Handbook of Pediatric Neurosurgery

[51] Ring D, Chin K, Jupiter JB. Radial nerve palsy associated with
high-energy humeral shaft fractures. J Hand Surg Am. 2004;
29(1):144–147
[52] Mehlman CT, Strub WM, Roy DR, Wall EJ, Crawford AH. The
e ect of surgical timing on the perioperative complications
of treatm ent of supracondylar humeral fractures in children.
J Bone Joint Surg Am. 2001; 83-A(3):323–327
[53] Kim DH, Murovic JA, Tiel R, Kline DG. Management and
outcomes in 353 surgically treated sciatic nerve lesions. J
Neurosurg. 2004; 101(1):8–17
[54] Patterson FP, Morton KS. Neurologic complications of
fractures and dislocations of the pelvis. Surg Gynecol Obstet.
1961; 112:702–706
[55] Kim DH, Kline DG. Surgical outcome for intra- and extrapelvic
femoral nerve lesions. J Neurosurg. 1995; 83(5):783–790
[56] Johnson EW, Jr, Vittands IJ. Nerve injuries in fractures of the
lower extremity. Minn Med. 1969; 52(4):627–633
[57] Morton KS. Traumatic dislocation of the hip: a follow up
study. Can J Surg. 1959; 3:67–74
[58] Roganovic´ Z. Missile-caused complete lesions of the
peroneal nerve and peroneal division of the sciatic nerve:
results of 157 repairs. Neurosurgery. 2005; 57(6):1201–1212,
discussion 1201–1212
[59] Gurdjian ES, Smathers HM. Peripheral nerve injury in
fractures and dislocations of long bones. J Neurosurg. 1945;
2:202–219
Trauma
408

51 Management of Pediatric Head Trauma
Linda W. Xu, Gerald A. Grant
51.1 Introduction
Traumatic brain injuries (TBIs) in children lead to
nearly 500,000 emergency room visits a year and
over 2,000 deaths a year. The most common cause
of injury in children of age 0 to 14 years are falls,
followed by being struck by an object, motor
vehicle accident, and assault. Trends for emer-
gency department visits, hospitalizations, deaths,
and mechanism are broken down by age and sum-
marized in Table 51.1. While falls are the most
common cause of TBI in children age 0 to 14 years,
children age 15 to 19 years are more commonly
injured from motor vehicle collisions (MVCs). Since
MVCs are more likely to be fatal than other mecha-
nisms, rates of fatal TBI are also highest in the 15-
to 19-year age group. Patients age 0 to 14 years old
have a 2 to 5% rate of death, but children age 15 to
19 years old have a 19% rate of death from TBI.1
Physical mechanisms of injury in traumatic
brain injuries involve acceleration, deceleration,
and rotational forces causing skull fractures, vascu-
lar injuries, direct impact to brain parenchyma,
and axonal shear injury. Levels of injury in TBI can
be loosely categorized into mild (Glasgow Coma
Score ([GCS] 13–15), moderate (GCS 9–12), and
severe (GCS≤8) based on GCS postresuscitation.
Mild TBI is vastly more common than severe and
often underreported as not all children with mild
TBI are brought to medical attention.
51.2 Initial Emergency Room
Evaluation
51.2.1 History
● Determine mechanism.
● Assess for seizures and loss-of-consciousness
events.
● Current headache, stable, increasing or
decreasing.
● Nausea or vomiting.
● Any history of bleeding disorders.
51.2.2 Physical
● Presence of scalp hematoma.
● Lacerations and abrasions on the scalp, assess
whether full thickness.
Table 51.1 Summary of number of emergency department visits, hospitalizations, deaths, and mechanisms of injury for
head trauma per year by age1
Age

ED visits

Hospitalizations

Deaths

Mechanism
0–4

251,546

15,239

998

5.1% MVC
64.2% Falls
0.1% Assault
21.4% Struck by object
9.1% Other
5–9

105,015

8,799

450

7.0% MVC
40.3% Falls
1.0% Assault
33.9% Struck by object
17.8% Other
10–14

117,387

11,098

726

5.6% MVC
36.5% Falls
9.7% Assault
29.5% Struck by object
18.8% Other
15–19

157,198

24,896

3,995

25.7% MVC
20.8% Falls
14.2% Assault
23.2% Struck by object
16.0% Other
Abbreviation: MVC, motor vehicle collision.
409

● Palpation for skull fractures.
● If fontanelle present, assess for bulging or
firmness.
● Focal neurological symptoms.
● Evidence of basilar skull fractures (ecchymosis
around eyes or ears, fluid drainage from the
nares or ears).
51.2.3 Neuroimaging
● When to image?
– Focal neurological findings.
– Concern for skull fracture on examination.
– Altered mental status.
– Irritability.
– Bulging fontanelle.
– Persistent vomiting.
– Seizure.
– Prolonged loss of consciousness.
– Concern for child abuse.2,3,4
● For patients with GCS 14 to 15 with mild head
trauma, chance of clinically significant finding
on computed tomography (CT) is 1%.2,5
– Can consider observation without CTscan if
very low risk.
– In low-risk patients with normal mental
status, no hematoma, no loss of consciousness,
no skull fracture, and low-risk mechanism.
○ <0.2% of patients <2 years old have clinically
significant findings on CT.
○ <0.05% of patients >2 years old have
clinically significant findings on CT.5
51.3 Management of Mild TBI
Minor head traum a can be defined as an injury to
the head in a patient that is awake, alert, and
remains responsive throughout the event. In a m ild
TBI, the patient may be currently awake, alert, and
responsive but have had a transient loss of con-
sciousness (LOC), disorientation, or emesis and GCS
14 to 15 on presentation. In this population, 0.1 to
1% will require neurosurgical intervention.3,5,6
Roughly 5% of patients with mild TBI will have
CT findings of either skull fracture or intracranial
abnormality and can be classified as a com pli-
cated m ild TBI.5,6,7 Although this is a small popu-
lation, there is some debate as to whether these
patients have an eventually di erent functional
outcome. Some adult studies show that those with
complicated mild TBI have outcomes more similar
to those with moderate head injuries (GCS 9–12)
with deficits on neuropsychiatric testing and lower
GCS scores while other studies suggest that while
there may be early di erences (prolonged return
to work), there are eventually no functional di er-
ences for those with complicated injuries than
those with uncomplicated TBI.7
As 99% of patients with mild TBI do not require
neurosurgical intervention, it is up for debate
which of these patients should be admitted for
monitoring in the hospital. In general, if there is
any suspicion of injury that may lead to further
decline, other medical issues that may make the
patient unstable, or concern about supervision or
mechanism of injury, patients should be admitted
for observation. In general, patients who have mild
TBI with no findings on initial CT have a low rate
of delayed decline.8,9 General criteria for admission
for mild TBI may thus include the following:
● Intracranial injury on CT
● Depressed skull fracture
● Persistent vomiting
● Any concern for nonaccidental trauma
Concussion is a subset of mild TBI specifically
defined as a low-velocity injury associated with a
rapid onset of short-lived impairment in neurolog-
ical function that resolves spontaneously. These
symptoms are thought to be related to a functional
disturbance rather than a structural disturbance.
Common symptoms are as follows:
● Headache.
● Disorientation.
● Loss of consciousness.
● Amnesia.
● Irritability.
● Insomnia.
● Emotional lability.
Initial on-site evaluation for concussion should
proceed as standard emergency care with evalua-
tion of ABCs and precautions for any associated
cervical spine injury. The patient needs to be
evaluated by a medical provider and if one is not
available on site, they should be taken for urgent
referral. The patient should not be left unattended
for the first hours after injury in case of neurologi-
cal decline. If the concussion occurred in the set-
ting of an athletic activity, the patient should not
be allowed to return to play on the day of injury.
Same day return to play can be associated with
delayed onset of symptoms and higher rates of
neuropsychological symptoms postinjury.10
There are several ways to grade concussions and
recommendations for return to play, which are
based on adult guidelines as summarized in
Trauma
410

