Elevated Intracranial Pressure

Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis - UpToDate 13/03/19 19.
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Elevated intracranial pressure (ICP) in children: Clinical manifestations and

diagnosis
Author: Robert C Tasker, MBBS, MD
Section Editors: Susan B Torrey, MD, Marc C Patterson, MD, FRACP, Adrienne G Randolph, MD, MSc
Deputy Editor: James F Wiley, II, MD, MPH
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2019. | This topic last updated: Apr 10, 2018.
INTRODUCTION
The clinical manifestations and diagnosis of elevated ICP in children will be reviewed here.
The management of elevated ICP in children, the evaluation of stupor and coma in children, and initial management of children
with severe traumatic brain injury are discussed separately. (See "Elevated intracranial pressure (ICP) in children: Management"
and "Evaluation of stupor and coma in children" and "Severe traumatic brain injury in children: Initial evaluation and management".)
BACKGROUND
Elevated ICP is a potentially devastating complication of neurologic injury. In children, 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 (table 1). Successful management of children with elevated
ICP requires prompt recognition and therapy directed at both reducing ICP and reversing its underlying cause. Early recognition of
elevated ICP can prevent neurologic sequelae and death.
PHYSIOLOGY
Intracranial pressure — The range of normal cerebrospinal fluid (CSF) pressure in children (10th to 90th percentile) at the time of
lumbar puncture is 12 to 28 cmH2O (9 to 21 mmHg) [1-3]. Measured ICP >20 mmHg (27 cmH2O) for longer than five minutes with
signs or symptoms is generally regarded as the threshold for treatment [4]. Occasional transient elevations may occur with
physiologic events, including sneezing, coughing, or Valsalva maneuvers. However, sustained elevations above this pressure are
abnormal [5].
The intracranial compartment is protected by the skull, a rigid structure with a fixed internal volume; the intracranial contents
include (by volume) [6]:
● Brain parenchyma – 80 percent

● Cerebrospinal fluid (CSF) – 10 percent
● Blood – 10 percent
ICP is the pressure of CSF inside the cerebral ventricles, which is determined by cerebral blood flow (CBF) and CSF circulation.
The Davson equation describes this relationship [7]:
ICP = Pss + (Iformation x RCSF)
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Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis - UpToDate 13/03/19 19.21
Where Pss is the sagittal sinus pressure, Iformation is the CSF formation rate, and RCSF is the resistance to CSF outflow. The range
of normal values for these variables are:
● Sagittal sinus pressure (Pss) – 5 to 8 mmHg

● CSF formation rate (Iformation) – 0.3 to 0.4 mL/min
● Resistance to CSF outflow (RCSF) – 6 to 10 mmHg/mL/min
Measured ICP is often greater than the calculated value because of a vascular component, which is probably a result of pulsation
in the arterial bed and the interaction between pulsatile arterial inflow and venous outflow curves, cardiac function, and cerebral
vasomotor tone [8]. Furthermore, all of these interrelationships may be altered in critically ill comatose patients with any of the
conditions that increase intracranial pressure (table 1).
The anatomy and development of the cranial vault, the brain, and its vascular and CSF compartments also have an effect on ICP.
The interrelationship between volume and compliance of each component of the intracranial compartment was recognized over
150 years ago and is known as the Monro-Kellie doctrine [9,10]. Because the overall volume of the cranial vault cannot change in
the patient with closed cranial sutures, an increase in the volume of one component or the presence of pathologic components
necessitates the displacement of other structures, an increase in ICP, or both [11]. Taken together with the Davson equation, it is
clear that ICP is affected by various pathologies including:
● Parenchymal brain swelling

● Interstitial and vasogenic edema
● Alterations in cerebral blood volume (CBV)
● Obstruction of CSF outflow
● Focal cerebral perfusion deficits
● Variable levels of CBF
● Cerebrovascular carbon dioxide (CO2) reactivity
● Cerebral vasculitis
The net result of this pathophysiology is elevated ICP along with significant risk of brain tissue herniation, ischemic syndromes, and
death.
This process is demonstrated in the figure (figure 1). Normally, the intracranial components are in equilibrium. In a “closed system”
(ie, closed sutures), initial compensation to increase in volume of a space-occupying lesion is by displacement of blood and CSF
along the spinal axis, and ICP remains normal. When the limits of this compensation are reached; any additional increase in the
volume of the mass lesion is accompanied by a corresponding increase in ICP (decompensated phase). The slope of the curve in
the decompensated phase is steep, such that small changes in volume cause significant changes in ICP (figure 2) [11]. In infants
with open cranial sutures and a non-ossified fontanel, the system should be considered as “open” and initial compensation occurs
with bulging at the anterior fontanel. In slowly progressive change in volume, head growth will be affected by splaying of the cranial
sutures, as seen in hydrocephalus.
Cerebral perfusion pressure — 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
Normal CPP in adults ranges from 50 to 70 mmHg; normal CPP in children younger than five years of age is probably lower than
that in older children or adults, because children have lower systolic blood pressures, but normal limits have not been well
established. However, based upon a normal ICP <20 mmHg and MAP >60 to 80 mmHg, depending upon age (where MAP = 1.5 x
Age + 55 mmHg [12]), normal CPP in children can be calculated to be at least 40 to 60 mmHg [13]. When CPP falls below a critical
level, either from hypotension or from a markedly elevated ICP, the brain receives inadequate CBF, and ischemic injury can occur
[5,11].
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Cerebral blood flow — When managing elevated ICP, the major goal is to maintain CBF. CBF is a function of the pressure drop
across the cerebral circulation divided by the cerebrovascular resistance (CVR), as predicted by Ohm's law:
CBF = (CAP - JVP) ÷ CVR
Where CAP is carotid arterial pressure, JVP is jugular venous pressure, and CVR is cerebrovascular resistance.
The following factors significantly impact CBF:
● Partial pressure of arterial oxygen (PaO2) – PaO2 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 [11].
● Partial pressure of arterial carbon dioxide (PaCO2) – Hypercapnia causes cerebral vasodilatation and increased CBF,
whereas hypocapnia reduces CBF [11]. Because the response to changes in PaCO2 is rapid, hyperventilation is an
emergency intervention as a temporizing measure before neurosurgery during the acute management of increased ICP
complicated by impending transtentorial and tonsillar herniation of brain tissue. (See "Elevated intracranial pressure (ICP) in
children: Management", section on 'Therapeutic hyperventilation'.)
● Autoregulation – In the intact and normal cerebral circulation, CBF is maintained at a relatively constant rate by intrinsic
cerebral mechanisms referred to as autoregulation. In addition to this global phenomenon, a region of brain tissue can also
bring about an acute regional change in CBF. This coupling of local blood flow to local changes in metabolic activity is
determined by a number of "neuro-energetic" signals [14]. A clinical illustration of this phenomenon is by the blood oxygen
level-dependent ("BOLD") time series used in functional magnetic resonance imaging (fMRI) that can show "activated" regions
with mental tasks. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Therapeutic
hyperventilation'.)
At a global level, cerebral autoregulation adjusts CBF through changes in CVR. In adults, changes in CVR can maintain
constant CBF at mean arterial pressures of 60 to 150 mmHg [15]. However, this "plateau" is under many influences including
level of sympathetic activity and baseline PaCO2. In infants and children, the range of the plateau (with upper and lower limits)
is going to differ to that identified in adults because of developmental differences in mean arterial pressure and level of
sympathetic activity. Consequently, we do not know the precise lower limit in mean blood pressure at which CBF falls with
declining blood pressure. Newer techniques, however, using near-infrared spectroscopy in babies with hypoxic-ischemic
encephalopathy suggest that optimum mean arterial pressure can be identified [16].
Outside this range, the compensatory mechanisms break down and inadequate or excessive perfusion can occur [11,15]. The
upper and lower limits of autoregulation are shifted to the right in patients with chronic hypertension, such as patients with
malignant hypertension and posterior reversible encephalopathy syndrome, in whom acute reductions in blood pressure can
produce ischemic symptoms (figure 3). In addition, autoregulation may be impaired in the setting of neurologic injury,
particularly in children, in whom rapid and severe brain swelling may result [17]. (See "Evaluation and management of
elevated intracranial pressure in adults", section on 'Autoregulation'.)
PATHOPHYSIOLOGY
Cerebral edema — Cerebral edema may arise from a variety of clinical conditions (table 2). Therapeutic options for cerebral
edema depend, in part, upon the type of 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.
● 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 [18]. Steroid therapy may be beneficial for vasogenic edema that occurs in the setting of mass lesions.
● 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.
Trauma — After head trauma, a complex series of pathophysiologic changes may occur and contribute to increased ICP [11]:
● Loss of autoregulation resulting in excessive cerebral blood flow (CBF)
● Increased CSF production in response to cerebral hyperemia
● Hypercapnia or hypoxia, which may cause vasodilation and increased CBF (see 'Cerebral blood flow' above)
● Cerebral vessel vasospasm, which may cause regional ischemia and swelling in a vascular distribution [19]
● Herniation, brain swelling, or subarachnoid hemorrhage, which may obstruct the flow of CSF
● 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
The combination of these changes can rapidly exceed the limits of intracranial compensation, leading to an increase in ICP and
subsequent herniation or ischemia (focal or global). Intracranial hypertension may manifest immediately but more often occurs in
the first 48 hours and peaks at day 3 to 5 after injury. (See 'Physiology' above.)
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 [20]:
● Transtentorial herniation is the most common type (figure 4). It results from downward displacement of supratentorial brain
tissue into the infratentorial compartment and can be caused by supratentorial mass lesions, diffuse brain swelling, focal
edema, or acute hydrocephalus. Transtentorial herniation can cause compression of the third cranial nerve, the upper
brainstem, and the cerebral peduncles as well as distortion or traction of the superior portion of the basilar artery and the
posterior cerebral arteries, leading to occipital lobe infarction.
Furthermore, increased pressure in the frontal lobes causes posterior displacement over the lesser wing of the sphenoid bone
which can cause carotid artery compression with anterior and middle cerebral artery infarction.
● Subfalcine herniation occurs when increased pressure in one hemisphere displaces brain tissue under the falx cerebri.
Subfalcine herniation can cause compression of the anterior cerebral artery and extensive infarction of the frontal and parietal
lobes.
● Foramen magnum herniation occurs when downward pressure forces the cerebellar tonsils into the foramen magnum, where
they compress the medulla oblongata and upper cervical spinal cord.
CLINICAL MANIFESTATIONS
The clinical presentation of elevated ICP varies by the age of the child and whether the rise in pressure is gradual or acute.
Features related to the underlying cause such as brain tumor or severe head trauma (including abusive head trauma) may also be
evident.
Patient age — Among infants with chronic, progressive elevation in ICP (eg, slow-growing brain tumor), macrocephaly for age
(figure 5 and figure 6) with a bulging anterior fontanel is the most common presenting feature because unfused cranial sutures can
accommodate rising ICP without acutely compromising neurologic status. In addition, infants and young children may be unable to
articulate certain symptoms (eg, headaches) and therefore are more likely to present with irritability. Alternatively, infants may
display lethargy, lack of interest in their surroundings, and poor feeding.
Nausea and vomiting are common presenting symptoms at any age. In older children and adolescents, other common findings
include headache, visual disturbance, abnormal gait, poor coordination, and papilledema.
Acutely elevated ICP — Acute elevation of ICP is an emergent condition that requires prompt recognition and management.
Important findings include:
● Headache – In verbal children, headache is an early sign of acute elevation of ICP and, as noted below, transtentorial
herniation.
● Vomiting – Vomiting frequently accompanies acute rises in ICP.
● Altered mental status – In patients with an acute increase in ICP (eg, severe head trauma or intracranial hemorrhage),
abrupt onset of altered mental status with obtundation or coma may arise from direct brain injury or herniation.
● Papilledema – Papilledema (picture 1), if present, can confirm the presence of intracranial hypertension. However,
papilledema may be absent in patients with acute elevation ICP because it takes several days to become apparent. Thus,
absence of papilledema does not exclude elevated ICP [21,22].
● Hypertension with bradycardia or tachycardia – In children, increased ICP causes hypertension and either bradycardia or
tachycardia. It is important to use age-based standards for heart rate (table 3) and blood pressure (table 4 and table 5). The
combination of systemic hypertension, bradycardia, and respiratory depression (Cushing triad) is a late sign of impending
herniation (table 6).
● Transtentorial herniation – In addition to vital sign changes, the earliest clinical signs of transtentorial herniation include
(figure 4 and table 6):
• Headache
• Altered level of consciousness
• Pupillary changes (eg, anisocoria) with intact oculocephalic reflex and cold caloric response (figure 7)
• Abnormal breathing patterns (eg, Cheyne Stokes respirations)
• Maintained localization of noxious stimuli if paralysis is not present
As transtentorial herniation progresses the respiratory pattern changes, pupils become midposition and fixed, and motor
response becomes decorticate, decerebrate, or absent (figure 8). Selected patients with posterior displacement of the brain
over the lesser wing of the sphenoid bone due to increased pressure in the frontal lobes of the brain may develop hemiplegia,
coma, and death due to compression of the anterior and middle cerebral arteries.
● Other herniation – Characteristic features identify other types of herniation:
• Foramen magnum herniation – Patients with foramen magnum herniation may have downbeat nystagmus, bradycardia,
bradypnea, and hypertension; these findings may be exacerbated by neck flexion and improve with neck extension.
• Subfalcine herniation – Clinical features of subfalcine herniation include unilateral or bilateral weakness, loss of bladder
control, and coma.
● 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 [23]
• Transient (5 to 15 minutes) epidermal flushing involving the upper chest, face, or arms during the period of deterioration
● Findings of child abuse – Retinal hemorrhages may be present in infants with acute brain injury and increased intracranial
pressure caused by abusive head trauma. Other findings such as cutaneous bruising, fractures, or visceral injuries may also
be present (table 7). (See "Child abuse: Eye findings in children with abusive head trauma (AHT)" and "Physical child abuse:
Recognition", section on 'Red flag physical findings'.)
Subacutely or chronically elevated ICP — Key findings of subacute or chronic elevation of ICP include:
● Headache – Headache is one of the earliest symptoms of increased ICP. Certain headache features suggest increased ICP
as described in the table (table 8). Infants and preverbal children who cannot express the presence of headache more
commonly present with irritability. (See "Headache in children: Approach to evaluation and general management strategies",
section on 'Worrisome findings'.)
● Vomiting – Vomiting, often worse in the morning, occurs due to buildup of ICP overnight while the patient is recumbent and
venous drainage is decreased.
● Abnormalities of vertical gaze (Parinaud syndrome) – Abnormalities of vertical gaze including sunsetting, a downward
gaze preference or an inability to look upwards are found in pediatric patients with hydrocephalus, brain tumor, or stroke due
to enlargement of the third ventricle (table 9).
● Visual changes – Visual changes, such as vision loss (typically peripheral before central vision) or double vision (caused by
palsies of cranial nerves III (oculomotor), IV (trochlear), or VI (abducens) suggest brainstem pathology (see "Detailed
neurologic assessment of infants and children", section on 'III (oculomotor), IV (trochlear), and VI (abducens)'). Infants and
young children who cannot complain of diplopia may squint, cover one eye with their hand, or tilt their head to one side
(picture 2).
● Papilledema – Papilledema (picture 1) is a specific finding of elevated ICP. However, an adequate funduscopic examination is
frequently difficult to obtain in infants or young children.
● Neurologic – Abnormal coordination and ataxia with gait disturbance suggests a posterior fossa lesion that is frequently
associated with elevated ICP. (See "Clinical manifestations and diagnosis of central nervous system tumors in children",
section on 'Tumor location'.)
● Findings of a brain tumor – Clinical features that suggest progressive elevation of ICP due to a brain tumor include (see
"Clinical manifestations and diagnosis of central nervous system tumors in children", section on 'Common presenting signs
and symptoms' and "Clinical manifestations and diagnosis of central nervous system tumors in children", section on
'Neurocutaneous syndromes'):
Growth abnormalities
• Neck pain or stiffness

