Pediatric Intracranial Hypertension

Shawn C. Aylward, MD,* Rachel E. Reem, MD†

*Department of Neurology and †Department of Ophthalmology, Nationwide Children’s Hospital, Columbus, OH

Education Gap
Intracranial hypertension can lead to significant morbidity; because it is a
rare disorder, the general practitioner can easily miss cases.

Objectives After completing this article, readers should be able to:

1. Recognize the clinical features of intracranial hypertension.

2. Understand the basics of the ophthalmologic examination.
3. Recognize potential causative factors contributing to intracranial
hypertension.
4. Appropriately initiate the evaluation in suspected cases and start
management in confirmed cases.

Abstract
Headaches are common in the clinical setting. Fortunately, intracranial
hypertension (IH) is rare, but when present it can lead to significant
morbidity. Early diagnosis and proper management are important to
lessen the potential morbidity. Careful headache history, ophthalmologic
examination, head imaging, and lumbar puncture (LP) are crucial tools in
the diagnosis of this condition. Management should be coordinated with
a neurologist, ophthalmologist, or neuro-ophthalmologist.

AUTHOR DISCLOSURE Drs Aylward and

Reem have disclosed no financial
relationships relevant to this article. This
commentary does contain a discussion of
an unapproved/investigative use of a
commercial product/device. CASE PRESENTATION

Two patients present to your general pediatric clinic with separate complaints but
ABBREVIATIONS
BID twice daily related pathology. The first is a 16-year-old girl with a chief complaint of headache.
CSF cerebrospinal fluid She reports a daily headache for the past 3 weeks that is worse in the morning and
ICP intracranial pressure improves over the course of the day but never resolves. On examination she is
IH intracranial hypertension obese (BMI, 29) but is otherwise well-appearing. Funduscopic examination
LP lumbar puncture
reveals blurred disc margins bilaterally. Visual field testing by direct confrontation
MRI magnetic resonance imaging
ONSF optic nerve sheath fenestration
notes constricted peripheral vision on the right side. The next patient is a well-
PIH primary intracranial hypertension appearing 6-year-old boy who presents after failing his vision screening at school.
SIH secondary intracranial hypertension He denies any symptoms, but his mother interjects that he has been complaining