Table 51.2. One concern about return to play
stems from the risk of second im pact syndrom e.
This phenomenon is seen when a second impact
occurs while the first injury has not been resolved
and triggers a synergistic response causing severe
and devastating results. The most severe cases of sec-
ond impact syndrome can appear as concussion
symptoms initially, but is then followed by collapse,
pupillary dilation, loss of eye movement, respiratory
failure, and death.11 This mechanism is thought to be
related to loss of vascular autoregulation with rapid
increase in intracranial pressure (ICP) and herniation,
which can result in neurological deterioration in a
matter of minutes. In a study of pediatric patients
with GCS 13 to 15, up to 28% demonstrated impaired
autoregulation following head trauma.12
More
Table 51.2 Concussion grading and return-to-play guidelines.
Grade I

Grade II

Grade III

Return to play (RTP)
Cantu guidelines No LOC<30 min
amnesia
LOC<5 min
30 min–24 h
amnesia
LOC>5 min
>24 h amnesia
Grade I:
● 1st time—1 wk
● 2nd time—2 wk
● 3rd time—end season
Grade II:
● 1st time—1 wk
● 2nd time—1 mo
● 3rd time—end season
Grade III:
● 1st time—1 mo
● 2nd time—end season
Colorado Medi-
cal Society
Guidelines
Confusion

Confusion
and amnesia
LOC

Grade I:
● 1st time—15 min
● 2nd time—1 wk
Grade II:
● 1st time—1 wk
● 2nd time—2 wk with
physician’s approval
Grade III:
● 1st time—1–6 mo based
on severity of LOC
● 2nd time–—6 mo–1 y with
physician’s approval
American Acad-
emy of Neurol-
ogy Guidelines
No LOC
and <15 min
confusion
No LOC
and >15 min
confusion
LOC

As summarized in Colorado
Medical Society Guidelines
4th International
Conference on
Concussion
No grading
guidelines
Summary of how to progress
through stepwise RTP
● Must be asymptomatic for 24
h in each step
● If any symptoms occur, drop
back to previous step where
patient was asymptomatic
● At least 1 wk to progress
through entire protocol
● Absolutely no same day re-
turn to play if any concussion
occurs
Stepwise RTP:
● Stage 1: No activity—rest
with goal of recovery
● Stage 2: Light aerobic
exercise—goal of increas-
ing heart rate
● Stage 3: Sport-specific
exercise—training drills
with no head impact
● Stage 4: Noncontact
training drills—complex
training drills with
resistive training
● Stage 5: Full-contact
practice—medical clea-
rance to participate in nor-
mal training with goal of
restoring functional skills
● Stage 6: Return to play
Abbreviation: LOC, loss of consciousness.
Source: Data from from Cantu guidelines, Colorado Medical Society Guidelines, American Academy of Neurology, and
the 4th International Conference on Concussion.13,14,15
Management of Pediatric Head Trauma
411

detailed discussion of cerebral physiology and autor-
egulation can be found later in this chapter. Most
physicians recommend a graduated return-to-play
protocol if the patient is asymptomatic, with a drop
down to previous activity level if the patient
becomes symptomatic.13,14,15 A general timeline is
proposed in the adult concussion literature, but
many choose to be more conservative with children
when recommending timing of return to play, which
may be left up to the prerogative of the individual
physician.
In patients with a history of prior concussions,
there may be long-term e ects. In the most imme-
diate period, postconcussion syndrom e can
develop in which the patient continues to have
symptoms after the first week with headaches,
dizziness, neuropsychiatric symptoms, or cognitive
impairment.15 About 10 to 15% of patients will
develop prolonged symptoms after the initial
period. Depression and other mental health prob-
lems can arise in this population as well. Sleep
problems and anxiety can also be common and
some will choose to treat these issues medically,
but of note, if these symptoms are medically sup-
pressed, the patient should not be considered at
their baseline and should not be considered for
return to play.13
After frequent and prolonged exposure to con-
cussions, “punch drunk,” dementia pugilistica, or
chronic traum atic encephalopathy (CTE) has
been well characterized and a real risk for those
with repeated injuries. First characterized in 1928,
those with multiple concussions later on in life
developed mood and emotional lability, memory
loss, tremor, and dysarthria. Autopsies at that time
showed microhemorrhages replaced with gliosis
or degenerative tissue.16 In particular, there was
destruction of the limbic system, atrophy of the
cerebellum, and widespread neurofibrillary tan-
gles. There does appear to be a correlation
between the level of exposure to concussion (i.e.,
years playing in the NFL) and worse pathological
findings on autopsy, although a direct link has not
been proven.10,17,18
51.4 Management of Severe TBI
and Polytrauma
Severe TBI is defined as GCS less than or equal
to 8 and 39% of severe pediatric TBIs are associ-
ated with m ultiple other traum atic injuries.19
Children with severe TBI have a 34% m ortality
rate, and only 16% survive with good outcom es
or moderate disabilities.20 These patients are
best m anaged in a specialized pediatric traum a
center.21,22,23,24
51.4.1 Cerebral Physiology
When a significant primary injury to the brain has
occurred, the principles of management are to
minimize the secondary insults to the brain. Pedia-
tric patients seem to be even more vulnerable than
their adult counterparts to subsequent di use cer-
ebral edema and injury, possibly from higher cere-
bral blood volume and flow.20,25,26
While many principles of cerebral physiology in
pediatrics are similar to adults, there are several
factors that do change with age. In adults, the aver-
age cerebral blood flow is about 50 mL/100 g/min
with more flow in the gray matter than white mat-
ter. It appears that this number is higher in young
children age 2 to 4 years old and then decreases
down to adult levels. Correspondingly, cerebral
vascular resistance is also lowest in this young age
group. Cerebral oxygen and glucose consumptions
start lower at birth and then increase during child-
hood until they plateau at 3 to 9 years old and then
decrease toward adult levels.27,28
As in adults, control of blood flow to the brain
varies by metabolism, carbon dioxide levels, oxy-
gen levels, blood viscosity, and autoregulation.
Carbon dioxide levels can very rapidly regulate
cerebral blood flow. There are studies in children
under anesthesia that they are even more sensitive
to these changes than adults are, with up to 14%
change in blood flow velocity per 1 mm Hg change
in end-tidal CO2. Autoregulation is mostly con-
trolled at the arteriole level and in adults, at mean
arterial pressures (MAPs) between 60 and 160 mm
Hg, cerebral blood flow is mostly constant as arte-
rioles constrict or relax to maintain a stable
amount of blood flow regardless of blood pressure
changes. Outside of these levels, autoregulation is
unable to compensate to maintain cerebral blood
flow constant and the child can experience ische-
mia or hyperemia. Although some assume children
can tolerate lower blood pressures than adults,
studies actually show a similar range with best
cerebral autoregulation with MAP above 60 mm
Hg.28
After brain trauma, cerebral blood flow can
become uncoupled from metabolism resulting in
either ischemia or hyperemia. In the immediate
hours after injury, ischemia is more common with
Trauma
412