• Behavior or personality change; in older children declining grades in school
• Known risk factor for intracranial pathology (eg, neurocutaneous syndrome, macrocephaly, or hormonal abnormalities)
• Focal weakness or paralysis
• Ataxia and gait abnormalities
DIAGNOSIS
Approach — Although discussed separately, the assessment and management of elevated ICP are performed jointly in practice.
The diagnosis of elevated ICP is typically established by neuroimaging or other noninvasive means in pediatric patients with
suggestive clinical findings (eg, headache, vomiting, vision changes, altered mental status, or findings of herniation (table 6)).
Papilledema, when present, is specific for intracranial hypertension but has low sensitivity. (See 'Clinical manifestations' above and
'Detection of papilledema' below.)
Direct measurement of increased ICP >20 mmHg (27 cmH2O) using an external ventricular drain or intraparenchymal ICP monitor
is the definitive way to confirm the presence of intracranial hypertension. However, invasive measurement of ICP is reserved for
the most severely affected children in whom the benefits of direct measurement outweigh the risks of bleeding and infection (eg,
Glasgow coma score [GCS] ≤8 (table 10) following head trauma or diagnosed with a condition that warrants aggressive treatment
to manage ICP) [24].
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 cmH2O) can establish the diagnosis of idiopathic intracranial hypertension (pseudotumor cerebri). (See "Idiopathic intracranial
hypertension (pseudotumor cerebri): Clinical features and diagnosis", section on 'Lumbar puncture' and "Idiopathic intracranial
hypertension (pseudotumor cerebri): Clinical features and diagnosis", section on 'Diagnosis'.)
The diagnosis of intracranial hypertension can be challenging, especially when the elevation is subacute or chronic. In infants with
unfused sutures, progressive enlargement of the cranial vault due to increased ICP can be initially accommodated without major
clinical decompensation. In older children, early symptoms such as headache or vomiting are nonspecific, and unless there is a
high index of suspicion, as the course progresses, an altered level of consciousness may hinder the diagnosis. Nonetheless, early
diagnosis is of utmost importance because appropriate therapy can minimize or prevent permanent neurologic injury.
Noninvasive detection of elevated ICP — In children, neuroimaging is the primary means of noninvasively detecting elevated
ICP [24]. However, findings of increased ICP take time to develop and are frequently not present during the first 24 hours in
patients with acute elevation of due to cerebral edema.
Computed tomography — For detection of acute elevation of ICP, computed tomography (CT) of the brain without contrast is
the initial study of choice because it is noninvasive, can be obtained quickly in most hospitals without sedating the patient, and is
more readily available than magnetic resonance imaging [24]. Head CT should be obtained as soon as the child is stabilized so
that emergency therapy, if indicated, can be initiated. 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 hydrocephalus). Head CT is also the best
imaging study for the initial evaluation of intracranial injuries caused by head trauma. (See "Severe traumatic brain injury in
children: Initial evaluation and management", section on 'Imaging'.)
Findings consistent with elevated ICP on head CT include [24,25]:
● Midline shift
● Effacement of the basilar cisterns (image 1)
● Effacement of the sulci (image 1)
● Thumbprinting referring to increased gyral markings on the inner table of the skull in patients with chronically elevated ICP
● In adults, increased optic nerve sheath diameter (>6 mm); specific criteria for children have not been established, but >6 mm
is used at the author’s institution. Based upon preliminary evidence using ocular ultrasound, different thresholds may exist for
infants with open fontanelles and children 1 year of age and younger [26]. (See 'Ocular ultrasound' below.)
Head CT may also demonstrate the underlying etiology of elevated ICP such as cerebral edema, mass lesion, or hemorrhage
(table 1).
However, based upon small observational studies in children with head trauma or nontraumatic coma and experience in adults with
severe head trauma, patients without these findings on initial CT may have elevated ICP in up to 15 percent of cases [27,28].
Abnormalities on head CT may develop within the first few days after a closed head injury in up to one-third of patients. (See
"Evaluation and management of elevated intracranial pressure in adults", section on 'Indications'.)
Thus, head CT findings must be interpreted cautiously, especially in children with head injury. Children with no findings of
increased ICP on head CT but in whom elevated ICP is suspected based upon clinical findings such as headache, vomiting, vision
changes, altered mental status, or findings of herniation should still receive expectant management and undergo alternative means
to identify elevated ICP as follows:
● Direct measurement of ICP by an external ventricular drain or intraparenchymal ICP monitor – Patients with head injury and a
GCS ≤8 or showing signs of impending herniation (see "Severe traumatic brain injury in children: Initial evaluation and
management", section on 'Management')
● Repeat CT or magnetic resonance imaging (MRI) at 12 to 24 hours – In general, if there has been no change in the patient’s
condition “routine” repeat imaging is not needed. However, repeat imaging is important in the following circumstances:
• For patients with head injury or a space-occupying lesion on initial head CT (eg, subdural hematoma, brain tumor, or
cerebral abscess), yet they have not undergone surgical intervention or direct measurement of ICP. Such imaging is
needed when clinical assessment is not possible because of other interventions (eg, endotracheal tube, mechanical
ventilation, sedation, and neuromuscular blockade)
• For patients with head injury or a space-occupying lesion on initial head CT, who in the intervening period have
deteriorated.
● Lumbar puncture – Only indicated in awake patients with features of elevated ICP (eg, headache, papilledema, peripheral
vision loss) but normal neurologic examination suggesting idiopathic intracranial hypertension (pseudotumor cerebri) (see
"Idiopathic intracranial hypertension (pseudotumor cerebri): Clinical features and diagnosis", section on 'Lumbar puncture')
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. It is also less available, takes longer to perform, and requires sedation in infants and young
children or otherwise uncooperative patients [24]. MRI is a suitable alternative to head CT in patients with intact mental status and
neurologic examination in whom chronically elevated ICP is suspected. As for CT, MRI findings of midline shift and effacement of
the basilar cisterns or sulci indicate elevated ICP.
Though pediatric evidence is limited or lacking, the following measurements have also been correlated with intracranial
hypertension in small studies:
● Elastance index that measures the ratio of intracranial pressure change to volume change during the cardiac cycle, high
elastance occurs in brains with low compliance due to elevated ICP [29]
● Cerebral blood flow [30]
● CSF flow velocity through the cerebral aqueduct [31]
● In adults, optic nerve sheath diameter, although pediatric criteria are emerging [32] (see 'Ocular ultrasound' below)
However, further studies are needed before these MRI measurements can be routinely employed in children.
MRI does have greater sensitivity for detecting conditions that can cause cerebral edema (table 2) 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 [25]. For example, three clinical illustrations of
interstitial edema, cytotoxic/cellular edema, and vasogenic edema are, respectively, acute hydrocephalus, cerebral infarction, and
posterior reversible encephalopathy syndrome (PRES). All three conditions show hyperintensity of signal in the affected region on
T2-W imaging. Signal hyperintensity on DW imaging is seen in regions affected by cerebral infarction and periventricular regions in
acute hydrocephalus. ADC is large and anisotropic in PRES, large in periventricular regions in acute hydrocephalus, and low with
reduced anisotropy in infarcted tissue [18].
By contrast, although CT of the head can identify the presence of cerebral edema, it does not distinguish the type of edema [25].
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) [33,34]. Furthermore,
papilledema takes time to develop and is typically not present in patients with increased ICP caused by acute head injury or
hemorrhage. However, when present, papilledema can be a specific indicator of elevated ICP.
Fundus photography and optical coherence tomography (OCT) provide alternative methods to detect elevated ICP using images of
the optic disk [35]. OCT has been used to monitor papilledema in children [35,36]. Although potentially better than funduscopy for
detecting papilledema caused by elevated ICP, these methods require patient cooperation and have the same limitations as
funduscopy for identifying acute intracranial hypertension.
Ocular ultrasound — Ocular nerve sheath diameter can be measured using ocular ultrasound. Based upon prospective data
from 174 children undergoing surgery, cutoff values that correlate with an ICP ≥20 mmHg may vary by age as follows [24,26]:
● ≤1 year or open fontanel: 5.2 mm (sensitivity 80 to 85 percent, specificity 75 to 76 percent)