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 of “seeing two of things” intermittently for the past few bacterial meningitis, probably due to cerebral hyperemia.
months. On examination he is a well-appearing boy with Later presentation of SIH is due to cerebral edema, obstruc-
normal growth indices. He has a slight left esotropia tive hydrocephalus, infarction, and venous thrombosis re-
and complains of diplopia when looking to the far left. sulting from the infection. The literature is filled with case
Funduscopic examination reveals blurred disc margins reports of disseminated Lyme infection and IH. Presenta-
bilaterally. tion is often early in the course and is believed to be the
result of decreased CSF absorption resulting from meningo-
vascular inflammation.
DEFINITION
Craniosynostosis due to premature closure of multiple
The first description of IH in the literature was by Quincke sutures can lead to IH due to reduced intracranial volume
in 1897, and he labeled it meningitis serosa. (1) Since this and distortion of the intracranial venous sinuses.
initial publication, advances in medicine have resulted in a The Table lists medications that have been strongly
multitude of names, including serous meningitis, toxic hydro- linked with SIH. Minocycline, tetracycline, and doxycy-
cephalus, otitic hydrocephalus, hypertensive meningeal hydrops, cline have long been known to cause SIH. This is notable
pseudotumor cerebri, benign intracranial hypertension, idio- because many pediatricians use minocycline as first-line
pathic intracranial hypertension, and pseudotumor cerebri syn- treatment of acne and are not aware of this potential
drome. Today, pseudotumor cerebri and idiopathic intracranial adverse effect. Secondary IH due to minocycline has 3
hypertension are the 2 terms most often used by physicians separate presentation periods in relation to medication
and the public. Unfortunately, the term pseudotumor cerebri initiation: early (2 months), delayed (>2 months), and
can become confusing when a cause for the IH is found; indeterminate (asymptomatic). Cessation of the medi-
thus, we prefer the terms primary IH (PIH) and secondary cation results in return to normal pressure within 1
IH (SIH). Primary refers to cases where no clear causative month, although rarely some patients continue to have
agent for the increased intracranial pressure (ICP) is found, symptoms.
replacing the terms idiopathic intracranial hypertension and Patients receiving growth hormone replacement for
pseudotumor cerebri. Individuals can have risk factors such as growth hormone deficiency can develop symptoms of IH.
female sex, postpubertal status, obesity, or polycystic ovarian The most common scenario is complaints of headache and
syndrome; however, these factors are not believed to directly subsequent discovery of optic nerve edema. Patients typi-
result in increased pressure. cally present during the first 12 weeks of treatment, although
The term SIH is reserved for patients whose IH is the it can occur at any time. Treatment consists of acetazolamide
direct result of another condition (Table). Cerebral venous and cessation of the growth hormone until symptom res-
sinus thrombosis is a common cause of SIH, with the most olution. Once all symptoms have resolved, patients can be
frequent locations being the superior sagittal and transverse started on a lower dose with gradual titration often without
sinuses. Standridge and O’Brien (2) found that 11% of return of symptoms.
patients with IH had evidence of thrombosis on imaging Long-term corticosteroid use can result in SIH; it is felt to
without clear risk factors, highlighting the importance of be due to the weight gain associated with long-term corti-
obtaining a magnetic resonance venogram on all patients. It costeroid use. A rapid wean or withdrawal is linked to a
used to be common for patients with otitis or mastoiditis to rebound increase in ICP and symptoms consistent with
present with IH due to sigmoid and/or jugular thromboses, SIH. Gradual weaning with reduction by no more than 50%
previously referred to as otitic hydrocephalus. Fortunately, over the course of a few weeks reduces the chance of
the modern use of antibiotics for these infections has greatly occurrence.
reduced the frequency of cases. Hypercoagulability in the The adult criteria for PIH are referred to as the modified
acute postpartum period, oral contraceptive use, cancer, and Dandy criteria. These criteria stipulate that a patient has 1)
various inherited coagulopathies can result in thrombosis signs and symptoms of raised ICP (headache, nausea,
and thus SIH. Because cerebrospinal fluid (CSF) is re- vomiting, transient visual obscurations, or papilledema),
absorbed into the venous circulation, the prevailing theory 2) absence of localizing neurologic signs except for unilat-
is that the increased venous pressure results in reduced eral or bilateral abducens nerve palsy, 3) CSF opening
reabsorption and thus increased ICP. pressure greater than 25 cm H2O with normal composi-
Infection involving the intracranial components, such tion, and 4) normal to small ventricles as demonstrated by
as meningitis or meningoencephalitis, can also result in computed tomography (today, magnetic resonance imaging
SIH. Intracranial hypertension is an early presentation in [MRI] is the modality of choice). (3)

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TABLE. Common Causes of Secondary Intracranial Hypertension
MEDICAL CONDITIONS MEDICATIONS

Cerebral venous thrombosis Tetracycline class (minocycline/tetracycline/

doxycycline)
Meningitis/meningoencephalitis Growth hormone
Intracranial hemorrhage Corticosteroids (especially withdrawal)
Brain tumor Lithium carbonate
Lyme disease Cyclosporine A
Demyelinating disease/multiple sclerosis Cytarabine
Leukemia/lymphoma Nalidixic acid
Pregnancy/eclampsia Retinoic acid
Crohn disease Vitamin A excess
Hydrocephalus Vitamin D (deficiency)
Craniofacial syndrome Oral contraceptives (likely secondary to venous
thrombosis)
Chiari malformation
Traumatic brain injury
Refeeding syndrome
Adrenal insufficiency (often on corticosteroids)
Hypoparathyroidism (early in correction)
Vitamin A deficiency