damage from hypoperfusion for the first 12 hours.
A second phase typically follows with hyperemia
and increased ICP. The third phase is associated
with vasospasm and ischemia which can again
become problematic.28
Ischemia causes secondary injury with infarc-
tion, but hyperemia also causes secondary injury
with increased chance of hemorrhage, di use
brain swelling, and higher ICPs. It has been sug-
gested that in young children that there is a
greater concern for hyperemia compared with
adults since baseline cerebral blood flow is higher.
In mild pediatric head trauma, 17 to 28% have
been found to have impaired autoregulation versus
42% in severe head injury.12,28
There is often a biphasic pattern of ICP eleva-
tion after severe head injury in children. After
the initial injury and temporary ischem ia, the
release of inflam m atory components from the
prim ary cell injury can cause the first phase of
dysregulation of cerebral blood flow, di use
edem a, and elevated ICP. A second phase often 3
to 7 days after initial injury when secondary
injury cellular cascades again increase inflam m a-
tory cerebral m arkers can cause a second phase
of elevated ICP.28,29 Although cerebral blood flow
and autoregulation are di cult to m easure clini-
cally, cerebral perfusion pressure (CPP) can often
be used as a surrogate and guidelines for use are
described later in this chapter.
Because of the principles of cerebral physiology
after trauma in a child, it is critical to manage vol-
ume status, ICP, CPP, ventilation, and cerebral
metabolism (seizures, sedation, paralysis) to mini-
mize additional secondary brain injury.
51.4.2 Pediatric Blood Loss and
Hypovolemia
In traum a, 39% of deaths can be attributed to
exsanguination.30 Children tend to have a higher
oxygen consumption, higher cardiac output to
blood volum e ratio, and for the very young, the
presence of fetal hem oglobin delivers less oxygen
to tissue.31 Despite having higher blood volum e
needs, children can m ask hypovolem ia and blood
loss due to their physiological reserve. In fact, the
blood pressure can rem ain norm al w ith 25 to
30% total blood volum e loss.32 Hypotension can
be di cult to recognize by those not fam iliar
w ith pediatric patients as their baseline blood
pressures can vary widely by age. By the tim e
hypotension or a drop in central venous pressure
is noted, a patient can proceed rapidly to cardio-
vascular collapse. Hypotension in the setting of
traum a is clearly associated w ith m orbidity and
m ortality.33,34
Many are not familiar with baseline normal
physiological ranges in pediatric patients. As a
rough estimate for blood volume:
Normal systolic blood pressure =90 +2 ×age
Hypotension =70 +2 ×age
Blood volume =80 mL/kg
In pediatric patients, less obvious signs of hypo-
volemia are particularly important such as:
● Decreased pulse pressure (<20 mm Hg) and
associated flattening in arterial line contour.
● Mottled skin.
● Drop in temperature.
● Lethargy.
● Metabolic acidosis.
● Decrease in palpable pulses.
● Decreased urine output.
● Increased capillary filling time.32
The pediatric guidelines for trauma suggest that
access for pediatric resuscitation is critical. If two
attempts at peripheral access have failed, the pro-
vider should move on to interosseus access.35
Resuscitation should proceed in a graded fashion
with the following protocol:
● Warm crystalloid boluses in 20 mg/kg units ×3.
● Type-specific or O-negative packed red blood
cells (PRBCs) in 10 mg/kg boluses and locate
source of bleeding as soon as possible.
● Monitor urine output to gauge success of
resuscitation with goal urine output of greater
than 2 mL/kg/h in infants and 1 to 1.5 mL/kg/h in
older children.36
Head traumas can contribute significantly to
blood loss as the scalp is especially vascular and
open lacerations can lead to rapid exsanguination.
Scalp hematomas can accumulate a significant
amount of blood compared to the overall blood
volume of a child. When assessing source of
blood loss in a child, cranial injuries are not an
insignificant potential source. Unlike adults though
where internal bleeding in long bones and the
abdominal cavities are typically the only spaces
where exsanguination can occur internally, an
infant with open sutures and the ability to expand
their overall cranial volume can hide a significant
amount of blood volume loss in the intracranial
space.37
Management of Pediatric Head Trauma
413

51.4.3 Coagulopathy
Coagulopathy can also particularly become a prob-
lem as platelets and coagulation factors are
actively consumed during active blood loss and
then subsequently become diluted as resuscitation
begins. While whole blood has normal clotting fac-
tors, patients are frequently transfused with PRBC,
transfusion of platelets or fresh frozen plasma
(FFP) should be considered in addition to PRBC.
Head injury patients are particularly prone to
developing dissem inated intravascular coagul-
opathy (DIC) as injured brain releases tissue
thromboplastin.37,38,39 DIC can be characterized by
a precipitous drop in platelets, elevation in pro-
thrombin time and partial thromboplastin time,
drop in fibrinogen, and elevation in D-dimer. Up to
40% of pediatric patients with severe TBI will
develop coagulopathy and this risk appears to cor-
relate with severity of injury, increasing age, and
intraparenchymal injuries.39
Providers should
therefore be especially vigilant in monitoring for
coagulopathy when a head injury is suspected.
51.4.4 ICP Monitoring
Numerous studies have shown that high ICP is
associated with poor outcome and aggressive
treatment of elevated ICP can improve outcome.
ICP monitoring provides a way to gauge current
ICP and whether subsequent treatments are work-
ing to bring ICP to a normal range.
Generally, after resuscitation, ICP monitoring is
indicated if the patient has GCS less than or equal
to 8 and CT evidence of intracranial injury.40 In
one study, up to 86% of pediatric patients with GCS
less than or equal to 8 had ICP greater than 20.41
Patients without obvious CT findings of intracra-
nial injury may also have elevated ICP and require
an ICP monitor.
Note: In infants with severe head injury, an open
fontanelle is not an adequate replacement for hav-
ing a definitive ICP monitor in place.42
51.4.5 Treatment of Intracranial
Hypertension
In studies of overall outcome, ICPs of greater than
40 mm Hg are highly associated with death and
ICPs ranging from 20 to 40 with significant mor-
bidity.43,44,45 In general, the goals of ICP manage-
ment are to keep ICPs below 20 mm Hg. However,
some pediatric studies show that control of CPP
may be more important than ICP in overall out-
come. CPP is calculated as MAP minus ICP and
studies in adults show better outcomes with CPP
above 40 to 60.46,47 In children, goal CPP tend to
vary by age with higher CPP goals in older age
groups than younger age groups with goals in the
40 s to 50 s in those ages 2 to 6 years and 50 s to
60 s in those ages 7 to 16 years.48,49 Below the
desired CPP goals the patient may experience cere-
bral ischemia and above the desired range the pa-
tient may experience hyperemia and subsequent
elevation in ICP.28,50,51 A biphasic increase in ICP
has been reported in children after severe TBI, one
immediately after injury, and one several days to a
week after injury.28,29,52
In general, strategies for lowering ICP and max-
imizing CPP rely on the following methods:
● Cerebrospinal fluid (CSF) drainage.
● Sedation and neuromuscular blockade.
● Hyperosmolar therapy.
● Hyperventilation.
● Barbiturates.
● Temperature regulation.
● Surgical decompression.42
CSF Drainage
Ventriculostomy has been known to reduce ICP
and in an adult study, CSF drainage to keep the ICP
less than 15 showed a significant improvement in
mortality down to 12% compared to 53% in medi-
cal management alone.41,53
In our practice, external ventricular drains
(EVDs) are often placed in the emergency room or
intensive care unit (ICU). We generally place EVDs
on the right side unless contraindicated by large
blood clots in the parenchyma or in the ventricle.
The hair is shaved on the corresponding side in a
generous area to allow for tunneling of the EVD
catheter into a clean area of scalp. The entry point
is generally at the mid-pupillary line about 1 cm
anterior to the coronal suture. The EVD is passed
to a premeasured length from available imaging
(usually between 3 and 5 cm) until CSF returns. If
there is a lower suspicion for a severe head injury
and the GCS is 7 to 8, one may also place a super-
ficial intraparenchymal strain gauge often called a
“bolt.” A bolt allows for ICP monitoring but does
not have the ability to drain CSF to improve the
elevations in ICP.
Hyperosmolar Therapy
The two most commonly used agents for hyperos-
molar therapy are mannitol and 3% hypertonic
Trauma
414