● >1 year: 5.8 mm (sensitivity 86 percent, specificity 70 percent)
However, further evidence from a much larger sample size is needed to determine the validity of ocular ultrasound measurement in
children and whether it provides useful clinical information.
Invasive measurement of ICP — Invasive measurement of ICP definitively establishes the presence of intracranial hypertension.
However, because of potential complications of infection and bleeding and the need for placement by a pediatric neurosurgeon,
invasive measurement is reserved for the most critically ill patients [24].
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 [4]. However, evidence is lacking to
guide this decision in children. Furthermore, in a retrospective, database, propensity-weighted analysis of the impact of ICP
monitors in over 3000 children suffering with severe TBI, functional outcomes, specifically survival, were not associated with the
use of invasive monitoring [37]. Further studies are needed to help with clinical decision-making (ie, examination of treatment used
along with the monitoring). Until that time, use of ICP monitoring remains a recommendation for severe TBI (GCS ≤8) in pediatric
patients.
Intracranial monitoring in adults is discussed separately. (See "Evaluation and management of elevated intracranial pressure in
adults", section on 'ICP monitoring'.)
A detailed discussion of neurologic monitoring in comatose children with elevated ICP is beyond the scope of this topic but is
addressed in the reference [38].
Ancillary studies — In addition to neuroimaging, ancillary studies serve to identify specific etiologies of elevated ICP (eg,
meningitis or encephalitis), comorbid conditions in children with severe head trauma, and to differentiate elevated ICP from other
causes of altered mental status (eg, hypoglycemia, metabolic encephalopathy, intoxication, or nonconvulsive status epilepticus).
Laboratory studies — Patients with known trauma or suspected abusive head injury should undergo laboratory evaluation for
other injuries as discussed separately. (See "Trauma management: Approach to the unstable child", section on 'Adjuncts to the
primary survey' and "Child abuse: Evaluation and diagnosis of abusive head trauma in infants and children", section on 'Laboratory
studies'.)
Patients presenting with altered consciousness but no evidence of trauma should undergo a rapid bedside test for blood glucose
and basic laboratory testing including (see "Evaluation of stupor and coma in children", section on 'Laboratory testing'):
● 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 include:
• Blood culture
• Urinalysis
• Urine culture
• If lumbar puncture can be safely performed, cerebrospinal fluid (CSF) studies including (see 'Lumbar puncture' below):
- CSF cell count
- CSF glucose and protein
- CSF Gram stain, culture, and, as indicated, polymerase chain reaction for specific pathogens (see "Bacterial
meningitis in children older than one month: Clinical features and diagnosis", section on 'Laboratory evaluation' and
"Acute viral encephalitis in children: Clinical manifestations and diagnosis", section on 'Laboratory evaluation')
● Additional studies in pediatric patients in whom intoxication is suspected based upon history or physical findings (table 11) are
as follows:
• Measured serum osmolality
• Blood ethanol concentration
• Urine drug screen for drugs of abuse
● In young infants in whom metabolic disease is suspected, evaluation according to presenting features (table 12) (see "Inborn
errors of metabolism: Metabolic emergencies", section on 'Evaluation of specific critical presentations')
Lumbar puncture — Lumbar puncture (LP), if necessary for diagnosis, should be deferred until after neuroimaging in any
patient in whom intracranial hypertension is suspected, especially those patients with findings of impending herniation (table 6).
(See 'Clinical manifestations' above.)
Furthermore, because neuroimaging does not always identify elevated ICP, patients with focal neurologic findings should not
routinely undergo LP, regardless of radiographic findings. (See 'Computed tomography' above and 'Magnetic resonance imaging'
above.)
These precautions are essential to avoid precipitating herniation across the tentorial notch or into the foramen magnum. LP
decreases pressure in the region below the tentorium. If elevated pressure above the tentorium exists, then the pressure gradient
between compartments, if large enough, can cause herniation.
In patients in whom central nervous system infection is a strong consideration, deferral of lumbar puncture should not delay the
initiation of empiric antibiotic therapy (table 13). (See "Bacterial meningitis in children older than one month: Treatment and
prognosis", section on 'Avoidance of delay'.)
When an LP is performed for evaluation of a child with suspected elevated ICP, an opening pressure should be obtained. (See
https://www.uptodate.com/contents/elevated-intracranial-pressure-…rch_result&selectedTitle=2~150&usage_type=default&display_rank=2 Page 10 of 53
"Lumbar puncture: Indications, contraindications, technique, and complications in children", section on 'Use of manometer'.)
The contraindications to lumbar puncture in children are discussed in detail separately. (See "Lumbar puncture: Indications,
contraindications, technique, and complications in children".)
Electroencephalogram — Rarely, nonconvulsive status can present with altered mental status and physical findings that
suggest increased ICP. EEG can identify this condition in patients whose neuroimaging and clinical progression do not correspond
with what is expected in patients with intracranial hypertension.
DIFFERENTIAL DIAGNOSIS
Whenever suspected, the first priority is to confirm the diagnosis of intracranial hypertension, prevent further decompensation, and
treat the underlying cause. The physician should also be aware of the conditions that can mimic acute or chronic elevations of ICP
as discussed below. (See "Elevated intracranial pressure (ICP) in children: Management", section on 'Ongoing Management'.)
Acute intracranial hypertension — Conditions that can mimic acute elevations of ICP consist of:
● Hypoglycemia – Hypoglycemia may present with abrupt onset of altered mental status and can cause coma with focal
seizures or a focal neurologic deficit. It warrants early recognition by measurement of rapid blood glucose and emergency
treatment to prevent permanent brain damage (table 14). (See "Approach to hypoglycemia in infants and children", section on
'Clinical features'.)
● Metabolic encephalopathies, other than hypoglycemia – Metabolic coma in children usually occurs as a progression from
delirium to stupor to coma, but more fulminant cases may present in coma. A fluctuating examination is common; deficits can
include abnormal brainstem reflexes, hypotonia, and even posturing in severe cases. However, focal neurologic findings and
anisocoria are uncommon in metabolic coma. Multifocal myoclonus is very suggestive of a metabolic etiology. Potential
etiologies of metabolic coma are provided in the table (table 15) and are discussed in detail separately. (See "Acute toxic-
metabolic encephalopathy in children".)
● Acute drug intoxication – Encephalopathy resulting from the toxic effect of medication is an important diagnostic
consideration in a patient in whom intracranial hypertension is suspected because of the typically abrupt onset of
encephalopathy. This condition can result from therapeutic overdose, unintentional ingestion, or deliberate abuse. Drugs that
result in coma when present in high concentration include sedatives, anticholinergic agents, and salicylates (table 16). In many
instances, physical findings can differentiate intoxication from increased ICP (table 11). Furthermore, drug intoxication with
these agents is not usually associated with focal neurologic findings. (See "Approach to the child with occult toxic exposure"
and "Acute toxic-metabolic encephalopathy in children", section on 'Drugs and toxins'.)
Chemotherapy may result in similar states regardless of drug level, and is often associated with signs of acute
leukoencephalopathy on brain magnetic resonance imaging (MRI) (high signal on T2 and fluid attenuated inversion recovery
[FLAIR]) and even changes in diffusion-weighted imaging (DWI), due to cytotoxic edema, especially with methotrexate use.
(See "Acute toxic-metabolic encephalopathy in children", section on 'Immunosuppressive agents'.)
● Nonconvulsive status epilepticus – Nonconvulsive status epilepticus may present with a variety of symptoms and signs,
including significant alterations in mental status. Electroencephalogram (EEG) confirms the diagnosis. EEG is warranted in
critically ill patients who are obtunded or comatose and do not have clear findings of intracranial hypertension. (See
"Nonconvulsive status epilepticus", section on 'Clinical features' and "Nonconvulsive status epilepticus", section on 'Patient
selection for EEG'.)
● Hemiplegic migraine headache – Hemiplegic migraine is characterized by migraine attacks with motor weakness during the
aura phase. Attacks may variably include severe headache, scintillating scotoma, visual field defect, numbness, paresthesia,
unilateral weakness, aphasia, fever, lethargy, coma, and seizures. The symptoms can last for hours to days, or rarely weeks.
The diagnosis is suggested by episodic occurrence of hemiplegia and response to specific treatment for migraine. (See
"Hemiplegic migraine", section on 'Clinical manifestations' and "Hemiplegic migraine", section on 'Diagnosis'.)
Chronic intracranial hypertension — Headache is the most common presenting symptom of chronically elevated ICP (table 8).
However, headache is also a frequent symptom of benign conditions in children, especially self-limited febrile illnesses (table 17). A
careful history and physical examination can usually identify patients with concerning findings of intracranial hypertension. (See
'Acutely elevated ICP' above and 'Subacutely or chronically elevated ICP' above.)
The acute evaluation of headaches in children is discussed separately. (See "Emergency department approach to nontraumatic
headache in children", section on 'Diagnostic approach'.)
SUMMARY AND RECOMMENDATIONS
● In children, 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 (eg, liver failure) (table 1). Measured ICP >20 mmHg (27 cmH2O) is generally regarded as the threshold for treatment.
(See 'Physiology' above and "Elevated intracranial pressure (ICP) in children: Management", section on 'Ongoing
Management'.)
● Acute elevation of ICP is an emergency condition. Important findings include (see 'Acutely elevated ICP' above):
• Headache (verbal children)

• Vomiting
• Abrupt onset of obtundation or coma
• Papilledema (picture 1) which may not be present in patients with acute elevations of ICP
• Hypertension (table 4 and table 5) with bradycardia or tachycardia (table 3)
• Signs of herniation (figure 4 and table 6)
• Spontaneous upper eyelid ecchymosis adjacent to the lid margin
• Retinal hemorrhages, cutaneous bruising, fractures, or visceral injury (table 7) in victims of abusive head trauma
● Among infants with chronic, progressive elevation in ICP (eg, slow-growing brain tumor), macrocephaly for age (figure 5 and
figure 6) with a bulging anterior fontanel is the most common presenting feature. In addition, infants and young children may
be unable to articulate certain symptoms (eg, headaches) and therefore are more likely to present with irritability. Alternatively,
infants may display lethargy, lack of interest in their surroundings, and poor feeding. (See 'Patient age' above.)
● Among children with chronically elevated ICP, key findings are as follows (see 'Subacutely or chronically elevated ICP' above):
• Headache (table 8)
• Vomiting, often worse in the morning due to buildup of ICP overnight while recumbent
• Abnormalities of vertical gaze (eg, downward gaze preference [sunsetting] or inability to look upwards)
• Vision loss or double vision; in young children diplopia may cause squinting or a head tilt (picture 2)
• Papilledema (picture 1)
• Ataxia, poor coordination, or abnormal gait suggesting a posterior fossa lesion
• Other findings of a brain tumor such as growth abnormalities, neck pain or stiffness, behavior change, or focal weakness
or paralysis
● Although discussed separately, the assessment and management of elevated ICP are performed jointly in practice (algorithm
1). The diagnosis of elevated ICP is typically established by neuroimaging or other noninvasive means in pediatric patients
with suggestive clinical findings (eg, headache, vomiting, vision changes, altered mental status, or findings of herniation (table
6)). Papilledema, when present, is specific for intracranial hypertension but has low sensitivity. (See 'Approach' above and
'Noninvasive detection of elevated ICP' above.)
● Invasive measurement of ICP definitively establishes the presence of intracranial hypertension. Intracranial monitoring with an
external ventricular drain or intraparenchymal ICP monitor placed by a neurosurgeon is usually indicated in pediatric patients
with a Glasgow coma score (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. (See
'Invasive measurement of ICP' above.)
● In addition to neuroimaging, ancillary studies serve to identify specific etiologies of elevated ICP (eg, meningitis or
encephalitis), comorbid conditions in children with severe head trauma, and to differentiate elevated ICP from other causes of
altered mental status (eg, hypoglycemia, metabolic encephalopathy, intoxication, or nonconvulsive status epilepticus). (See
'Ancillary studies' above and 'Differential diagnosis' above.)
● Lumbar puncture (LP), if necessary for diagnosis, should be deferred until after neuroimaging in any patient in whom
intracranial hypertension is suspected, especially those patients with findings of impending herniation. Furthermore, because
neuroimaging does not always identify elevated ICP, patients with focal neurologic findings should not routinely undergo LP,
regardless of radiographic findings.
● The treatment of elevated ICP in children is discussed in greater detail separately. (See "Elevated intracranial pressure (ICP)
in children: Management".)
ACKNOWLEDGMENT
The editorial staff at UpToDate would like to acknowledge Warren K Brasher, MD, who contributed to an earlier version of this topic
review.
Use of UpToDate is subject to the Subscription and License Agreement.
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17. Aldrich EF, Eisenberg HM, Saydjari C, et al. Diffuse brain swelling in severely head-injured children. A report from the NIH
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Topic 6077 Version 16.0
GRAPHICS
Causes of intracranial hypertension*
Traumatic brain injury/intracranial hemorrhage
Subdural, epidural, or intraparenchymal hemorrhage
Ruptured aneurysm
Diffuse axonal injury
Arteriovenous malformation or other vascular anomalies
Central nervous system infections (eg, encephalitis, meningitis, abscess)
Ischemic stroke
Neoplasm
Vasculitis
Hydrocephalus
Hypertensive encephalopathy
Idiopathic intracranial hypertension (pseudotumor cerebri)
* For further information on clinical manifestations, diagnosis, or treatment of these conditions, refer to specific UpToDate topics.
Graphic 69683 Version 9.0
Intracranial compensation for mass
Normally, the intracranial components are in equilibrium as shown in

chamber 1. Initially, the volume of a space-occupying lesion is compensated
for by displacement of blood and CSF and ICP remains normal (chamber 2).
When the limits of this compensation is reached; any additional increase in
the volume of the mass lesion is accompanied by a corresponding increase in
ICP (chamber 3, decompensated phase).
Data from Pathophysiology and management of the intracranial vault. In: Textbook
of Pediatric Intensive Care, 3rd ed, Rogers, MC (Ed), Williams and Wilkins 1996. p.
646; figure 18.1.
The relationship between intracranial volume and

pressure is nonlinear
An initial increase in volume results in a small increase in pressure because

of intracranial compensation (blue line). Once intracranial compensation is
exhausted, additional increases in intracranial volume result in a dramatic
rise in intracranial pressure (red line).
Cerebral autoregulation in hypertension
Schematic representation of autoregulation of cerebral blood flow in

normotensive and hypertensive subjects. In both groups, initial increases or
decreases in mean arterial pressure are associated with maintenance of
cerebral blood flow due to appropriate changes in arteriolar resistance. More
marked changes in pressure are eventually associated with loss of
autoregulation, leading to a reduction (with hypotension) or an elevation
(with marked hypertension) in cerebral blood flow. These changes occur at
higher pressures in patients with hypertension, presumably due to arteriolar
thickening. Thus, aggressive antihypertensive therapy will produce cerebral
ischemia at a higher mean arterial pressure in patients with underlying
hypertension.
Redrawn from: Kaplan NM. Management of hypertensive emergencies. Lancet 1994;

