical treatment of sustained intracranial
hypertension or impending herniation
 Osmolar therapy with either mannitol or hypertonic saline is initially
effective. When combined treatment is given with both agents ?,
hypertonic saline administration helps to offset the hyponatremia and
hypovolemia that frequently follow the rapid diuresis associated with
mannitol treatment.

• On the other hand, mannitol helps to offset potential worsening of vasogenic

cerebral edema that may occur with prolonged use of hypertonic saline as
described below.
Medical treatment of sustained intracranial
hypertension or impending herniation
 Mannitol — There is limited evidence to compare mannitol with hypertonic
saline for intracranial hypertension. Because mannitol may lower ICP more
rapidly, it is preferred by some experts for the acute treatment of brain
herniation and for children with severe head trauma although other experts
prefer hypertonic saline in this situation.
 The recommended initial dose for mannitol is 0.5 to 1 g/kg (2.5 to 5 mL/kg of
the 20 percent solution which contains 200 mg/mL mannitol concentration)
given as an IV infusion through an in-line filter over 20 to 30 minutes .
Mannitol has a rapid onset of action and maintains its effect for a period of
1.5 to 6 hours.
Medical treatment of sustained intracranial
hypertension or impending herniation
 Mannitol administration also has the potential side effects of
hyperosmolarity, hypovolemia, electrolyte imbalance, and acute renal
failure .
Hypertonic saline
 Initial intravenous bolus of 5 mL/kg of 3 percent saline which corresponds to
an expected rise in serum sodium of 5 mEq/L; this dose may be repeated,
hourly, as needed until the serum sodium reaches 160 mEq/L. Hypertonic
saline typically fails to further reduce ICP when the serum sodium exceeds
160 mEq/L.
 Continuous infusion of 3 percent saline at rates of 0.5 to 1.5 mL/kg per hour
adjusted to maintain ICP <20 mmHg may also be used after the ICP is
controlled by hypertonic saline boluses.
Hypertonic saline
 Additional proposed benefits include
• Restoration of normal cellular resting membrane potential and cell volume,
• Stimulation of atrial natriuretic peptide release,
• Inhibition of inflammation, and
• Enhancement of cardiac output.
Hypertonic saline
 Rebound increased ICP has occurred after 3 percent hypertonic saline
administration
 Other potential complications associated with hypertonic saline
administration include hypernatremia and hyperosmolality with acute
kidney injury, fluid overload with pulmonary edema and/or heart failure,
metabolic acidosis, and osmotic demyelination syndrome (formerly called
central pontine myelinolysis)
Refractory intracranial hypertension
criteria?
 Options include:
 CSF drainage
 Barbiturate coma : It decreases the cerebral metabolic rate, which causes a
reduction in cerebral blood flow and, thus, in ICP .
 Surgical decompression :decompressive craniectomy (DC) may be helpful
for patients with rapid deterioration from a focal space-occupying brain
lesion (eg, brain tumor, cerebral abscess, and lobar parenchymal
hemorrhages) and is performed at the neurosurgeon's discretion.
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