saline infusion. Mannitol was first introduced in
1961 and is felt to work by both a rapid mecha-
nism of decreased blood viscosity and thus
decreasing blood vessel diameter and total intra-
cranial blood volume, and a slower mechanism
that acts directly by osmosis.52,54,55,56,57 Mannitol
can decrease ICP by about 10% with mean time for
return to baseline being roughly 3 hours.57 Manni-
tol is felt to have some risks for renal injury, having
led to acute tubular necrosis and renal failure in
early studies, however, at that time, patients were
often kept hypovolemic while mannitol was
administered. It is unclear if the renal toxicity
would be significantly less if the patient is kept
euvolemic during that time. However, it is also
important to note that due to this quick and robust
diuretic e ect, volume status can be hard to man-
age in a very small child after mannitol adminis-
tration. Mannitol is generally administered
between 0.25 g/kg and 1 g/kg boluses with goal se-
rum osmolarity of 320 mOsm/L.42 We caution the
use of mannitol in young children due to the risk
for hypovolemia.
Three percent hypertonic saline has been used
since the early 1900s with e cacy in lowering ICP
and overall improved ICU courses when used in
severe TBI. It has been studied in children with
good results and no significant renal failure
noted.58,59,60,61 Some propose that with 3%, the
Osm goal can be higher and that 0.1 to 1.0 mL/kg
hour can be used with goal serum osmolarity up
to 360 mOsm/L.42,59
Hyperventilation
The goal of hyperventilation is to reduce the serum
pCO2 and cause vasoconstriction and thus limit
the total blood volume intracranially. Hypocapnia
leads quickly to cerebral vasoconstriction, cerebral
blood flow, cerebral blood volume, and can quickly
change ICP. In children, as described above, they
appear to be even more sensitive than adults to
pCO2 changes.28 However, vasoconstriction also
leads to risks of decreased cerebral perfusion.62
Chronic hyperventilation can lead to a variety of
problems including depleted bicarbonate supplies,
causing the patient to become hyperresponsive to
subsequent pCO2 levels, left shift of the hemoglo-
bin curve with decreased oxygen delivery, and
increased brain ischemia.63,64,65,66 Thus, hyperven-
tilation is meant only for short-term use and only
if ICP has been demonstrated to be high. There is
no indication for prophylactic hyperventilation. As
it is not a long-term mechanism for decreasing ICP,
hyperventilation is generally used only for brief
periods in cases of herniation or acute deteriora-
tion to help while awaiting a more definitive
method for lowering ICP. Hyperventilation goals
can be to increase respiratory rate until PaCO2
equals 30, less than 30 if used very aggressively. If
planning for aggressive hyperventilation, one
could consider monitoring for cerebral ischemia
with brain tissue oxygen monitors or jugular
venous oxygen monitors.42
Sedation
Sedation and paralysis are felt to reduce secondary
injury after head trauma by reducing cerebral
metabolism, minimizing patient agitation, and
facilitating ventilation. There are number of agents
that can be used for sedation which are often used
in conjunction and thus di cult to study inde-
pendently. The only sedative with strong evidence
of correlation with lowering ICP more e ectively
than other agents is barbiturates which are dis-
cussed in the next section. Common sedatives
used in pediatric trauma are summarized in
Table 51.3. Opiates for pain management and
benzodiazepines for sedation are commonly used
for sedation to control ICP. Propofol is commonly
used in neurosurgical patients as there is often a
reduction in ICP from the agent itself, however,
there have been concerns about propofol infusion
syndrome, particularly in children. Therefore,
long-term use is generally avoided.67,68,69,70
Neuromuscular blockade can decrease ICP by
decreasing airway and thoracic pressures, decreas-
ing shivering, posturing, and fighting the ventila-
tor.71 However, conversely it is also associated with
pneumonia, cardiovascular side e ects, increased
ICU stay, myopathy, patient stress if not concomi-
tantly sedated well, and inability to detect neuro-
logical changes.42,72
Barbiturates
Use of barbiturates was first described as a treat-
ment for elevated ICP in the 1970s and have been
correlated with improved outcomes.73 It is thought
that the mechanism of ICP reduction is threefold
by suppressing overall metabolism, changing vas-
cular tone, and eliminating free radicals with sta-
bilization of neuronal membranes.74,75 Generally
pentobarbital and thiopental can both be used and
there are no studies that directly compare the e -
cacy of either agent against each other. When ini-
tiating barbiturate coma, the patient should be
Management of Pediatric Head Trauma
415

concomitantly on electroencephalogram (EEG) to
titrate doses to maximal burst suppression to min-
imize cerebral metabolism. While you can check
serum levels, studies have shown that serum levels
don’t predict well when a patient is truly burst
suppressed. The drawback of barbiturate coma is
that it often induces hemodynamic instability and
requires concurrent use of cardiovascular drips to
maintain adequate blood pressures and may be
di cult to use in patients that are already hemo-
dynamically unstable. In pediatric studies, use of
barbiturates in patients without refractory intra-
cranial hypertension may actually increase mortal-
ity due to hemodynamic problems, and thus it
should never be used prophylactically or unless
other methods of ICP control have failed.76,77
When to stop a barbiturate coma can be up to the
practitioner, but some suggest that ICP should be
stable for at least 24 hours before trialing a barbi-
turate taper.
Pentobarbital:
Loading dose 10 mg/kg.
Maintenance 1 mg/kg/h with adjustments for
burst suppression.78
Thiopental:
Loading dose 10 to 20 mg/kg.
Maintenance 3 to 5 mg/kg/h with adjustments
for burst suppression.79
Temperature Regulation
Hyperthermia after a cerebral injury is thought to
lead to increased metabolism, inflammation, exci-
totoxicity, and seizures. Thus, it was suggested that
perhaps cooling a patient may improve neurologi-
cal outcomes. A study in children in the 1970s
showed 19/20 children survived with initial GCS of
4 after cooling, which is significantly better than
historical controls.80 There have been several adult
studies more recently showing improved ICP and
improved outcomes at 3 and 6 months from
injury.81,82,83 In one phase II trial in children, hypo-
thermia did lower ICPs but were associated with
some increase in arrhythmias and showed no
Table 51.3 Comparison of sedative agents frequently used in pediatrics for ICP management67,68,69,70
Agents

Pros

Cons

Use

Notes
Propofol

Rapid onset
Rapid clearance
Decreases cerebral
metabolism and ICP
Increases seizure
threshold
Hypotension
Pancreatitis
Liver failure
Propofol infusion
syndrome
Induction: 1–2.5 mg/kg
Maintenance: 1.5–
4.5 mg/kg/h and titrate
to sedation
Propofol infusion
syndrome
● First reported in
children
● Lactic acidosis
● Cardiovascular
collapse
● At risk if using more
than 4 mg/kg/h
for >48 h
Benzodiazepines

Less hypotension
Raises seizure
threshold
Reduces cerebral
metabolism and ICP
Slow wake up due to
buildup of metabo-
lites
Withdrawal
Delirium
Respiratory depres-
sion
Plateau with no in-
crease in ICP control
at high doses
Induction: 0.1 mg/kg
Maintenance: 0.01–
0.2 mg/kg/h
Narcotics

Pain control
Little effect on
blood pressure
Could possibly in-
crease ICP in high-
dose boluses
Adjunct to other
sedatives
Dexmedetomidine No respiratory
depression
Can be used in
patients who are not
intubated
Decreases delirium
Hypotension
Bradycardia
Arrhythmia
Induction: 1 µg/kg
Infusion: 0.42–1 µg/kg/h
Abbreviation: ICP, intracranial pressure.
Trauma
416