344:1335.
Causes of cerebral edema in children*
Severe head trauma

Brain tumor
Hydrocephalus
Hypoxic-ischemic encephalopathy
Infectious
Cerebral abscess
Meningitis
Encephalitis
Diabetic ketoacidosis
Stroke
Venous thrombosis
Arteriovenous malformations
Vasculitis
*These conditions may result in one or more types of cerebral edema; cytotoxic, vasogenic, and/or interstitial.
Transtentorial herniation
Data from: Plum F, Posner JB. The Diagnosis of Stupor and Coma III. FA Davis, Philadelphia 1995. p.
103.
Head circumference-for-age percentiles, girls 0 to 36 months, CDC

growth charts
Head circumference-for-age percentiles, boys birth to 36 months, CDC

growth charts
Papilledema
Papilledema, characterized by blurring of the optic disc margins, loss of

physiologic cupping, hyperemia, and fullness of the veins, in a 5-year-old girl
with intracranial hypertension due to vitamin A intoxication.
Courtesy of Gerald Striph, MD.
Pediatric respiratory rate and heart rate lower limit, normal range, and upper limit by age*
Respiratory rate (breaths/minute) Heart rate (beats/minute)
Age Normal range Normal range

Lower limit Upper limit Lower limit Upper limit
(10 th-90 th (10 th-90 th
(1 st percentile) (99 th percentile) (1 st percentile) (99 th percentile)
percentile) percentile)
0 to 3 months 25 34-57 66 107 123-164 181
3 to <6 months 24 33-55 64 104 120-159 175
6 to <9 months 23 31-52 61 98 114-152 168
9 to <12 months 22 30-50 58 93 109-145 161
12 to <18 months 21 28-46 53 88 103-140 156
18 to <24 months 19 25-40 46 82 98-135 149
2 to <3 years 18 22-34 38 76 92-128 142
3 to <4 years 17 21-29 33 70 86-123 136
4 to <6 years 17 20-27 29 65 81-117 131
6 to <8 years 16 18-24 27 59 74-111 123
8 to <12 years 14 16-22 25 52 67-103 115
12 to <15 years 12 15-21 23 47 62-96 108
15 to 18 years 11 13-19 22 43 58-92 104
* The respiratory and heart rates provided are based upon measurements in awake, healthy infants and children at rest. Many clinical findings besides the actual
vital sign measurement must be taken into account when determining whether a specific vital sign is normal in an individual patient. Values for heart rate or
respiratory rate that fall within normal limits for age may still represent abnormal findings that are caused by underlying disease in a particular infant or child.
Data from: Fleming S, Thompson M, Stevens R, et al. Normal ranges of heart rate and respiratory rate in children from birth to 18 years of age: A systematic
review of observational studies. Lancet 2011; 377:1011.
Blood pressure levels for girls by age and height percentile
Systolic BP (mmHg) Diastolic BP (mmHg)

BP
Height percentile or measured height Height percentile or measured height
(percentile)
5% 10% 25% 50% 75% 90% 95% 5% 10% 25% 50% 75% 90% 95%
1 year
Height (in) 29.7 30.2 30.9 31.8 32.7 33.4 33.9 29.7 30.2 30.9 31.8 32.7 33.4 33.9
Height (cm) 75.4 76.6 78.6 80.8 83.0 84.9 86.1 75.4 76.6 78.6 80.8 83.0 84.9 86.1
50 th 84 85 86 86 87 88 88 41 42 42 43 44 45 46
90 th 98 99 99 100 101 102 102 54 55 56 56 57 58 58
95 th 101 102 102 103 104 105 105 59 59 60 60 61 62 62
95 th + 12 mmHg 113 114 114 115 116 117 117 71 71 72 72 73 74 74
2 years
Height (in) 33.4 34.0 34.9 35.9 36.9 37.8 38.4 33.4 34.0 34.9 35.9 36.9 37.8 38.4
Height (cm) 84.9 86.3 88.6 91.1 93.7 96.0 97.4 84.9 86.3 88.6 91.1 93.7 96.0 97.4
50 th 87 87 88 89 90 91 91 45 46 47 48 49 50 51
90 th 101 101 102 103 104 105 106 58 58 59 60 61 62 62
95 th 104 105 106 106 107 108 109 62 63 63 64 65 66 66
95 th + 12 mmHg 116 117 118 118 119 120 121 74 75 75 76 77 78 78
3 years
Height (in) 35.8 36.4 37.3 38.4 39.6 40.6 41.2 35.8 36.4 37.3 38.4 39.6 40.6 41.2
Height (cm) 91.0 92.4 94.9 97.6 100.5 103.1 104.6 91.0 92.4 94.9 97.6 100.5 103.1 104.6
50 th 88 89 89 90 91 92 93 48 48 49 50 51 53 53
90 th 102 103 104 104 105 106 107 60 61 61 62 63 64 65
95 th 106 106 107 108 109 110 110 64 65 65 66 67 68 69
95 th + 12 mmHg 118 118 119 120 121 122 122 76 77 77 78 79 80 81
4 years
Height (in) 38.3 38.9 39.9 41.1 42.4 43.5 44.2 38.3 38.9 39.9 41.1 42.4 43.5 44.2
Height (cm) 97.2 98.8 101.4 104.5 107.6 110.5 112.2 97.2 98.8 101.4 104.5 107.6 110.5 112.2
50 th 89 90 91 92 93 94 94 50 51 51 53 54 55 55
90 th 103 104 105 106 107 108 108 62 63 64 65 66 67 67
95 th 107 108 109 109 110 111 112 66 67 68 69 70 70 71
95 th + 12 mmHg 119 120 121 121 122 123 124 78 79 80 81 82 82 83
5 years
Height (in) 40.8 41.5 42.6 43.9 45.2 46.5 47.3 40.8 41.5 42.6 43.9 45.2 46.5 47.3
Height (cm) 103.6 105.3 108.2 111.5 114.9 118.1 120.0 103.6 105.3 108.2 111.5 114.9 118.1 120.0
50 th 90 91 92 93 94 95 96 52 52 53 55 56 57 57
90 th 104 105 106 107 108 109 110 64 65 66 67 68 69 70
95 th 108 109 109 110 111 112 113 68 69 70 71 72 73 73
95 th + 12 mmHg 120 121 121 122 123 124 125 80 81 82 83 84 85 85
6 years
Height (in) 43.3 44.0 45.2 46.6 48.1 49.4 50.3 43.3 44.0 45.2 46.6 48.1 49.4 50.3
Height (cm) 110.0 111.8 114.9 118.4 122.1 125.6 127.7 110.0 111.8 114.9 118.4 122.1 125.6 127.7
50 th 92 92 93 94 96 97 97 54 54 55 56 57 58 59
90 th 105 106 107 108 109 110 111 67 67 68 69 70 71 71
95 th 109 109 110 111 112 113 114 70 71 72 72 73 74 74
95 th + 12 mmHg 121 121 122 123 124 125 126 82 83 84 84 85 86 86
7 years
Height (in) 45.6 46.4 47.7 49.2 50.7 52.1 53.0 45.6 46.4 47.7 49.2 50.7 52.1 53.0
Height (cm) 115.9 117.8 121.1 124.9 128.8 132.5 134.7 115.9 117.8 121.1 124.9 128.8 132.5 134.7
50 th 92 93 94 95 97 98 99 55 55 56 57 58 59 60
90 th 106 106 107 109 110 111 112 68 68 69 70 71 72 72

th
95 th 109 110 111 112 113 114 115 72 72 73 73 74 74 75
95 th + 12 mmHg 121 122 123 124 125 126 127 84 84 85 85 86 86 87
8 years
Height (in) 47.6 48.4 49.8 51.4 53.0 54.5 55.5 47.6 48.4 49.8 51.4 53.0 54.5 55.5
Height (cm) 121.0 123.0 126.5 130.6 134.7 138.5 140.9 121.0 123.0 126.5 130.6 134.7 138.5 140.9
50 th 93 94 95 97 98 99 100 56 56 57 59 60 61 61
90 th 107 107 108 110 111 112 113 69 70 71 72 72 73 73
95 th 110 111 112 113 115 116 117 72 73 74 74 75 75 75
95 th + 12 mmHg 122 123 124 125 127 128 129 84 85 86 86 87 87 87
9 years
Height (in) 49.3 50.2 51.7 53.4 55.1 56.7 57.7 49.3 50.2 51.7 53.4 55.1 56.7 57.7
Height (cm) 125.3 127.6 131.3 135.6 140.1 144.1 146.6 125.3 127.6 131.3 135.6 140.1 144.1 146.6
50 th 95 95 97 98 99 100 101 57 58 59 60 60 61 61
90 th 108 108 109 111 112 113 114 71 71 72 73 73 73 73
95 th 112 112 113 114 116 117 118 74 74 75 75 75 75 75
95 th + 12 mmHg 124 124 125 126 128 129 130 86 86 87 87 87 87 87
10 years
Height (in) 51.1 52.0 53.7 55.5 57.4 59.1 60.2 51.1 52.0 53.7 55.5 57.4 59.1 60.2
Height (cm) 129.7 132.2 136.3 141.0 145.8 150.2 152.8 129.7 132.2 136.3 141.0 145.8 150.2 152.8
50 th 96 97 98 99 101 102 103 58 59 59 60 61 61 62
90 th 109 110 111 112 113 115 116 72 73 73 73 73 73 73
95 th 113 114 114 116 117 119 120 75 75 76 76 76 76 76
95 th + 12 mmHg 125 126 126 128 129 131 132 87 87 88 88 88 88 88
11 years
Height (in) 53.4 54.5 56.2 58.2 60.2 61.9 63.0 53.4 54.5 56.2 58.2 60.2 61.9 63.0
Height (cm) 135.6 138.3 142.8 147.8 152.8 157.3 160.0 135.6 138.3 142.8 147.8 152.8 157.3 160.0
50 th 98 99 101 102 104 105 106 60 60 60 61 62 63 64
90 th 111 112 113 114 116 118 120 74 74 74 74 74 75 75
95 th 115 116 117 118 120 123 124 76 77 77 77 77 77 77
95 th + 12 mmHg 127 128 129 130 132 135 136 88 89 89 89 89 89 89
12 years
Height (in) 56.2 57.3 59.0 60.9 62.8 64.5 65.5 56.2 57.3 59.0 60.9 62.8 64.5 65.5
Height (cm) 142.8 145.5 149.9 154.8 159.6 163.8 166.4 142.8 145.5 149.9 154.8 159.6 163.8 166.4
50 th 102 102 104 105 107 108 108 61 61 61 62 64 65 65
90 th 114 115 116 118 120 122 122 75 75 75 75 76 76 76
95 th 118 119 120 122 124 125 126 78 78 78 78 79 79 79
95 th + 12 mmHg 130 131 132 134 136 137 138 90 90 90 90 91 91 91
13 years
Height (in) 58.3 59.3 60.9 62.7 64.5 66.1 67.0 58.3 59.3 60.9 62.7 64.5 66.1 67.0
Height (cm) 148.1 150.6 154.7 159.2 163.7 167.8 170.2 148.1 150.6 154.7 159.2 163.7 167.8 170.2
50 th 104 105 106 107 108 108 109 62 62 63 64 65 65 66
90 th 116 117 119 121 122 123 123 75 75 75 76 76 76 76
95 th 121 122 123 124 126 126 127 79 79 79 79 80 80 81
95 th + 12 mmHg 133 134 135 136 138 138 139 91 91 91 91 92 92 93
14 years
Height (in) 59.3 60.2 61.8 63.5 65.2 66.8 67.7 59.3 60.2 61.8 63.5 65.2 66.8 67.7
Height (cm) 150.6 153.0 156.9 161.3 165.7 169.7 172.1 150.6 153.0 156.9 161.3 165.7 169.7 172.1
50 th 105 106 107 108 109 109 109 63 63 64 65 66 66 66
90 th 118 118 120 122 123 123 123 76 76 76 76 77 77 77
95 th 123 123 124 125 126 127 127 80 80 80 80 81 81 82
95 th + 12 mmHg 135 135 136 137 138 139 139 92 92 92 92 93 93 94
15 years
Height (in) 59.7 60.6 62.2 63.9 65.6 67.2 68.1 59.7 60.6 62.2 63.9 65.6 67.2 68.1
Height (cm) 151.7 154.0 157.9 162.3 166.7 170.6 173.0 151.7 154.0 157.9 162.3 166.7 170.6 173.0
50 th 105 106 107 108 109 109 109 64 64 64 65 66 67 67
90 th 118 119 121 122 123 123 124 76 76 76 77 77 78 78
95 th 124 124 125 126 127 127 128 80 80 80 81 82 82 82
95 th + 12 mmHg 136 136 137 138 139 139 140 92 92 92 93 94 94 94
16 years
Height (in) 59.9 60.8 62.4 64.1 65.8 67.3 68.3 59.9 60.8 62.4 64.1 65.8 67.3 68.3
Height (cm) 152.1 154.5 158.4 162.8 167.1 171.1 173.4 152.1 154.5 158.4 162.8 167.1 171.1 173.4
50 th 106 107 108 109 109 110 110 64 64 65 66 66 67 67
90 th 119 120 122 123 124 124 124 76 76 76 77 78 78 78
95 th 124 125 125 127 127 128 128 80 80 80 81 82 82 82
95 th + 12 mmHg 136 137 137 139 139 140 140 92 92 92 93 94 94 94
17 years
Height (in) 60.0 60.9 62.5 64.2 65.9 67.4 68.4 60.0 60.9 62.5 64.2 65.9 67.4 68.4
Height (cm) 154.4 154.7 158.7 163.0 167.4 171.3 173.7 154.4 154.7 158.7 163.0 167.4 171.3 173.7
50 th 107 108 109 110 110 110 111 64 64 65 66 66 66 67
90 th 120 121 123 124 124 125 125 76 76 77 77 78 78 78
95 th 125 125 126 127 128 128 128 80 80 80 81 82 82 82
95 th + 12 mmHg 137 137 138 139 140 140 140 92 92 92 93 94 94 94
The 50 th, 90 th, and 95 th percentiles were derived by using quantile regression on the basis of normal-weight children (BMI <85 th percentile). BP
stages are defined as elevated BP ≥90 th percentile but <95 th percentile; stage 1 HTN: ≥95 th percentile or 130/80 to 139/89 mmHg; and stage 2
HTN: ≥95 th percentile + 12 mmHg or >140/90 mmHg.
BP: blood pressure; BMI: body mass index; HTN: hypertension.
Reproduced with permission from: Pediatrics, Vol. 140, doi: 10.1542/peds.2017-1904. Copyright © 2017 by the AAP.
Blood pressure levels for boys by age and height percentile
Systolic BP (mmHg) Diastolic BP (mmHg)