Further revisions to the criteria for PIH by Friedman patients diagnosed as having demyelinating disorders and
and colleagues (4) have attempted to update the criteria found that they had a mean opening pressure of 21.5 cm
and include requirements for pediatric cases and those H2O, higher than the total population mean of 20.3 cm
presenting without optic nerve edema. Concerns have H2O. Morgan-Followell and Aylward (7) evaluated age-
been raised that these stringent criteria will result in and sex-matched cohorts of patients with demyelinating
missed cases and increased potential morbidity. The pedi- conditions and PIH for comparison and found no statis-
atric normative values for CSF opening pressure have tically significant difference in the opening pressure
recently received scrutiny. Older studies determined nor- between the 2 groups. This suggests that demyelinating
mal opening pressures of 18 cm H2O or less for children conditions have elevated opening pressures and that
younger than 8 years and of 25 cm H2O or less for children including them in a normative population may falsely
8 years or older (mirrors adult normal values). Recent elevate the average. Fortunately, the debate surrounding
articles have questioned these values. Using 44 pediatric the normal pressure is rarely needed because patients
patients who had a sedated LP, Lee and Vedanarayanan (5) often have opening pressures well above either cutoff
found a mean opening pressure of 20.3 cm H2O. Avery point. However, to avoid additional morbidities by miss-
et al (6) observed a mean opening pressure of 19.8 cm ing cases, the authors prefer to use the older criteria.
H2O, and the 90th percentile for their cohort was 28 cm
H2O. They also found increases with moderate sedation
EPIDEMIOLOGY
and increased BMI. Both studies included patients with
demyelinating and white matter disorders as well as Traditionally, PIH is thought of as a rare disease. Outside
healthy patients. Other published studies have shown the United States, the annual pediatric incidence is esti-
increased opening pressures in patients with demyelin- mated to be 0.47 per 100,000 in Germany and 0.6 to 0.9
ating conditions. Lee et al conducted a separate analysis of per 100,000 in the provinces of Nova Scotia and Prince

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 Edward Island. A recent study found an annual US PIH understood, and those lacking edema are believed to have
incidence of 0.63 per 100,000 children in a typical Mid- unique anatomical variants at the level of the optic canal.
western city. (8) At presentation, up to 85% of patients able to participate in
Pediatric PIH is typically divided into prepubertal and visual field testing demonstrate a visual field abnormality.
pubertal groups. Those who have entered or completed Enlarged blind spots are the most common visual field defect,
puberty have the same risk factors as adults. Studies have with peripheral constriction, nasal field loss, and inferior
shown a near 1:1 female to male distribution in prepubertal arcuate defects also seen. Visual acuity is often not affected
patients compared with the 4:1 ratio seen in adults. (9) In 2 unless severe edema is present and thus should not be used as
separate studies, obesity was not shown to increase the risk a method to exclude the diagnosis of IH or to monitor prog-
of PIH in prepubertal patients. Examination of pediatric ress. Transient visual obscurations are often reported as brief
patients in a large IH registry found a significantly higher episodes (<30 seconds) of monocular or binocular blurring or
BMI (30.7 versus 21.6) in postpubertal patients with PIH “graying out” of vision. Events occur multiple times per day
compared with their prepubertal counterparts. (10) and can be provoked by position changes.