definitive functional di erence at 6 months from
injury.84 In general, all brain traumas should avoid
hyperthermia and those with medically refractory
ICP can be considered for a cooling protocol down
to a temperature of 34 °C. During cooling it is
important to monitor for coagulopathy, which can
worsen existing bleeding, arrhythmias, and also to
minimize shivering which can increase cerebral
metabolism. Patients being cooled may need to be
simultaneously paralyzed to minimize the e ects
of shivering. As cooling protocols limit examina-
tions if the patient requires sedation and paralysis,
and can worsen coagulopathy, it is also generally
reserved for patients with refractory ICP to other
methods of treatment.
Steroids
Steroids are used commonly in other neurosurgi-
cal pathologies like tumors and infections but in
studies of steroid use in trauma, it has been
correlated with increased infection rates but no cor-
responding improvement in outcomes.85,86,87,88 Thus,
there is no indication for steroid use in trauma.
Surgical Treatment
In general, if the patient has elevated ICP from a
mass lesion, it is easy to make the decision to pro-
ceed with operative intervention to remove the
mass lesion, whether it be a subdural, epidural, or
intraparenchymal hematoma.
Epidural hematomas are classically associated
with an immediate loss of consciousness with a
lucid interval afterward, followed by headache,
vomiting, and altered mental status. Often there
are associated skull fractures and on CT the pattern
of blood typically takes a lentiform shape and does
not cross suture lines of the skull. Although previ-
ously it was felt that epidural hematomas are usu-
ally the result of arterial bleeding and thus can
progress quickly and should all be surgically
decompressed, more recent studies suggest that it
is possible to manage patients who are neurologi-
cally intact with nonoperative treatment. In a
study of 13 intact patients with epidural hema-
toma, all but one was successfully managed with
nonoperative treatment and made a full recovery
at follow-up after 4 months with follow-up CT
scans showing complete resolution of bleed.89
However, others argue nonoperative treatment
can lead to prolonged hospitalization with contin-
ued issues with headache, nausea, and vomiting
than a simple evacuation of an epidural.
Subdural hematomas typically result from shear
injury to a cortical vein. In infants, it can be a result
of shaken baby syndrome and nonaccidental
trauma, which is addressed in a separate chapter.
In general, patients with a subdural hemorrhage,
evidence of brain compression, midline shift, and
neurological deficit should be considered for evac-
uation. In an acute subdural, blood typically cannot
be drained through burr holes and requires a full
craniotomy, but chronic subdurals from distant
trauma is often liquefied and can be successfully
drained with just burr holes.
Less straightforward is deciding which patients
require decompressive craniectomy. Goals for
decompression are to reduce ICP, increase CPP, and
prevent herniation. Decompressive craniectomy is
e cacious in reducing ICP with a drop in ICP of 9
to 47 points at the time of durotomy.45,90 However,
as patients requiring decompressive craniectomy
are also patients with very severe injuries, there is
some question to whether this overall leads to
desirable outcomes. There is some evidence that
there are overall improved outcomes with craniec-
tomy with better results in pediatric trauma
patients than adults.45,90,91 It is worth considering
early in a child with refractory ICPs and a unilat-
eral injury. In general, it is felt that patients should
be considered if the patient meets the following
criteria:45,90,91,92
1. Di use swelling on CTscan
2. Patient is within 48 hours of initial injury
3. No episodes of sustained ICP greater than 40
prior to surgery
4. GCS greater than 3 at some point after injury
5. Secondary deterioration after initial good
clinical presentation
6. Evidence of herniation
Surgical technique for decompression can be a uni-
lateral frontotemporalparietal decompression or
bifrontal craniotomy. No studies directly compare
these techniques but preference may depend on
appearance on CT and whether there is more
concern for unilateral or bilateral edema. Most
surgeons also perform a duraplasty at the time of
surgery. Generally, size of craniotomy is recom-
mended to be as large as is safely possible as small
craniectomy can cause sustained ICP problems and
cerebral infarction at the borders of the craniec-
tomy that undergo the most pressure to herniate
outward.
Summary of treatment of elevated ICP
(Fig. 51.1).42
● Tier 1: Basic management of head trauma
Management of Pediatric Head Trauma
417

● Tier 2: Suspected or confirmed ICP elevation
● Tier 3: Refractory elevated ICP
51.4.6 Seizures
Posttraumatic seizures are common and can be
classified as either early (within the first 7 days) or
late (>7 days from injury). Seizures after initial
injury can cause increased brain metabolism and
ICP, leading to additional brain injury. In children,
20 to 39% of patients with severe TBI experience
early posttraumatic seizures. Infants and children
already have lower seizure threshold than adults
and may have di cult to detect clinical seizures.
Antiepileptics in severe TBI patients have been
shown to decrease the percentage of patients that
experience early seizures and has been associated
with improved survival.42,93,94
Late posttraumatic seizures present in 7 to 12%
of TBI patients and is not felt to be prevented by
early use of prophylactic antiepileptics.42 The risk
of developing epilepsy is two times higher in the
first 5 years after injury than those without head
injury.95 It can lead to further accidental injury
and psychological changes, and these patients
should generally be referred to a neurologist for
long-term seizure management.
51.5 Surgical Pearls
● Head trauma is common in pediatrics with
younger populations having more falls and older
populations having more MVCs, leading to
higher fatalities in older children.
● Mild TBI is defined as a patient with GCS greater
than 13 on presentation and complicated mild
TBI if the patient has an associated CT finding,
who may functionally behave more like a patient
with a moderate TBI. Only 1% will eventually
need surgical intervention. Concussion is a
functional disturbance in neurological
dysfunction without any noted structural
findings and is a subset of mild TBI.
● The principles of graded return to play indicate
that the patient should return to activity
through various stages starting with light
activity to full activity, and drop back down to
previous activity level if any symptoms are
experienced. This is to minimize the occurrence
of second impact syndrome which can be a fatal
dysregulation of cerebral blood flow.
● Patient with multiple concussions or mild TBIs
should be counseled on chronic traumatic
encephalopathy (CTE) and implications later in
life.
● Because of improved compensatory mechanisms
in children to maintain heart rate and blood
pressure, clinical signs of hypovolemia are more
important to note early on rather than changes
in vital signs.
● DIC is common in pediatrics and coagulation
factors should be transfused in conjunction with
PRBC.
● There is a basic tiered approach to elevated ICP
management with baseline management of all
head traumas, treatment methods for suspected
or confirmed ICP elevation, and refractory ICP.
● CPP goals vary by age with goals of 40 to 50 in
younger children and 50 to 60 in older children.
● Surgical decompression should be considered
when there is a defined mass lesion.
● Surgery decompression should be considered
early for di use brain edema if patient had an
initially better neurological presentation and
Fig. 51.1 Summary of treatment of
elevated intracranial pressure. Tier 1:
Basic management of head trauma.
Tier 2: Suspected or confirmed ICP
elevation. Tier 3: Refractory elevated
ICP.
Trauma
418

had a subsequent decline due to herniation and
surgical intervention can be o ered quickly.
51.6 Common Clinical
Questions
1. If ICP remains elevated after initiation of EVD
placement and CSF drainage, 3% infusion, and
sedation, what other steps can be taken at this
point to lower ICP?
2. Are antiepileptic medications needed after head
trauma? Do they reduce the chance of
developing late posttraumatic seizures?
3. After a concussion, when should a child return
to activities?
4. What is chronic traumatic encephalopathy?
51.7 Answers to Common
Clinical Questions
1. If ICP is refractory to initial treatments, the next
steps to consider are barbiturate coma and
possibly hypothermia. If there is a mass lesion,
surgical evacuation should be considered. If
there is di use edema, overall clinical status
should be considered and if appropriate for
decompressive craniectomy, this step should be
taken quickly. Hyperventilation can be used as a
bridge therapy until another more definitive
therapy can be initiated.
2. Antiepileptics should be considered for severe
TBIs and has been shown to improve survival. It
does not change the risk for late posttraumatic
seizures.
3. After a concussion, the child should never
return to play on the day of the event and
should seek evaluation by a physician. Return to
activities is based on a graded return to play
where the child proceeds through graded steps
of no activity, light activity, moderate activity,
and full return to play with stop and drop back
to previous activity level if the patient
experiences any symptoms such as headache,
nausea/vomiting, confusion, dizziness,
dyscoordination, or mood changes. Recent
recommendations are also encouraging return
to school prior to return to play.
4. CTE is a condition after repeated head injuries
where microhemorrhages are progressively
replaced with degenerative tissue especially in
the limbic system and cerebellum leading to
permanent mood changes, memory loss,
tremor, and dysarthria. There is a direct
correlation between exposure to concussions
and severity of CTE.
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[78] Eisenberg HM, Frankowski RF, Contant CF, Marshall LF,
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Trauma
422