BP
Height percentile or measured height Height percentile or measured height
(percentile)
5% 10% 25% 50% 75% 90% 95% 5% 10% 25% 50% 75% 90% 95%
1 year
Height (in) 30.4 30.8 31.6 32.4 33.3 34.1 34.6 30.4 30.8 31.6 32.4 33.3 34.1 34.6
Height (cm) 77.2 78.3 80.2 82.4 84.6 86.7 87.9 77.2 78.3 80.2 82.4 84.6 86.7 87.9
50 th 85 85 86 86 87 88 88 40 40 40 41 41 42 42
90 th 98 99 99 100 100 101 101 52 52 53 53 54 54 54
95 th 102 102 103 103 104 105 105 54 54 55 55 56 57 57
95 th + 12 mmHg 114 114 115 115 116 117 117 66 66 67 67 68 69 69
2 years
Height (in) 33.9 34.4 35.3 36.3 37.3 38.2 38.8 33.9 34.4 35.3 36.3 37.3 38.2 38.8
Height (cm) 86.1 87.4 89.6 92.1 94.7 97.1 98.5 86.1 87.4 89.6 92.1 94.7 97.1 98.5
50 th 87 87 88 89 89 90 91 43 43 44 44 45 46 46
90 th 100 100 101 102 103 103 104 55 55 56 56 57 58 58
95 th 104 105 105 106 107 107 108 57 58 58 59 60 61 61

th
95 + 12 mmHg 116 117 117 118 119 119 120 69 70 70 71 72 73 73
3 years
Height (in) 36.4 37.0 37.9 39.0 40.1 41.1 41.7 36.4 37.0 37.9 39.0 40.1 41.1 41.7
Height (cm) 92.5 93.9 96.3 99.0 101.8 104.3 105.8 92.5 93.9 96.3 99.0 101.8 104.3 105.8
50 th 88 89 89 90 91 92 92 45 46 46 47 48 49 49
90 th 101 102 102 103 104 105 105 58 58 59 59 60 61 61
95 th 106 106 107 107 108 109 109 60 61 61 62 63 64 64
95 th + 12 mmHg 118 118 119 119 120 121 121 72 73 73 74 75 76 76
4 years
Height (in) 38.8 39.4 40.5 41.7 42.9 43.9 44.5 38.8 39.4 40.5 41.7 42.9 43.9 44.5
Height (cm) 98.5 100.2 102.9 105.9 108.9 111.5 113.2 98.5 100.2 102.9 105.9 108.9 111.5 113.2
50 th 90 90 91 92 93 94 94 48 49 49 50 51 52 52
90 th 102 103 104 105 105 106 107 60 61 62 62 63 64 64
95 th 107 107 108 108 109 110 110 63 64 65 66 67 67 68
95 th + 12 mmHg 119 119 120 120 121 122 122 75 76 77 78 79 79 80
5 years
Height (in) 41.1 41.8 43.0 44.3 45.5 46.7 47.4 41.1 41.8 43.0 44.3 45.5 46.7 47.4
Height (cm) 104.4 106.2 109.1 112.4 115.7 118.6 120.3 104.4 106.2 109.1 112.4 115.7 118.6 120.3
50 th 91 92 93 94 95 96 96 51 51 52 53 54 55 55
90 th 103 104 105 106 107 108 108 63 64 65 65 66 67 67
95 th 107 108 109 109 110 111 112 66 67 68 69 70 70 71
95 th + 12 mmHg 119 120 121 121 122 123 124 78 79 80 81 82 82 83
6 years
Height (in) 43.4 44.2 45.4 46.8 48.2 49.4 50.2 43.4 44.2 45.4 46.8 48.2 49.4 50.2
Height (cm) 110.3 112.2 115.3 118.9 122.4 125.6 127.5 110.3 112.2 115.3 118.9 122.4 125.6 127.5
50 th 93 93 94 95 96 97 98 54 54 55 56 57 57 58
90 th 105 105 106 107 109 110 110 66 66 67 68 68 69 69
95 th 108 109 110 111 112 113 114 69 70 70 71 72 72 73
95 th + 12 mmHg 120 121 122 123 124 125 126 81 82 82 83 84 84 85
7 years
Height (in) 45.7 46.5 47.8 49.3 50.8 52.1 52.9 45.7 46.5 47.8 49.3 50.8 52.1 52.9
Height (cm) 116.1 118.0 121.4 125.1 128.9 132.4 134.5 116.1 118.0 121.4 125.1 128.9 132.4 134.5
50 th 94 94 95 97 98 98 99 56 56 57 58 58 59 59
90 th 106 107 108 109 110 111 111 68 68 69 70 70 71 71

th
95 th 110 110 111 112 114 115 116 71 71 72 73 73 74 74
95 th + 12 mmHg 122 122 123 124 126 127 128 83 83 84 85 85 86 86
8 years
Height (in) 47.8 48.6 50.0 51.6 53.2 54.6 55.5 47.8 48.6 50.0 51.6 53.2 54.6 55.5
Height (cm) 121.4 123.5 127.0 131.0 135.1 138.8 141.0 121.4 123.5 127.0 131.0 135.1 138.8 141.0
50 th 95 96 97 98 99 99 100 57 57 58 59 59 60 60
90 th 107 108 109 110 111 112 112 69 70 70 71 72 72 73
95 th 111 112 112 114 115 116 117 72 73 73 74 75 75 75
95 th + 12 mmHg 123 124 124 126 127 128 129 84 85 85 86 87 87 87
9 years
Height (in) 49.6 50.5 52.0 53.7 55.4 56.9 57.9 49.6 50.5 52.0 53.7 55.4 56.9 57.9
Height (cm) 126.0 128.3 132.1 136.3 140.7 144.7 147.1 126.0 128.3 132.1 136.3 140.7 144.7 147.1
50 th 96 97 98 99 100 101 101 57 58 59 60 61 62 62
90 th 107 108 109 110 112 113 114 70 71 72 73 74 74 74
95 th 112 112 113 115 116 118 119 74 74 75 76 76 77 77
95 th + 12 mmHg 124 124 125 127 128 130 131 86 86 87 88 88 89 89
10 years
Height (in) 51.3 52.2 53.8 55.6 57.4 59.1 60.1 51.3 52.2 53.8 55.6 57.4 59.1 60.1
Height (cm) 130.2 132.7 136.7 141.3 145.9 150.1 152.7 130.2 132.7 136.7 141.3 145.9 150.1 152.7
50 th 97 98 99 100 101 102 103 59 60 61 62 63 63 64
90 th 108 109 111 112 113 115 116 72 73 74 74 75 75 76
95 th 112 113 114 116 118 120 121 76 76 77 77 78 78 78

th
95 + 12 mmHg 124 125 126 128 130 132 133 88 88 89 89 90 90 90
11 years
Height (in) 53.0 54.0 55.7 57.6 59.6 61.3 62.4 53.0 54.0 55.7 57.6 59.6 61.3 62.4
Height (cm) 134.7 137.3 141.5 146.4 151.3 155.8 158.6 134.7 137.3 141.5 146.4 151.3 155.8 158.6
50 th 99 99 101 102 103 104 106 61 61 62 63 63 63 63
90 th 110 111 112 114 116 117 118 74 74 75 75 75 76 76
95 th 114 114 116 118 120 123 124 77 78 78 78 78 78 78
95 th + 12 mmHg 126 126 128 130 132 135 136 89 90 90 90 90 90 90
12 years
Height (in) 55.2 56.3 58.1 60.1 62.2 64.0 65.2 55.2 56.3 58.1 60.1 62.2 64.0 65.2
Height (cm) 140.3 143.0 147.5 152.7 157.9 162.6 165.5 140.3 143.0 147.5 152.7 157.9 162.6 165.5
50 th 101 101 102 104 106 108 109 61 62 62 62 62 63 63
90 th 113 114 115 117 119 121 122 75 75 75 75 75 76 76
95 th 116 117 118 121 124 126 128 78 78 78 78 78 79 79
95 th + 12 mmHg 128 129 130 133 136 138 140 90 90 90 90 90 91 91
13 years
Height (in) 57.9 59.1 61.0 63.1 65.2 67.1 68.3 57.9 59.1 61.0 63.1 65.2 67.1 68.3
Height (cm) 147.0 150.0 154.9 160.3 165.7 170.5 173.4 147.0 150.0 154.9 160.3 165.7 170.5 173.4
50 th 103 104 105 108 110 111 112 61 60 61 62 63 64 65
90 th 115 116 118 121 124 126 126 74 74 74 75 76 77 77
95 th 119 120 122 125 128 130 131 78 78 78 78 80 81 81
95 th + 12 mmHg 131 132 134 137 140 142 143 90 90 90 90 92 93 93
14 years
Height (in) 60.6 61.8 63.8 65.9 68.0 69.8 70.9 60.6 61.8 63.8 65.9 68.0 69.8 70.9
Height (cm) 153.8 156.9 162.0 167.5 172.7 177.4 180.1 153.8 156.9 162.0 167.5 172.7 177.4 180.1
50 th 105 106 109 111 112 113 113 60 60 62 64 65 66 67
90 th 119 120 123 126 127 128 129 74 74 75 77 78 79 80
95 th 123 125 127 130 132 133 134 77 78 79 81 82 83 84
95 th + 12 mmHg 135 137 139 142 144 145 146 89 90 91 93 94 95 96
15 years
Height (in) 62.6 63.8 65.7 67.8 69.8 71.5 72.5 62.6 63.8 65.7 67.8 69.8 71.5 72.5
Height (cm) 159.0 162.0 166.9 172.2 177.2 181.6 184.2 159.0 162.0 166.9 172.2 177.2 181.6 184.2
50 th 108 110 112 113 114 114 114 61 62 64 65 66 67 68
90 th 123 124 126 128 129 130 130 75 76 78 79 80 81 81
95 th 127 129 131 132 134 135 135 78 79 81 83 84 85 85
95 th + 12 mmHg 139 141 143 144 146 147 147 90 91 93 95 96 97 97
16 years
Height (in) 63.8 64.9 66.8 68.8 70.7 72.4 73.4 63.8 64.9 66.8 68.8 70.7 72.4 73.4
Height (cm) 162.1 165.0 169.6 174.6 179.5 183.8 186.4 162.1 165.0 169.6 174.6 179.5 183.8 186.4
50 th 111 112 114 115 115 116 116 63 64 66 67 68 69 69