The literature contains few reports of familial links with Cranial nerve VI palsy is seen in 12% to 60% of patients.
PIH, mostly parent and offspring relationships. Affected Patients often note diplopia when looking in the direction of
siblings have also been reported. the nerve palsy. Often unreported until asked, pulsatile
tinnitus is experienced by up to 44.3% of patients. Distinct
from common tinnitus, it is often described as a “whoosh-
CLINICAL ASPECTS AND DIAGNOSIS
ing” sound coinciding with the heartbeat.
There is variability in clinical presentation depending on age Direct funduscopic examination is used to visualize the
(see the case presentations at the beginning of the article), optic nerve for the presence of edema and, if present, is
with symptoms tending to be less evident in younger graded using the Frisén scale. (11) The Figure contains clear
individuals. In prepubertal children, optic disc edema inci- examples of the different grades of optic edema. (9) Spon-
dentally discovered on routine eye examination is reported taneous venous pulsations are seen in 87% to 90% of the
in up to 33% of patients. Asymptomatic children are typically healthy population. They have also been seen in those with
boys, younger, and less likely to be obese compared with documented elevated ICP, making decisions regarding
their symptomatic counterparts. further evaluation and treatment difficult. The help of an
The most common symptom reported is headache, in up ophthalmologist should be solicited for detailed evaluation
to 96.5% of patients. The headaches are usually constant, of these findings.
with some variability in severity throughout the day. They If the child is able to cooperate, Humphrey or Goldmann
are most often severe in the morning and can be exacerbated visual field testing is performed at the initial and subsequent
by maneuvers such as Valsalva, lying supine, bending over, visits. These tests evaluate the peripheral vision using a
or coughing. dome-shaped screen on which visual targets are projected in
The ophthalmic examination is crucial for the diagnosis static (Humphrey) or dynamic (Goldmann) fashion. The
and subsequent management of IH. The fundamental ability to maintain gaze fixation for 15 to 30 minutes is
parts include pupillary and ocular motility assessments, essential for visual field test reliability; thus, usually these
color vision testing, visual acuity, and funduscopic exam- tests are performed on older, more cooperative children.
ination (with attention to the optic nerve). Humphrey Optical coherence tomography is a noninvasive test that
or Goldmann visual field testing, optical coherence to- evaluates the thickness of the retinal nerve fiber layer
mography of the retinal nerve fiber layer, and fundus surrounding the optic nerve and is used to monitor the
autofluorescence are useful tools for initial evaluation resolution of papilledema during treatment.
and serial monitoring. It is important to note that optic disc drusen, globular
Optic disc edema is frequently seen in IH and is often aggregates of hyaline and calcium salts on the optic nerve,
bilateral. Any patient presenting with unilateral edema can mimic optic nerve edema. When this occurs, the pa-
should raise concerns for other diagnoses, such as optic tient is said to have pseudopapilledema. B-scan ultrasonog-
neuritis. Up to 17.8% lack optic edema at presentation but raphy and fundus autofluorescence photography can be
have other symptoms consistent with elevated ICP (head- used by the ophthalmologist to differentiate between true
ache, nausea, vomiting, transient visual obscurations) and papilledema and pseudopapilledema. Optical coherence
documented elevated opening pressure. The exact mecha- tomography has been explored as a method of differen-
nism by which optic disc edema develops is poorly tiating between the two as well, but as yet this method is