52 Abusive Head Trauma
Mark S. Dias
52.1 Definitions and
Nomenclature
Abusive head trauma reflects a combination of
injuries to an infant, most commonly less than 24
months of age, resulting from child abuse. The
injuries were originally described by Guthkelch in
1972 and Ca ey in 1974; the term shaken baby
syndrome was adopted in 1984 to emphasize the
contribution of shaking as a mechanistic injury. In
1987, Duhaime and colleagues first described
impact injuries in a significant proportion of cases
and suggested the term shaken impact syndrome.1
Multiple studies have described both shaking as
well as impact; the literature confirms both that
(1) shaking can cause brain injury, subdural hema-
toma (SDH), retinal hemorrhage (RH), and even
death, and (2) evidence of impact injuries may be
lacking even when impact has occurred. Therefore,
the term abusive head trauma (AHT) has been
more recently proposed by many, including the
American Academy of Pediatrics,2 to account for
the contributions of shaking, impact, and other
injury mechanisms. The term abusive head trauma
should be used rather than shaken baby syndrome
since, in any particular case, the injury mechanism(s)
are not known with absolute certainty.
AHT produces a constellation of injuries, not all
of which need to be present to make the diagnosis.
AHT is an important type of childhood head
trauma, the proper and accurate recognition of
which is vital both for the protection of the child
from harm and the caregiver from wrongful
prosecution. The principal injuries include the
following:
● Subdural hematoma: SDHs are present, on
average, in 80% of cases of AHT. They may be
hyperdense, isodense, hypodense, or of mixed
density. Mixed-density SDH are more common
in AHT than in accidental injuries; some of these
likely reflect multiple episodes of injury
although more recent studies suggest that some
may occur after a single trauma and may reflect
an admixture of clotted and unclotted blood,
cerebrospinal fluid (CSF), and serum.3 Some, but
not all, studies have suggested a preponderance
of interhemispheric and tentorial SDH in AHT.4
● Primary brain injury: Brain injuries can include
superficial or deep contusions and cortical
lacerations, deeper white matter injuries, and
hypoxic-ischemic injuries. Contusions are mostly
superficial and are visible as hyperdense
punctate hemorrhages on computed
tomography (CT). In contrast, ischemic-anoxic
injuries are hypodense on CTscans, and
hyperintense on T2- and fluid-attenuated
inversion recovery (FLAIR)-weighted magnetic
resonance imaging (MRI) sequences; di usion
and apparent di usion coe cient (ADC) MRI
sequences establish these as ischemic-anoxic in
nature. A particular pattern involves a reversal of
the densities of the hemispheres compared with
either the deep gray nuclei or the cerebellum
(reversal sign). At the extreme, the entire
hemisphere is hypodense ("big black brain").
● Retinal hemorrhages: RHs are seen, on average,
in 80% of cases of AHT.5 The number and
location may vary widely. Not all RHs are
diagnostic of AHT; RHs are increasingly specific
for AHTwhen they are (1) more numerous in
number, (2) extend beyond the posterior pole
(the perimacular region) to the edges (ora
serrata) of the retina, (3) involve multiple retinal
layers (preretinal, intraretinal, and subretinal),
and (4) include retinoschisis or macular folds.
Retinoschisis is the retinal finding that is most
specific to AHT and represents a physical tearing
within the layers of the retina producing a
hemorrhagic cavity within the neural retina. As
of this writing only five cases of traumatic
retinoschisis have been reported outside of the
setting of AHT (these include cases of crush
injuries to the head, high-speed vehicular
trauma, and fall from great height). RHs are
present in only 3 to 5% of accidentally injured
children and, when present, they are usually
few, limited to the posterior pole and
intraretinal in location. Other conditions that
may produce RH are covered in an excellent
reference by Levin.5
● Signs of cranial impact injury: Impact injuries are
reported in about one-quarter to one-half of
cases of AHT, and skull fractures in about one-
quarter.6,7,8 Evidence of impact may include both
physical signs such as soft tissue swelling,
bruising, lacerations or abrasions, and
radiographic evidence such as soft tissue
swelling or skull fractures.
423

● Spine injuries: Spine and spinal cord injuries
have previously been thought to be rare in AHT.
However, more recent studies, using more
modern autopsy techniques that do not cut
across the cervicomedullary junction, have
increasingly demonstrated evidence of
ligamentous or bony cervical spine injuries, as
well as injuries to the spinal cord and upper
cervical roots and ganglia, in up to 78% of cases
on MRI scans9 and 70% of fatal cases at
autopsy.10 Posterior ligamentous and bony
injuries are more common than are vertebral
body fractures. Spinal SDH may also be present,
particularly in cases having posterior fossa SDH;
thoracolumbar SDH likely reflect dropdown of
blood from the cranium to the most dependent
portion of the spine.
● Other injuries: The presence of other, noncranial
traumatic injuries is important to document and
needs to be considered in the holistic evaluation
of AHT. Bruises, burns, or patterned marks on
the skin should be sought, particularly on
padded surfaces and torso, and particularly
among nonambulatory infants. Rib fractures are
present in approximately one-third of cases;
although any part of the rib may be fractured,
many studies demonstrate that posterior rib
fractures, where the rib abuts the vertebral
transverse process, is the most common
location. Long bone fractures are present in
about one-quarter of cases; classic metaphyseal
lesions (CMLs), also known as corner fractures,
of the limb metaphases are particularly
suggestive of abuse. Liver, spleen, pancreatic, or
bowel injuries reflect coexisting occult
abdominal trauma.
52.2 Clinical Presentation
Children with AHT are young; 80 to 90% are under
12 months of age at diagnosis.11 The type, severity,
and extent of injuries are typically inconsistent with
either the story provided or the developmental age
of the child (e.g., a fall from height in an infant <4
months of age who can’t roll, or multiple bruises in
a child who is not yet cruising). Often the story
changes as time goes on as additional injuries are
discovered that the alleged perpetrator can’t
explain. The most common presentations include
the following, virtually always while alone with a
single adult, and without an adequate explanation:
● Sudden and unexplained screaming, crying, or
extreme irritability.
● Sudden lethargy or alteration in level of
consciousness.
● Eyes rolling back in head.
● Apnea or disordered breathing.
● Seizures.
● Loss of motor tone or limpness.
● Emesis.
The presence of coma, disordered breathing or
apnea, significant RHs or retinoschisis, and multi-
ple seizures over the first 72 hours that are di -
cult to control are all significant indicia of AHT.
The history is a vital part of the evaluation for
AHT. It should be obtained from both parents and/
or any witnesses to the events independently
using open-ended questions, and the entire con-
versation should be recorded in the medical record
immediately after the interview, being as accurate
and complete as possible. Questions will obviously
be dependent on the situation, but important
questions to record include What exactly hap-
pened? Where and how was the baby positioned
at the time? Where were you when it happened?
What exactly did the baby do? If an accidental
trauma was described, how exactly did it happen?
If the baby fell, how far, o of what, on what sur-
face did they land, did they hit anything else on
the way down? Who else was in the room with, or
in proximity to you? What were you doing with
the baby at the time? What did you do in response
to the changes in the baby? How did the baby react
to that? Did you perform cardiopulmonary resusci-
tation (CPR) (including chest compressions)? Were
you injured (e.g., if the story involves an adult fall-
ing with the baby)? Who else cares for the baby
and at what times? When did each person last care
for the baby? Have you witnessed any other inju-
ries prior to the day this happened?
It is also vital to carefully document an injury
time line as completely and accurately as possible.
When was the baby last seen by another adult act-
ing normally? When did they last eat and how
much (head injured babies will not eat much)?
Have they been unusually fussy or irritable lately
(perhaps suggesting a prior injury)? Have there
been any recent seizures or abnormal motor
movements? Radiological interpretation can also
provide clues as to when an injury occurred; for
example, studies suggest that (1) a hypodense
component of an acute SDH most commonly
appears within 3 to 12 days after AHT and (2)
parenchymal hypodensities appear commonly
within 1 to 3 hours.4,9 One must be careful about
correlating the clinical and imaging findings to
Trauma
424