th
90 126 127 128 129 131 131 132 77 78 79 80 81 82 82
95 th 130 131 133 134 135 136 137 80 81 83 84 85 86 86
95 th + 12 mmHg 142 143 145 146 147 148 149 92 93 95 96 97 98 98
17 years
Height (in) 64.5 65.5 67.3 69.2 71.1 72.8 73.8 64.5 65.5 67.3 69.2 71.1 72.8 73.8
Height (cm) 163.8 166.5 170.9 175.8 180.7 184.9 187.5 163.8 166.5 170.9 175.8 180.7 184.9 187.5
50 th 114 115 116 117 117 118 118 65 66 67 68 69 70 70
90 th 128 129 130 131 132 133 134 78 79 80 81 82 82 83
95 th 132 133 134 135 137 138 138 81 82 84 85 86 86 87
95 th + 12 mmHg 144 145 146 147 149 150 150 93 94 96 97 98 98 99
The 50 th, 90 th, and 95 th percentiles were derived by using quantile regression on the basis of normal-weight children (BMI <85 th percentile). BP
stages are defined as elevated BP ≥90 th percentile but <95 th percentile; stage 1 HTN: ≥95 th percentile or 130/80 to 139/89 mmHg; and stage 2
HTN: ≥95 th percentile + 12 mmHg or >140/90 mmHg.
BP: blood pressure; BMI: body mass index; HTN: hypertension.
Reproduced with permission from: Pediatrics, Vol. 140, doi: 10.1542/peds.2017-1904. Copyright © 2017 by the AAP.
Clinical progression of transtentorial herniation
Headache
Altered level of consciousness
Dilation of ipsilateral pupil
Cranial nerve III palsy

Ptosis
Loss of medial gaze
Decerebrate posturing
Hemiparesis
Dilation of opposite pupil
Alteration of respiration
Bradycardia
Hypertension
Respiratory arrest
Oculocephalic and caloric response
Oculocephalic (doll's eyes) response: This test should not be performed if a

cervical spine injury is suspected. Observe the motion of the eyes while passively
moving the head. In a comatose patient, conjugate movement of the eyes in the
direction opposite to the head movement is expected. An absent or asymmetric
response in an unconscious patient implies brainstem dysfunction.
Caloric response: After visually checking that the tympanic membrane is intact,
ice cold water is used to irrigate the ear canal and should produce a slow
conjugate deviation toward the irrigated side. An absent or asymmetric response
indicates brainstem dysfunction. Intact eye deviation with nystagmus suggests
that the patient may not be in coma.
Adapted from: Bateman DE. Neurologic assessment of coma. J Neurol Neurosurg Psychiatry
2001; 71 Suppl 1:13.
Decorticate/decerebrate postures
Red flags for child physical abuse on examination
Bruises
Any bruising in infants four months of age or younger

More than one bruise in a pre-mobile infant and more than two bruises in a crawling child
Bruises located on the trunk, ear, neck, jawline, cheek, or buttocks
Bruises with a pattern of the striking object (eg, slap, belt, or loop marks; spoons; spatulas; or other objects)
Human bite marks
Oral injuries
Lip lacerations or bruising, especially in nonambulatory infants

Lingual or labial frenulum tears, especially in nonambulatory infants
Tongue lacerations, especially in nonambulatory infants
Bruising or wounds of the buccal mucosa, gums, or palate, especially in nonambulatory infants
Missing or fractured teeth with an absent or implausible history
Maxillary or mandibular fractures with an absent or implausible history
Bruising, lichenification, or scarring at the corners of the mouth from being gagged
Burns
Scalds in children <5 years of age that do not fit an unintentional spill pattern
Scalds from hot tap water due to immersion, demonstrating a sharp upper line of demarcation ("high tide mark"), affecting both sides of the body
symmetrically, or involving the lower extremities and/or perineum
Burns that have a sharply demarcated edge in the shape of the burning object (eg, clothing iron, spatulas, spoons, grates, metal hairdryer grids,
curling irons, or the metal tops of butane cigarette lighters)
Cigarette burns that appear as discreet circular burns 8 to 12 mm in diameter and are deep (eg, third degree burns)
Fractures
Metaphyseal corner fractures

Rib fractures
Fractures of the sternum, scapula, or spinous processes
Long bone fracture in a nonambulatory infant
Multiple fractures in various stages of healing
Bilateral acute long-bone fractures
Vertebral body fractures and subluxations in the absence of a history of high force trauma
Digital fractures in children younger than 36 months of age
Epiphyseal separations
Severe skull fractures in children younger than 18 months of age
Serious injury without explanation*
Subdural hematoma or retinal hemorrhage in a young child, without a significant public trauma such as a fall out a tall building window or a car crash
Other intracranial injury without a clear trauma history
Abdominal injury (perforation or hematoma of the bowel, pancreas, or bladder; solid organ [eg, liver, spleen, or kidney] hematoma or laceration)
* Any major traumatic injury without a plausible explanation is concerning for child abuse. More minor injuries may also warrant further evaluation for child
abuse depending upon the patient's age. Refer to UpToDate content on diagnostic evaluation for physical child abuse.
Clinical features that may indicate intracranial pathology in children and adolescents with headache
Headache characteristics
Headache awakens the child or occurs consistently upon awakening from sleep
Short or paroxysmal headache; thunderclap headache (uncommon in children)
Associated neurologic signs and symptoms (eg, persistent nausea/vomiting, altered mental status, ataxia, etc)
Headache worsened in recumbent position or by cough, micturition, defecation, or physical activity
Absence of aura
Chronic progressive headache pattern
Change in quality, severity, frequency, or pattern of headache
Occipital headache
Recurrent localized headache
Lack of response to medical therapy
Headache duration of less than six months
Patient history
Inadequate history (description of headache and relative features)
Risk factor for intracranial pathology (eg, sickle cell disease, immune deficiency, malignancy or history of malignancy, coagulopathy, cardiac disease with
right-to-left intracardiac shunt, head trauma, neurofibromatosis type 1, tuberous sclerosis complex, pre-existing hydrocephalus or shunt)
Age <6 years
Personality change
Deterioration of school work
Associated symptoms in the neck or back
Family history
Absence of family history of migraine
Examination findings
Child uncooperative (unable to complete neurologic examination)
Abnormal neurologic examination (eg, ataxia, weakness, diplopia, abnormal eye movements, other focal signs)
Papilledema or retinal hemorrhages
Growth abnormalities (increased head circumference, short stature or deceleration of linear growth, abnormal pubertal progression, obesity)
Nuchal rigidity
Signs of trauma
Cranial bruits
Skin lesions that suggest a neurocutaneous syndrome (neurofibromatosis, tuberosis sclerosis complex)
Data from:
1. Lewis DW, Ashwal S, Dahl G, et al. Practice parameter: Evaluation of children and adolescents with recurrent headaches: Report of the Quality Standards
Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology 2002; 59:490.
2. Newton RW. Childhood headache. Arch Dis Child Educ Pract Ed 2008; 93:105.
3. Prince JS, Gunderman R, Coley BD, et al. Expert Panel on Pediatric Imaging. ACR Appropriateness Criteria. Headache - Child. American College of
Radiology, Reston, VA, 2008.
www.acr.org/SecondaryMainMenuCategories/quality_safety/app_criteria/pdf/ExpertPanelonPediatricImaging/HeadacheChildDoc3.aspx (Accessed on March
17, 2011).
4. Strasburger VC, Brown RT, Braverman PK, et al. Headache. In: Adolescent Medicine: A Handbook for Primary Care, Lippincott Williams & Wilkins,
Philadelphia 2006. p.25.
5. Wilne S, Koller K, Collier J, et al. The diagnosis of brain tumours in children: A guideline to assist healthcare professionals in the assessment of children
who may have a brain tumour. Arch Dis Child 2010; 95:534.
6. Seshia SS, Abu-Arafeh I, Hershey AD. Tension-type headache in children: The Cinderella of headache disorders! Can J Neurol Sci 2009; 36:687.
Ophthalmic findings in the Parinaud syndrome
Vertical gaze abnormalities, especially upgaze
Downward gaze preference or tonic downward deviation of the eyes ("setting-sun sign")
Primary position upbeat or downbeat nystagmus
Impaired convergence and divergence
Excessive convergence tone
Convergence-retraction nystagmus
Skew deviation, often with the higher eye on the side of the lesion
Alternating adduction hypertropia or alternating adduction hypotropia
Bilateral upper eyelid retraction (Collier "tucked-lid" sign)
Bilateral ptosis
Pupillary abnormalities (large with light-near dissociation)
Modified with permission from: Lee AG, Brazis PW. Clinical Pathways in Neuro-ophthalmology: An Evidence-based Approach, Thieme, New York 1998.
Congenital superior oblique palsy of the left eye
(A) A typical abnormal head position is shown. The head is tilted to the right, away from
the side of the palsied muscle. The chin is tilted downward slightly. In this head posture,
the child fuses and avoids diplopia.
(B) There is a small left hypertropia (upward deviation) in primary gaze when the head
is nearly straightened; this is the first step in the "three-step test".
(C) The left hypertropia is worse in gaze to the right; this is the second step in the
"three-step test".
(D) A large left hypertropia is seen on forced (by the mother's hand) left head tilt; this is
the third step in the "three-step test".
Reproduced with permission from: Tasman W, Jaeger E. The Wills Eye Hospital Atlas of Clinical
Ophthalmology, 2nd ed, Lippincott Williams & Wilkins, Philadelphia 2001. Copyright ©2001
Lippincott Williams & Wilkins.
Glasgow Coma Scale and Pediatric Glasgow Coma Scale
Glasgow Coma
Sign Pediatric Glasgow Coma Scale [2] Score
Scale [1]
Eye opening Spontaneous Spontaneous 4
To command To sound 3
To pain To pain 2
None None 1
Verbal Oriented Age-appropriate vocalization, smile, or orientation to sound, interacts (coos, babbles), follows 5
response objects
Confused, disoriented Cries, irritable 4
Inappropriate words Cries to pain 3
Incomprehensible sounds Moans to pain 2
None None 1
Motor Obeys commands Spontaneous movements (obeys verbal command) 6

response
Localizes pain Withdraws to touch (localizes pain) 5
Withdraws Withdraws to pain 4
Abnormal flexion to pain Abnormal flexion to pain (decorticate posture) 3
Abnormal extension to pain Abnormal extension to pain (decerebrate posture) 2
None None 1
Best total score 15
The Glasgow Coma Scale (GCS) is scored between 3 and 15, 3 being the worst, and 15 the best. It is composed of three parameters: best eye
response (E), best verbal response (V), and best motor response (M). The components of the GCS should be recorded individually; for example,
E2V3M4 results in a GCS of 9. A score of 13 or higher correlates with mild brain injury, a score of 9 to 12 correlates with moderate injury, and a
score of 8 or less represents severe brain injury. The pediatric Glasgow coma scale (PGCS) was validated in children two years of age or younger.
Data from:
1. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 1974; 2:81.
2. Holmes JF, Palchak MJ, MacFarlane T, Kuppermann N. Performance of the pediatric Glasgow coma scale in children with blunt head trauma. Acad Emerg
Med 2005; 12:814.
Radiographic findings suggestive of elevated ICP
Evidence of contusions with surrounding edema (top arrow), effacement of

cisterns (middle arrow), and effacement of sulci (lowest arrow).
Common poisoning syndromes (toxidromes)
Mental
Toxidrome Pupils Vital signs Other manifestations Examples of toxic agents
status
Sympathomimetic Hyperalert, Mydriasis Hyperthermia, Diaphoresis, tremors, hyperreflexia, Cocaine, amphetamines, cathinones,
agitation, tachycardia, seizures ephedrine, pseudoephedrine,
hallucinations, hypertension, phenylpropanolamine, theophylline,
paranoia widened pulse caffeine
pressure,
tachypnea,
hyperpnea
Anticholinergic Hypervigilance, Mydriasis Hyperthermia, Dry flushed skin, dry mucous Antihistamines, tricyclic antidepressants,
agitation, tachycardia, membranes, decreased bowel cyclobenzaprine, orphenadrine,
hallucinations, hypertension, sounds, urinary retention, antiparkinson agents, antispasmodics,
delirium with tachypnea myoclonus, choreoathetosis, phenothiazines, atropine, scopolamine,
mumbling picking behavior, seizures (rare) belladonna alkaloids (eg, Jimson Weed)
speech, coma
Hallucinogenic Hallucinations, Mydriasis Hyperthermia, Nystagmus Phencyclidine, LSD, mescaline, psilocybin,