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Figure. Optic nerve edema stages. Left to right. Top row: normal (0), stage 1. Middle row: stage 2, stage 3 (note cotton wool spot with hemorrhage at 5
o’clock). Bottom row: stage 4 (note hemorrhages at 1-2 and 6-8 o’clock, retinal striae due to severity of edema), stage 5. (Reprinted with permission from
Elsevier. [9])

somewhat less reliable. The most reliable method is cur- mass lesion, hydrocephalus, or other conditions that would
rently fluorescein angiography. (12) be a contraindication to performing the LP. All pediatric
Neuroimaging (computed tomography or MRI) should patients diagnosed as having IH should eventually undergo
be performed as an initial step in the evaluation to rule out MRI and magnetic resonance venography to rule out other

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 secondary causes, such as sinus venous thrombosis. Al- complete resolution of symptoms in addition to resolution
though the MRI should be devoid of structural abnormal- of their papilledema.
ities, subtle findings suggestive of IH can sometimes occur, The goal of pharmacologic management is to decrease
including empty or partially empty sella turcica, dilation of CSF production and in turn lower the ICP. Acetazolamide
the optic nerve sheath, flattening of the posterior globe, is considered the first-line treatment for IH due to its
anterior protrusion of the optic nerve head, tortuosity of the relative tolerability and lack of need for repeated laboratory
optic nerve, and distal transverse sinus stenosis. Although monitoring. Patients may complain of food having a
the presence of 1 or more of these subtle radiographic metallic taste to it, especially carbonated beverages. Tran-
findings increases the probability of IH, lack of these sient paresthesia, metabolic acidosis, and slight increase in
findings does not decrease its likelihood. Bilateral transverse urination are other common adverse effects. The meta-
sinus stenosis is thought to be a consequence and not a bolic acidosis is often asymptomatic, and patients tolerate
cause of the IH as studies have shown normalization of the serum carbon dioxide levels down to 15 mmol/L without
stenosis after high-volume LP. (13) the need for supplementation. The typical adolescent
One of the most important diagnostic tools, and also dosing is 1 to 2 g divided twice daily (BID). Doses greater
the most fraught with error, is the LP. The most common than 2 g failed to show much added benefit at the risk of
error is improper positioning. Opening pressure mea- increased adverse effects. In younger children, doses of
surements should not be performed with the patient in approximately 20 to 25 mg/kg per day divided BID are
the seated position. Accepted positioning is in lateral typical, although doses as high as 100 mg/kg per day can be
decubitus with the legs and head extended at the time tolerated.
of pressure measurement. For sedated patients, sponta- Furosemide is the second-line agent due to its diuretic
neous respirations with normal arterial carbon dioxide is nature and requirement to monitor for hypokalemia. For-
preferred. One pediatric study found that an increase of 1 tunately, most pediatric patients taking furosemide do not
kPa in end-tidal carbon dioxide increases CSF pressure by need potassium replacement above increased dietary intake.
3.5 to 12 cm H2O. Typical dosing is 1 to 2 mg/kg per day divided BID. Studies
Popular convention is for withdrawal of large CSF have shown a synergistic effect when used in combination
volumes and normalization of the pressure in an effort with acetazolamide.
to protect the vision. An adult study found that the Due to similar chemical structures to sulfonamides,
average time to return to initial pressure after LP is 82 there is a potential risk of cross-reactivity to acetazolamide
minutes. The authors’ experience found that normalizing and furosemide in patients with reported allergy. An adult
higher pressures results in increased rates of post-LP study reviewed the medical records of patients with self-
headache. Reduction of less than 10 cm H2O of pressure reported sulfa allergy who were given regimens of acetazol-
still results in transient headache relief with fewer post- amide, furosemide, or a combination for treatment of IH.
LP headaches. (15) No evidence of cross-reactivity was found, and the study
suggests that patients with a reported sulfa allergy can safely
take these medications.
MANAGEMENT
Topiramate is also used in patients who are not able to
Management of a patient with IH often requires a multi- tolerate acetazolamide or furosemide. It is similar to acet-
disciplinary approach with neurology and ophthalmology. If azolamide and has a similar mode of action. In an open-label
clinically indicated, neurosurgery, psychology, psychiatry, study, 40 adult patients were alternately assigned to receive
dietetics, physical therapy, hematology, and/or endocrinol- topiramate (100–150 mg/d) or acetazolamide (1,000–1,500
ogy may be involved. mg). Visual field grades were followed, and both treatment
Often, pubertal and adult patients report weight gain in groups demonstrated statistically significant improvement.
the 12 months before diagnosis. Numerous adult studies Long-term use or rapid weaning of corticosteroids can
have shown that aside from removing an offending med- result in SIH, although they used to be the first-line choice
ication, weight loss is the only other modifiable risk factor for treatment of PIH before acetazolamide. Their use has
shown to affect the ICP. One of the first studies treated declined given the improved outcomes and fewer adverse
patients with a low-calorie rice diet to treat their IH. (14) effects with medications used today. However, in instances
Study participants lost 11 to 56 kg over the treatment of severe visual deficits at presentation, corticosteroids used
period, resulting in papilledema resolution without in conjunction with acetazolamide does result in a better
medication use. The 2 symptomatic patients reported outcome. The recommended dose is largely anecdotal,