establish a time frame during which the abuse
might have occurred.
52.3 Di erential Diagnosis
of AHT
The history and physical findings in combination
usually suggest the possibility of AHT. However, it
is important to keep an open mind and contem-
plate other potential causes of the injuries. The dif-
ferential diagnosis of AHT includes a large number
of other diseases,5,6,12,13 only a few of which are
discussed in detail here. Obviously whether to
consider any of these depends on the circumstan-
ces of the injury, the clinical findings, and the
results of ancillary tests.
Di erentiating AHT from accidental injury is the
most frequent dilemma. However, multiple studies
of accidental injuries in children confirm the
following:
● The overwhelming majority of household and/or
short falls are benign. Significant brain injury,
prolonged coma, disordered breathing and/or
apnea, multiple seizures, and radiographic
evidence of ischemic-anoxic brain injury are
extraordinarily uncommon in short falls (<4 ft).
The risk of dying from a short fall is, at greatest,
approximately 0.25%.14 When they do occur,
coma and/or death are most frequently due to
large and expanding extra-axial mass lesions.15
● SDH is statistically much less frequent in
accidental trauma than in AHT (where it
averages 80%). Moreover, when it occurs in the
setting of accidental injury, SDH is usually small,
focal, and underlying a site of impact injury. In
contrast, AHT more commonly produces di use,
bilateral, panhemispheric, interhemispheric,
and/or tentorial SDH.
● Intracranial injuries from short falls more
commonly include scant, focal cortical
subarachnoid hemorrhage and/or tiny
superficial cortical contusions that are almost
always associated with a skull fracture and/or
soft tissue scalp swelling; hypodensities and
deeper white matter injuries are rare.
● Epidural hematomas occur more commonly in
association with accidental injuries and, in young
children, may not be associated with a skull
fracture; on occasion they may be associated
with a small number of RH as well.
Birth trauma is another consideration. Birth
trauma is a known cause of RH in 40% of
newborns.5 However, most resolve within days of
birth, and all reported cases have resolved by 4
postnatal weeks. Similarly, recent studies have
demonstrated that birth-related SDH are common
in asymptomatic infants (8–46%).16,17,18 They are
more common in vaginal and assisted deliveries.
Most are located in the occipital and infratentorial
locations, and virtually all are gone by 4 weeks
postnatal. Rebleeding has only been described in
one asymptomatic case.17 Birth trauma should not
be a cause for acute deterioration in an infant more
than 4 weeks’ postnatal. Although rebleeding into
a chronic birth-related SDH has been proposed as
a potential cause for acute deterioration weeks or
months later, there is not a single reported case to
support this theory.
An underlying coagulopathy should be excluded.
Many institutions perform only a complete blood
count (CBC) with platelet counts and a prothrom-
bin time (PT), partial thromboplastin time (PTT),
and international normalized ratio (INR); others
recommend more sophisticated testing to include
fibrinogen and fibrin split products (to evaluate for
disseminated intravascular coagulopathy [DIC]),
von Willebrand’s factor, and factors VIII, IX, and
XIII.19 Hemorrhagic disease of the newborn should
be considered in the infant up to 6 months of
age with a greatly prolonged PT, particularly in a
child who is breast-fed, has significant diarrhea,
has been on prolonged antibiotics, or has had
neonatal hepatitis/biliary atresia, and whose PT
corrects readily with the administration of vitamin
K. A significant coagulopathy other than DIC
should prompt a hematology consult for further
evaluation.
Vascular malformations and aneurysms are rare
causes of intracranial hemorrhage in infancy, and
are usually readily distinguished by the location of
the hemorrhage as subarachnoid or intraparen-
chymal rather than subdural. Although RH may
occur in the setting of aneurysmal intracranial
hemorrhage in adults (Terson’s syndrome), these
are extraordinarily rare in childhood if they occur
at all, and are readily distinguished from RH associ-
ated with AHT. A brain MRI, magnetic resonance
angiography (MRA), and magnetic resonance venog-
raphy (MRV) will usually exclude these conditions.
Intracranial infections are rarely confused with
AHT. Neither meningitis nor viral encephalitis are
associated with SD or severe RH. Fevers, nuchal
rigidity, and an elevated white blood cell (WBC),
erythrocyte sedimentation rate (ESR), and C-
reactive protein (CRP) are usually present. Postme-
ningitic subdural hygromas can develop (especially
Abusive Head Trauma
425

after pneumococcal and Haemophilus influenzae
meningitis), but acute SDH does not occur. Sub-
dural empyema is usually readily distinguished
from SDH based on the history, laboratory tests,
and neuroimaging; a contrast-enhanced CT or MRI
will disclose leptomeningeal enhancement.
Genetic, metabolic, and other conditions that
can mimic AHT in infants may include the
following:
● Glutaric aciduria (GA): Produces episodic
neurological decline with extensor motor
movements, hyper- or hypotonia, and seizures;
choreoathetoid movements develop later in life.
Neuroimaging demonstrates enlarged extra-
axial CSF spaces, temporal fossa arachnoid cysts,
and, later, characteristic putaminal
hyperintensities.20 A routine newborn metabolic
screen (mandated in most states) virtually
excludes GA.
● Menkes’ kinky-hair disease: X-linked recessive
disorder characterized by short, friable, and
twisted hair (pili torti); poor growth; severe and
early neurological deterioration; characteristic
skeletal deformities (wormian skull bones,
metaphyseal defects); and characteristic facies.
Neuroimaging demonstrates atrophy, enlarged
extra-axial CSF spaces with tortuous cerebral
vessels, and SDHs or e usions.
● Ehlers–Danlos syndrome: A disorder
characterized by hypermobile joints,
hyperelastic skin, dystrophic scarring
particularly around the flexor creases of joints,
and poor healing of skin wounds. Approximately
30% of a ected individuals also have a
qualitative functional platelet disorder. A family
history may reveal ruptured cerebral or thoracic
aortic aneurysms in other family members.
SDHs can rarely be present.
● Arachnoid cysts: Temporal fossa cysts may be
associated with SDH or hygroma either
spontaneously or in response to trauma; RHs
are extraordinarily rare and if present
are intraretinal and limited to the posterior
pole.
● Benign extra-axial collections of infancy (BECI):
BECI is characterized by macrocrania with
progressive cranial enlargement over the first 12
to 18 months of life; neuroimaging
demonstrates an accumulation of CSF in the
subarachnoid spaces, associated with mild
ventricular enlargement in 40%. A family history
of macrocephaly is present in 40% of families.
The infants are asymptomatic and develop
normally. The fluid is subarachnoid in location;
therefore, the fluid is isointense to CSF on CT and
all MRI sequences, it does not compress the sulci
(in fact, the sulci are typically widened giving
the erroneous picture of brain atrophy), and the
cortical bridging blood vessels cross the space to
the overlying arachnoid. In contrast, a subdural
hematoma or hygroma is not entirely isointense
to CSF and causes compression of both the sulci
and the bridging vessels. An associated SDH may
occur in approximately 2 to 3% of cases of
BECI.21,22 In virtually every case, the infant is
asymptomatic and the BECI and SDH are is
discovered during an evaluation for
macrocephaly; there is no associated brain
injury or other evidence of trauma and RH have
been described in only one case.23
52.4 Work-up of AHT
In addition to a thorough history and physical
examination, the following studies that should be
considered (depending on the circumstances)
include the following:
● A complete coagulation profile as described
above.
● Brain MRI, MRA, and MRV, as well as a cervical
spine MRI. A complete spine MRI should be
considered as spinal SDH in the thoracic or
lumbar regions may be missed.
● A retinal examination by a pediatric or retinal
ophthalmologist who is experienced in
interpreting RH.
● A complete skeletal survey.
● Liver function tests, amylase, urinalysis, and/or
abdominal CT if abdominal trauma is suspected.
● Consultation with a geneticist if an underlying
metabolic or genetic condition is suspected.
● A child abuse pediatrician should always be
consulted if available.
● If a reasonable suspicion of abuse is present, all
health care providers are mandated to report
suspected abuse to legal agencies (usually a state
Department of Children and Youth).
52.5 Treatment
The medical and surgical treatment of AHT is
largely identical to the treatment of any severe
traumatic brain injury and includes the following:
● Intubation for the child with Glasgow Coma
Score (GCS) less than 8 for airway control.
● Seizure prophylaxis is particularly important
given both the frequency with which seizures
Trauma
426