perceptual (usually) tachycardia, designer amphetamines (eg, MDMA
distortions, hypertension, ["Ecstasy"], MDEA)
depersonalization, tachypnea
synesthesia,
agitation
Opioid CNS depression, Miosis Bradypnea, apnea Hyporeflexia, pulmonary edema, Opioids (eg, heroin, morphine,
coma characteristic; May needle marks methadone, oxycodone, hydromorphone),
develop: diphenoxylate
hypothermia,
bradycardia,
hypotension
Sedative-hypnotic CNS depression, Variable Often normal, but Hyporeflexia Benzodiazepines, barbiturates,
confusion, stupor, may develop: carisoprodol, meprobamate, glutethimide,
coma hypothermia, alcohols, zolpidem
bradycardia,
hypotension,
apnea, bradypnea
Cholinergic Confusion, coma Miosis Bradycardia, Salivation, urinary and fecal Organophosphate and carbamate
hypertension or incontinence, diarrhea, emesis, insecticides, nerve agents, nicotine,
hypotension, diaphoresis, lacrimation, GI pilocarpine, physostigmine, edrophonium,
tachypnea or cramps, bronchoconstriction, bethanechol, urecholine
bradypnea muscle fasciculations and
weakness, seizures
Serotonin Confusion, Mydriasis Hyperthermia, Tremor, myoclonus, hyperreflexia, MAOIs alone or with: SSRIs, meperidine,
syndrome agitation, coma tachycardia, clonus, diaphoresis, flushing, dextromethorphan, TCAs, L-tryptophan
hypertension, trismus, rigidity, diarrhea
tachypnea
LSD: lysergic acid diethylamide; MDMA: 3,4-methylenedioxymethamphetamine; MDEA: methylenedioxymethamphetamine; CNS: central nervous system; GI:
gastrointestinal; MAOI: monoamine oxidase inhibitor; SSRI: selective serotonin reuptake inhibitor; TCA: tricyclic antidepressant.
Laboratory evaluation for suspected inborn errors of metabolism
Comments
Initial evaluation*
Blood tests
CBC with
differential
Blood glucose
Electrolytes,
BUN, creatinine,
uric acid
Arterial blood
gas
Plasma ammonia Should be obtained from artery or vein without a tourniquet. The tube should be placed on ice for transport to the laboratory and
analyzed immediately. If the plasma ammonia concentration is >100 micromol/L (1.7 mcg/mL), the measurement should be
repeated immediately.
AST, ALT, If the patient has signs of liver disease.

bilirubin, PT
LDH, aldolase,
creatine, kinase
Urine tests
Color, odor
Urinalysis
Reducing
substances
Myoglobin If the patient has signs or symptoms of myopathy.
Specialized tests
Blood tests
Quantitative Plasma amino acid analysis must be performed quantitatively rather than qualitatively.
plasma amino
acids
Lactate and Lactate and pyruvate should be measured in arterial blood and transported on ice.
pyruvate
Acylcarnitine Analysis of acylcarnitine conjugates is performed by tandem mass spectrometry and can be measured in a plasma sample or a
profile filter-paper bloodspot. Serum is preferred because of inherent problems in quantitating compounds from a filter-paper blood spot
Urine tests
Qualitative urine Minimum of 2 to 5 mL in sterile container without preservative.

organic acids
CBC: complete blood count; BUN: blood urea nitrogen; AST: aspartate aminotransferase; ALT: alanine aminotransferase; PT: prothrombin time; LDH: lactate
dehydrogenase.
* If possible, blood and urine samples should be obtained for both the initial and specialized tests at the time of presentation. Samples for specialized tests
should be processed and stored appropriately for further testing if indicated.
Rapid overview: Emergency management of infants (≥1 month) and children with suspected bacterial meningitis
Clinical findings
Infants: Fever, hypothermia, bulging fontanel, lethargy, irritability, seizures, respiratory distress, poor feeding, vomiting.
Older children: Fever, headache, photophobia, meningismus, nausea/vomiting, confusion, lethargy, irritability.
Evaluation
Laboratory testing – Initial laboratory testing should include (STAT):
Blood cultures (two sets).
CBC with differential and platelet count.
Serum electrolytes, BUN, creatinine, glucose.
PT, INR, and PTT.
Lumbar puncture:
LP should be performed in all children with suspected meningitis unless there is a specific contraindication to LP.
Contraindications to LP include: Cardiopulmonary compromise, clinical signs of increased intracranial pressure, papilledema, focal neurologic signs,
and skin infection over the site for LP. If there is a contraindication to or inability to perform an LP, or if the LP is delayed by the need for cranial
imaging, antimicrobial therapy should not be delayed. Blood cultures should be obtained and empiric antibiotics administered as soon as is
possible.
CSF should be sent for the following (STAT): Cell count and differential, glucose and protein concentration, Gram stain, and culture.
Neuroimaging (eg, head CT):

In children who require neuroimaging before LP, blood cultures should be obtained and empiric antibiotics administered before imaging.
LP should be performed as soon as possible after neuroimaging is completed, provided that the imaging has not revealed any contraindications.
Indications for neuroimaging before LP include: Severely depressed mental status (coma), papilledema, focal neurologic deficit (with the exception
of cranial nerve VI or VII palsy), history of hydrocephalus and/or presence of a CSF shunt, recent history of CNS trauma or neurosurgery.
Management
Supportive care:
Ensure adequate oxygenation, ventilation, and circulation.
Obtain venous access and initiate cardiorespiratory monitoring while obtaining laboratory studies.
Keep the head of bed elevated at 15 to 20 degrees.
Treat hypoglycemia, acidosis, and coagulopathy, if present.
Antimicrobial therapy – Antibiotic therapy should be initiated immediately following the LP if the clinical suspicion for meningitis is high:
Administer first dose of empiric antimicrobial therapy:
Vancomycin (15 mg/kg IV), plus
Ceftriaxone (50 mg/kg IV) or cefotaxime (100 mg/kg IV; where available).
Consider dexamethasone therapy* (0.15 mg/kg IV) in patients with certain risk factors (eg, unimmunized patients, young children [age ≥6 weeks
to ≤5 years], children with sickle cell disease, asplenic patients) or if there is known or suspected Haemophilus influenzae infection (eg, based on
Gram stain results).
If dexamethasone is given, it should be administered before, or immediately after, the first dose of antimicrobial therapy.
STAT: intervention should be performed emergently; CBC: complete blood count; BUN: blood urea nitrogen; PT: prothrombin time; INR: international normalized
ratio; PTT: partial thromboplastin time; LP: lumbar puncture; CSF: cerebrospinal fluid; CT: computed tomography; CNS: central nervous system; IV:
intravenous.
* Decisions regarding the administration of dexamethasone should be individualized. The use of dexamethasone in children with suspected meningitis is
controversial, and the opinions of UpToDate authors regarding this issue differ. One UpToDate author would administer dexamethasone only to children who are
known or highly suspected to have H. influenzae (Hib) at the time the LP is performed (a fairly uncommon scenario), whereas another UpToDate author would
administer dexamethasone to all young children (age ≥6 weeks to ≤5 years old) with community-acquired meningitis and to children with sickle cell disease or
asplenia with suspected bacterial meningitis. The 2015 Red Book statement on dexamethasone use in pneumococcal meningitis also acknowledges that expert
opinion differs on this issue. Evidence supporting the efficacy of dexamethasone in reducing the risk of hearing loss in children with meningitis is most clearly
established for infections caused by Hib. For other bacterial pathogens (eg, pneumococcus, meningococcus), the efficacy of dexamethasone is uncertain. For
further details, refer to UpToDate topics on bacterial meningitis in children, pneumococcal meningitis in children, and the use of dexamethasone and other
measures to prevent neurologic complications of pediatric bacterial meningitis.
Rapid overview for hypoglycemia in adolescents and children, other than neonates
Clinical features
Any patient with acute lethargy or coma should have an immediate measurement of blood glucose to determine if hypoglycemia is a possible cause
Other findings of hypoglycemia are nonspecific* and vary by age:
Infants
Irritability
Lethargy
Jitteriness
Feeding problems
Hypothermia
Hypotonia
Tachypnea
Cyanosis
Apnea
Seizures
Older children and adolescents
Autonomic response (tends to occur with blood glucose <50 to 65 mg/dL)
Sweating
Tachycardia
Palpitations
Tremor
Nervousness
Hunger
Paresthesias
Pallor
Neuroglycopenia
Irritability
Confusion
Uncharacteristic behavior
Weakness
Seizures
Coma
Occasionally, transient focal neurologic deficits
Diagnosis
Obtain rapid bedside blood glucose concentration (and β-hydroxybutyrate, if available as a point-of-care measurement)
Confirm the presence of hypoglycemia with a simultaneously drawn plasma glucose
Treat, as outlined below, if the bedside value is low (<70 mg/dL [3.89 mmol/L]) in symptomatic patients
Obtain a blood sample for additional diagnostic studies prior to glucose administration, if possible, and collect the first voided urine after the
hypoglycemic event in all infants and young children who are not being treated for diabetes mellitus or do not have a known cause for hypoglycemia ¶
Treatment
Do not delay treatment if symptomatic hypoglycemia is suspected. However, every reasonable effort should be made to obtain a rapid blood glucose
measurement prior to administering glucose.
Give glucose based upon the patients level of consciousness and ability to swallow safely (ie, alert enough to do so and with intact
gag reflex) as follows:
Conscious and able to drink and swallow safely:
Administer 0.3 g/kg (10 to 20 g) of a rapidly-absorbed carbohydrate. 15 g is supplied by 3 glucose tablets, a tube of gel with 15 g, 4 oz (120
mL) sweetened fruit juice, 6 oz non-diet soda, or a tablespoon (15 mL) of honey or table sugar. May repeat in 10 to 15 minutes.
Altered mental status, unable to swallow, or does not respond to oral glucose administration within 15 minutes:
Give an initial IV bolus of glucose of 0.25 g/kg of dextrose (maximum single dose 25 g). Δ The volume and concentration of glucose bolus is
infused slowly at 2 to 3 mL per minute and based upon age:
2.5 mL/kg of 10% dextrose solution (D10W) in infants and children up to 12 years of age (10% dextrose is 100 mg/mL)
1 mL/kg of 25% dextrose (D25W) or 0.5 mL/kg of 50% dextrose (D50W) in adolescents (25% dextrose is 250 mg/mL; 50% dextrose is 500
mg/mL)
Unable to receive oral glucose and unable to obtain IV access:
Give glucagon 0.03 mg/kg IM or SQ (maximum dose 1 mg): ◊
Perform blood glucose monitoring every 10 to 15 minutes as the effects of glucagon may be transient
Establish vascular access as soon as possible
After initial hypoglycemia is reversed, provide additional glucose and treatment based upon suspected etiology:
Give children and adolescents with type I diabetes mellitus a normal diet
Give patients with an unknown cause of hypoglycemia intravenous infusion of dextrose 10% (6 to 9 mg/kg per minute) titrated to maintain blood
glucose in a safe and appropriate range (70 to 150 mg/dL [3.89 to 8.33 mmol/L])
Give patients, who have ingested a sulfonylurea and have recurrent hypoglycemia, octreotide (dose: 1 to 1.5 mcg/kg IM or SQ, maximum dose
150 mcg every 6 hours) in addition to glucose. (Refer to UpToDate topic on sulfonylurea poisoning.)
Measure a rapid blood and plasma glucose 15 to 30 minutes after the initial IV glucose bolus and then monitor every 30 to 60 minutes until stable
(minimum of four hours) to ensure that plasma glucose concentration is maintained in the normal range (>70 to 100 mg/dL [>3.89 to 5.55 mmol/L])
Obtain pediatric endocrinology consultation for patients with hypoglycemia of unknown cause
Obtain medical toxicology consultation for patients with ingestion of oral hypoglycemic agents by calling the United States Poison Control Network at
1-800-222-1222 or access the World Health Organization's list of international poison centers
Admit the following patients:
Cannot maintain normoglycemia with oral intake
Hypoglycemia of unknown cause
Ingestion of long-acting hypoglycemic agents
Recurrent hypoglycemia during the period of observation
IV: intravenous; IM: intramuscular; SQ: subcutaneous; D10W: 10% dextrose in water; D25W: 25% dextrose in water; D50W: 50% dextrose in water.
* These findings may also occur in infants with sepsis, congenital heart disease, respiratory distress syndrome, intraventricular hemorrhage, other metabolic
disorders, and in children and adolescents with a variety of underlying conditions.
¶ Specific laboratory studies to obtain in children include blood samples for glucose, insulin, C-peptide, beta-hydroxybutyrate, lactate (free flowing blood must be
obtained without a tourniquet), plasma acylcarnitines, free fatty acids, growth hormone, and cortisol.
Δ Higher doses of glucose (eg, 0.5 to 1 g/kg [5 to 10 mL/kg of 10% dextrose in water or 2 to 4 mL/kg of 25% dextrose in water]) may be needed to correct
hypoglycemia caused by sulfonylurea ingestion. (For more detail, refer to UpToDate topic on sulfonylurea agent poisoning.)
◊ Glucagon will reverse hypoglycemia caused by excess endogenous or exogenous insulin and will not be effective in patients with inadequate glycogen stores
(prolonged fasting), ketotic hypoglycemia, or are unable to mobilize glycogen (glycogen storage diseases). Of note, children may exhaust their glycogen stores in
as little as 12 hours. Other conditions in which glycogen cannot be effectively mobilized include ethanol intoxication in children, adrenal insufficiency, and certain
inborn errors of metabolism (eg, a disorder of glycogen synthesis and glycogen storage diseases).
Causes of coma
I. Symmetrical, nonstructural II. Symmetrical, structural
Toxins Supratentorial
Lead Bilateral internal carotid occlusion
Thallium Bilateral anterior cerebral artery occlusion
Mushrooms Sagittal sinus thrombosis
Cyanide Subarachnoid hemorrhage
Methanol Thalamic hemorrhage*
Ethylene glycol Trauma-contusion, concussion*
Carbon monoxide Hydrocephalus
Drugs Infratentorial
Sedatives Basilar occlusion*
Barbiturates* Midline brainstem tumor
Other hypnotics Pontine hemorrhage*
Tranquilizers Central pontine myelinolysis
Bromides III. Asymmetrical, structural