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mirroring what is used in optic neuritis and other inflam- hearing loss on the treated side are the most common
matory neurologic disorders. Patients are initially given adverse effects reported. Rarer adverse effects include hem-
intravenous methylprednisolone 20 mg/kg (maximum 1 g) orrhage, venous perforation due to the guidewire, and
daily for 5 days followed by an oral taper. temporary unsteadiness. Use of stenting has not been
In pediatrics, surgical interventions for IH are rarely studied in pediatrics.
necessary. Surgery is considered in patients for whom
medical therapy cannot be tolerated, patients with severe
PROGNOSIS
optic nerve swelling with concerns of permanent vision loss,
or patients with persistently elevated ICP with associated Despite the previously held belief that this is a relatively
papilledema or pain despite maximizing pharmacologic benign condition, the potential for permanent vision
options. The main procedures considered involve CSF loss and chronic pain are significant morbidities. When
shunting and optic nerve sheath fenestration (ONSF). properly treated, headaches typically resolve within the
It is believed that ONSF preserves optic nerve function by first few weeks. Resolution of papilledema averages 4.2
redirecting pressure away from the optic nerve head, the to 5 months. Minor visual field deficits often fully resolve,
area of the most tenuous blood supply. It does not directly sometimes lagging behind resolution of the papilledema.
address the elevated ICP. Surgery involves exposing the There is literature to suggest that grade 3 or higher
optic nerve and making openings in the sheath to relieve the papilledema is a high predictor of permanent visual deficits.
pressure. Risks include ischemic optic neuropathy (espe- Another study found that postpubertal status resulted in a
cially in severely edematous or ischemic nerves), transient worse visual outcome. Recurrence is seen in 18% to 20%
blindness, pupillary mydriasis and retrobulbar hemorrhage. of patients. A series of adult patients were followed after
Unilateral fenestration can result in resolution of edema in weaning off acetazolamide for recurrence of their optic
the unfenestrated eye; however, common practice is to nerve edema. (17) All the patients lost weight from the time
perform bilateral fenestration. Typically, ONSF is not per- of diagnosis to medication wean, and those with recurrence
formed on an acutely swollen nerve but rather when the had an average BMI 5.5% higher than at diagnosis. This was
swelling is more under control. Signs of optic nerve ische- compared with an average decrease of 17.9% in BMI in
mia, including cotton wool spots, increase the risk to the those without recurrence.
optic nerve and thus should resolve before the procedure is Up to two-thirds of patients develop new headache
performed. symptoms that are reported as different from their IH
A CSF diversion is more effective in patients when pain headache. Most are diagnosed as having migraine without
is the primary symptom. In addition, it is used to protect aura or episodic tension-type headache and respond to
vision in the acute presentation, where the risk of ischemic common prophylactics used for these conditions.
neuropathy due to ONSF is high. There are 2 options for
shunt placement: lumboperitoneal or ventriculoperito-
neal. The goal is to mechanically reduce the CSF pressure
by direct CSF diversion. Unfortunately, the myth that
ventricular diversion is superior still persists. In one study,
the outcomes of 25 patients shunted for their IH were Summary
reviewed. (16) Shunt failure was defined as continuation or • Based on research evidence, obesity does not play as large of a
role in primary intracranial hypertension in prepubertal patients.
return of presenting symptoms with radiographically ver-
(6)(7)
ified shunt placement and normal opening pressure.
• Consensus supports the crucial role of the ophthalmic
Those requiring revision had radiographic evidence of
examination in diagnosis and subsequent management
shunt disturbance, blockage, or increased opening pres- of intracranial hypertension. This includes pupillary
sure. Failure rates were similar at 11% and 14% for lumbar and ocular motility assessments, color vision testing,
and ventricular shunts, respectively. Revisions were more visual acuity, funduscopic examination, Humphrey or
common in lumbar versus ventricular shunts (60% versus Goldmann visual field testing, and optical coherence
tomography.
30%).
• Based on strong research and consensus, the
Attempts have been made to stent sinus venous stenosis
lumber puncture opening pressure measurement
in adults with varying success. Headache resolution is seen
should be performed with the patient in the lateral
in up to 84.6% of patients, and resolution of papilledema in decubitus position with the legs and head
62.5% to 100%. Transient postoperative headache or partial

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 extended. Sedated patients should have spontaneous To view teaching slides that accompany this article,
respirations with normal arterial carbon dioxide
visit http://pedsinreview.aappublications.org/
concentrations.
content/39/3/121.supplemental.
• The literature supports the consensus that minocycline, and
the related tetracycline class of medications, can cause
secondary intracranial hypertension. This is of concern
because many pediatricians use minocycline in the
treatment of acne and are not aware of this potential
adverse effect.
• Based on strong research studies, aside from
removing an offending medication, weight loss
is the only modifiable risk factor shown to
affect the intracranial pressure and prevent recurrence.
(11)(14)
• Based on research and consensus, acetazolamide is the first-
line treatment for intracranial hypertension due to its relative
tolerability and lack of need for repeated laboratory
monitoring.
• Some research has shown that lumbar shunts
have equal failure rates compared with ventricular
shunts. (13)
References for this article are at http://pedsinreview.aappubli-
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 Pediatric Intracranial Hypertension
Shawn C. Aylward and Rachel E. Reem
Pediatrics in Review 2018;39;121
DOI: 10.1542/pir.2016-0226

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 Pediatric Intracranial Hypertension
Shawn C. Aylward and Rachel E. Reem
Pediatrics in Review 2018;39;121
DOI: 10.1542/pir.2016-0226

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://pedsinreview.aappublications.org/content/39/3/121

Data Supplement at:

http://pedsinreview.aappublications.org/content/suppl/2018/02/28/39.3.121.DC1

Pediatrics in Review is the official journal of the American Academy of Pediatrics. A monthly
publication, it has been published continuously since 1979. Pediatrics in Review is owned,
published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point
Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 2018 by the American Academy of
Pediatrics. All rights reserved. Print ISSN: 0191-9601.

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