Alcohol
Supratentorial
Opiates
Thrombotic thrombocytopenic purpura ¶
Paraldehyde
Disseminated intravascular coagulation
Salicylate
Nonbacterial thrombotic endocarditis (marantic endocarditis)
Psychotropics
Subacute bacterial endocarditis
Anticholinergics
Fat emboli
Amphetamines
Unilateral hemispheric mass (tumor, abscess, bleed) with herniation
Lithium
Subdural hemorrhage bilateral
Phencyclidine
Intracerebral bleed
Monoamine oxidase inhibitors
Pituitary apoplexy ¶
Metabolic
Massive or bilateral supratentorial infarction
Hypoxia
Multifocal leukoencephalopathy
Hypercapnia Creutzfeldt-Jakob disease
Hypernatremia*
Adrenal leukodystrophy
Hypoglycemia* Cerebral vasculitis
Hyperglycemic nonketotic coma
Cerebral abscess
Diabetic ketoacidosis
Subdural empyema
Lactic acidosis Thrombophlebitis ¶
Hypercalcemia
Multiple sclerosis
Hypocalcemia Leukoencephalopathy associated with chemotherapy
Hypermagnesemia
Acute disseminated encephalomyelitis
Hyperthermia
Infratentorial
Hypothermia
Brainstem infarction
Reye syndrome
Brainstem hemorrhage
Aminoacidemia
Brainstem thrombencephalitis
Wernicke encephalopathy
Porphyria
Hepatic encephalopathy*
Uremia
Dialysis encephalopathy
Addisonian crisis
Hypothyroidism
Infections
Bacterial meningitis
Viral encephalitis
Postinfectious encephalomyelitis
Syphilis
Sepsis
Typhoid fever
Malaria
Waterhouse-Friderichsen syndrome
Psychiatric
Catatonia
Other
Postictal seizure*
Diffuse ischemia (myocardial infarction, heart failure, arrhythmia)
Hypotension
Fat embolism*
Hypertensive encephalopathy
Hypothyroidism
Nonconvulsive status epilepticus
Heat stroke
* Relatively common asymmetrical presentation.

¶ Relatively symmetrical presentation.
Reproduced with permission from: Berger JR. Clinical Approach to Stupor and Coma. In: Neurology in Clinical Practice: Principles of Diagnosis and Management,
4th ed, Bradley WG, Daroff RB, Fenichel GM, Jankovic J (Eds), Butterworth Heinemann, Philadelphia, PA 2004. p.46. Copyright © 2004 Elsevier.
Drug- and toxin-induced mental status alterations
Central nervous system depression Agitation

Anticholinergics Amantadine
Antihistamines Sympathomimetics
Belladonna alkaloids Amphetamines
Phenothiazines Cocaine
Antidepressants Caffeine
Cyclic antidepressants Phenylpropanolamine
Selective serotonin reuptake inhibitors Theophylline
Monoamine oxidase inhibitors Cathinones
Antipsychotics Anticholinergics
Simple asphyxiants Antihistamines
Carbon dioxide Atropine
Inert gases Scopolamine
Cellular asphyxiants Antiparkinson agents
Antispasmodics
Carbon monoxide
Muscle relaxants
Cyanide
Plants containing belladonna alkaloids
Hydrogen sulfide
Phenothiazines
Methemoglobinemia
Tricyclic antidepressants
Lithium
Salicylates
Cholinergics
Central hallucinogens
Organophosphates
Lysergic acid diethylamide (LSD)
Carbamates
Phencyclidine
Sympatholytics
Mescaline
Beta blockers
Psilocybin
Clonidine
Ketamine
Sedative-hypnotics
Designer amphetamines
Benzodiazepines
Synthetic cannabinoids
Barbiturates
Drug withdrawal states
Muscle relaxants
Lithium
Hypoglycemic agents
Carbon monoxide
Heavy metals
Hypoglycemic agents
Opiates
Heavy metals
Antiepileptics
Mushrooms
Salicylates
Gamma-hydroxybutyrate
Volatile inhalants
Alcohols
Life-threatening and common causes of headache in children
Infection
Bacterial meningitis*
Viral encephalitis*
Orbital or cerebral abscess*
Viral infection, including viral meningitis ¶
Lyme meningitis
Pharyngitis ¶
Otitis media ¶
Sinusitis ¶
Dental infection ¶
Increased intracranial pressure

Tumor*
Hydrocephalus*
Intracranial hemorrhage*
Idiopathic intracranial hypertension
Other conditions
Carbon monoxide poisoning*
Hypertensive encephalopathy*
Temporomandibular joint dysfunction
Cluster headache
Primary headache
Migraine ¶
Tension-type headache ¶
Chronic daily headache
* Life-threatening condition.
¶ Common condition.
Treatment of acute brain herniation or symptomatic intracranial hypertension (ICP >20 mmHg [27 cm H 2 0]) in
children*
RSI: rapid sequence intubation; GCS: Glasgow coma scale; ICP: intracranial pressure.
* This algorithm is intended for children in whom increased ICP is diagnosed based upon neuroimaging or intracranial monitoring, or in whom it is strongly suspected
based upon signs of brain herniation. Refer to UpToDate topics on elevated ICP in children.
¶ A large diuresis is expected with mannitol and may require normal saline boluses to prevent hypotension. Thus, placement of a urinary Foley catheter is suggested.
Monitoring of serum osmolal gap is necessary to avoid complications. Refer to UpToDate topics on the management of elevated ICP in children.
Δ When administering 3% saline, the expected serum sodium rise is 1 mEq/L for every 1 mL/kg bolus, and 1 mEq/L/hour for every 1 mL/kg/hour of continuous
infusion. Monitoring of serum sodium is necessary to avoid complications. Patients with a serum sodium level >160 mEq/L are unlikely to benefit from hypertonic
saline administration. Refer to UpToDate topics on management of elevated ICP in children.
◊ Temporary therapeutic hyperventilation (PaCO 2 30 to 35 mmHg) may be initiated under direction by a neurosurgeon for patients with signs of impending
herniation in whom surgical intervention is planned. If used, avoid hyperventilation for longer than 2 hours.
§ Monitor total dose of lidocaine administered to avoid lidocaine toxicity.
Adapted from: Stevens RD, Shoykhet M, Cadena R. Emergency Neurological Life Support: Intracranial Hypertension and Herniation. Neurocrit Care 2015; 23 Suppl
2:S76.
Contributor Disclosures
Robert C Tasker, MBBS, MD Nothing to disclose Susan B Torrey, MD Nothing to disclose Marc C Patterson, MD,
FRACP Grant/Research/Clinical Trial Support: Orphazyme [Niemann-Pick disease, type C (Arimoclomol)]; Shire [Metachromatic leukodystrophy
(Enzyme replacement therapy)]. Consultant/Advisory Boards: Actelion [Niemann-Pick C (Miglustat)]; Agios [CGD]; Alexion [General lysosomal
diseases, lysosomal acid lipase deficiency (Sebelipase alfa)]; Amicus [Fabry, Gaucher, Pompe (Migalastat)]; Cerecor [Congenital disorders of
glycosylation]; IntraBio [General lysosomal diseases and ataxic disorders]; Novartis [Multiple sclerosis (Sphingolimod)]; Orphazyme [Niemann-Pick
disease, type C]; Shire [Metachromatic leukodystrophy]; Vtesse [Niemann-Pick disease, type C (Cyclodextrin)]. Equity Ownership/Stock Options:
IntraBio [General lysosomal diseases and ataxic disorders]. Other Financial Interest: Sage [Honorarium as Editor-in-Chief of Journal of Child
Neurology and Child Neurology Open]. Adrienne G Randolph, MD, MSc Grant/Research/Clinical Trial Support: Genentech [lipid biomarkers in
influenza critical illness]. Consultant/Advisory Boards: La Jolla Pharmaceuticals [Angiotensin 2 in pediatric refractory shock]; Bristol Myers Squibb
[PD1 inhibitors in sepsis induced immunoparalysis]. James F Wiley, II, MD, MPH Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level
review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

Elevated Intracranial Pressure

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Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis - UpToDate 13/03/19 19.

Official reprint from UpToDate®

Elevated intracranial pressure (ICP) in children: Clinical manifestations and

● Brain parenchyma – 80 percent

ICP = Pss + (Iformation x RCSF)

● Sagittal sinus pressure (Pss) – 5 to 8 mmHg

● Parenchymal brain swelling

CPP = MAP - ICP

CBF = (CAP - JVP) ÷ CVR

The following factors significantly impact CBF:

Interstitial edema responds to therapies to reduce CSF pressure.

● Loss of autoregulation resulting in excessive cerebral blood flow (CBF)

● Increased CSF production in response to cerebral hyperemia

● Vomiting – Vomiting frequently accompanies acute rises in ICP.

● Other herniation – Characteristic features identify other types of herniation:

• A natural preference for the "knee-chest" position

• Neck pain or stiffness

Findings consistent with elevated ICP on head CT include [24,25]:

● Cerebral blood flow [30]

● CSF flow velocity through the cerebral aqueduct [31]

● ≤1 year or open fontanel: 5.2 mm (sensitivity 80 to 85 percent, specificity 75 to 76 percent)

● Serum electrolytes, calcium, magnesium

SUMMARY AND RECOMMENDATIONS

• Headache (verbal children)

Use of UpToDate is subject to the Subscription and License Agreement.

Topic 6077 Version 16.0

Causes of intracranial hypertension*

Traumatic brain injury/intracranial hemorrhage

Subdural, epidural, or intraparenchymal hemorrhage

Diffuse axonal injury

Arteriovenous malformation or other vascular anomalies

Central nervous system infections (eg, encephalitis, meningitis, abscess)

Idiopathic intracranial hypertension (pseudotumor cerebri)

Graphic 69683 Version 9.0

Intracranial compensation for mass

Normally, the intracranial components are in equilibrium as shown in

Graphic 65853 Version 5.0

The relationship between intracranial volume and

An initial increase in volume results in a small increase in pressure because

Graphic 54602 Version 2.0

Cerebral autoregulation in hypertension

Schematic representation of autoregulation of cerebral blood flow in

Redrawn from: Kaplan NM. Management of hypertensive emergencies. Lancet 1994;

Graphic 57676 Version 4.0

Causes of cerebral edema in children*

Severe head trauma

Graphic 106133 Version 2.0

Graphic 76974 Version 5.0

Head circumference-for-age percentiles, girls 0 to 36 months, CDC

Graphic 59076 Version 3.0

Head circumference-for-age percentiles, boys birth to 36 months, CDC

Graphic 80863 Version 3.0

Papilledema, characterized by blurring of the optic disc margins, loss of

Courtesy of Gerald Striph, MD.

Graphic 50378 Version 1.0

Respiratory rate (breaths/minute) Heart rate (beats/minute)

Age Normal range Normal range

0 to 3 months 25 34-57 66 107 123-164 181

3 to <6 months 24 33-55 64 104 120-159 175

6 to <9 months 23 31-52 61 98 114-152 168

9 to <12 months 22 30-50 58 93 109-145 161

12 to <18 months 21 28-46 53 88 103-140 156

18 to <24 months 19 25-40 46 82 98-135 149