occur in AHT and the di culty in controlling
them. Prophylaxis with phenobarbital,
phenytoin, or levetiracetam should be instituted
at the onset; a second agent may be necessary if
seizures continue despite maximal doses of a
single agent. Seizures usually subside after the
first 3 to 4 days.
● Standard intracranial pressure (ICP)
management using osmotic diuretics and/or
hypertonic saline and external ventricular
drainage as primary measures.
● Surgical management is rarely needed. SDH are
usually small and nonoperative; larger acute
SDH should be evacuated. Chronic SDH may be
treated with either repeated aspirations (usually
through the anterior fontanelle), a subdural
drain, or a subdural-peritoneal shunt if
necessary.
● Consideration may be given to decompressive
craniotomy if ICP cannot be controlled and/or
there is significant shift on neuroimaging
studies.
52.6 Outcome
Outcome from AHT is poorer than for other types
of traumatic brain injury.
● Mortality averages 20 to 25%.
● Half of survivors will su er significant
neurological deficits such as spasticity, seizures,
blindness (from RH and/or cortical injury), and
focal neurological deficits.
● As many as 80% will su er measurable cognitive
and/or behavioral deficits.
● Neuroimaging studies often demonstrate
multifocal encephalomalacia or global brain
atrophy, evidence of cortical laminar necrosis
(tram-track hyperdensities that follow the gyral
surfaces), ex vacuo ventricular enlargement, and
widened subarachnoid spaces.
● Rebleeding into chronic SDH occurs in about
15%, but is virtually always asymptomatic and
usually discovered incidentally on routine
follow-up neuroimaging studies.9 It does not, in
itself, indicate repeated abuse.
52.7 Other Considerations
● Medical information gathering is critical to the
successful evaluation and prosecution of AHT.
The evaluation of AHTshould be left to
physicians who are experienced in its evaluation
and knowledgeable about the di erential
diagnosis.
● It is no longer acceptable to naively equate SDH
and RH with AHTwithout careful consideration
of alternate diagnoses. A thorough history and
work-up looking both for associated injuries and
evidence of other medical conditions is
important.
● Chart documentation is extremely important
from a medicolegal standpoint. Avoid the use of
the word shaken baby syndrome as the
mechanism(s) are unknown in individual cases
and this generates unnecessary confusion. Stick
to the facts, avoiding inflammatory or
judgmental statements about the alleged
perpetrator and/or family, particularly
concerning social or demographic issues.
● Don’t jump to conclusions. Avoid making overly
dogmatic statements about causation—one way
or another—before the history has been fully
obtained and all of the medical information is
available.
● Do not testify in court as an expert witness
without first knowing all of the clinical
information and the pertinent literature on AHT.
It is easy for the uninformed clinician to derail a
medicolegal investigation with ill-considered or
incorrect remarks in the courtroom.
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Neurosurg Focus. 1999; 7(4):e4
Trauma
428

X
Section X
Infections
53 Evaluation and Management
of Pediatric Intracranial
Infections

430
54 Evaluation and Management
of Pediatric Spinal Infections 448
55 Surgical Considerations in
Tuberculosis, Fungal, and
Parasitic Infections of CNS in
Children

460

53 Evaluation and Management of Pediatric
Intracranial Infections
Jonathan R. Ellenbogen, Richard P.D. Cooke, Conor L. Mallucci
53.1 Introduction
Central nervous system (CNS) infections in the
pediatric population are life-threatening diseases
in which early recognition and appropriate treat-
ment may prevent long-term brain injury or death.
The causal agents are di erent in the pediatric
population when compared to the adult popula-
tion, and so are the presenting symptoms. It is
therefore important to know and understand the
clinical presentations of these conditions in children
in order to evaluate and manage these conditions
appropriately. This chapter will focus on epidural
and brain abscesses, subdural empyema, bacterial
and viral meningitis, and encephalitis. Tuberculous,
fungal, and parasitic infections of the CNS will be
discussed in a di erent chapter.
53.2 Bacterial Meningitis
53.2.1 Background
Meningitis is the most common CNS infection and
can be classified according to causative agent, for
example, viral or bacterial, or on the basis of the
duration of symptoms, that is, acute, subacute, or
chronic. Subacute meningitis is defined as the one
that ongoing for more than 1 week. Chronic men-
ingitis occurs if the symptoms have been ongoing
for a month or longer.
Bacterial meningitis usually arises via hematog-
enous spread from mucosal surfaces. Other modes
of transmission include contiguous spread from an
infected mastoid/middle ear or paranasal sinus,
rupture of a parenchymal abscess, transmission
from dysraphic lesions, and penetrating trauma.
In neonates (<28 days old) the most common
causative organisms are likely to be acquired
around the time of birth from the maternal genital
and gastrointestinal tract, and are Streptococcus
agalactiae (group B Streptococcus), Escherichia coli,
Streptococcus pneumoniae, and Listeria monocyto-
genes.1 L monocytogenes meningitis is rare (~ 5% of
neonatal meningitis) with most cases occurring in
the first week of life in predominantly premature
infants, and are related to maternal infection. The
neonatal case fatality rate is around 10 to 12.4%.2
The risk factors for neonatal meningitis include
antenatal chorioamnionitis, premature rupture of
membranes, less than 37 weeks’ gestation, and
having a previous newborn with early-onset dis-
ease.3
In children over the age of 3 months the most
common pathogens arise from the upper respira-
tory tract and include Neisseria meningitidis
(meningococcus), S. pneumoniae (pneumococcus),
and Haemophilus influenzae type b (Hib). The case
fatality rate in this group varies between 1.9 and
11%.2 N. meningitidis infection leading to meningo-
coccal disease is the leading infectious cause of
death in early childhood (case fatality rate ~ 10%)
and can be fatal within hours of the first symptoms
appearing. The highest incidence occurs among
children aged under 2 years; another period of
increased risk occurs in adolescence and early
adulthood. The disease is more frequent in winter
months and is associated with smoking, crowding,
and recent viral respiratory illness. It most com-
monly presents as bacterial meningitis (15%) or
septicemia (25%), or as a combination of the two
syndromes (60%).2 Rarely the disease presents as
pneumonia, arthritis, osteomyelitis, pericarditis,
endophthalmitis, or conjunctivitis.
The epidemiology of pediatric bacterial menin-
gitis has changed dramatically following the intro-
duction of routine vaccination. Hib was the main
cause of bacterial meningitis in children under 5
years old before the introduction of the Hib conju-
gate vaccine in 1992. It is now the third most com-
mon causative organism after N. meningitidis and
S. pneumoniae. Similar results have been found
since the introduction of the meningococcal C
(MenC) conjugate vaccine in 1999 against
serogroup C meningococcus, and the pneumococ-
cal conjugate vaccine in 2006 against pneumococ-
cal disease. Serogroup B meningococcus is now the
most common cause of bacterial meningitis (and
septicemia) in children and young people aged 3
months or older. A vaccine is available but not in
routine use.
53.2.2 Evaluation
Most children with meningitis present with a tem-
perature over 38 °C or fever (90%), vomiting (70%),
and headache (3–58%). Respiratory symptoms are
430

not an uncommon finding. Under one-third of
children present having had a seizure (13–30%),
with shock being a less common finding at presen-
tation (8–17%). Over two-thirds of children with
meningitis experience impaired consciousness
(60–87%), with around 10% presenting with coma.
Most are “irritable” or “agitated.” Between 62 and
75% will report neck sti ness or some back
rigidity.2
Brudzinski’s sign can be elicited in
approximately two-thirds of children and Kernig’s
sign is present in approximately half of children.
Approximately 80% of children will have one of
these signs; neck sti ness, Kernig’s sign, or
Brudzinski’s sign.2
Children under 2 years old present similarly but
two-thirds will present with poor feeding and the
prevalence of seizures ranges from 22 to 55.2%.2
Approximately half present with a bulging fontanelle.
In neonates, fever and irritability is common
(79%), however, the classical symptoms of nuchal
rigidity and bulging fontanelle are not usually evi-
dent (17% and 13%, respectively). A quarter of neo-
nates present with lethargy and 17% with seizures.
Nonspecific gastrointestinal symptoms (anorexia
and/or vomiting, diarrhea, and abdominal disten-
sion) are more frequent (50, 29, and 17%, respec-
tively) than respiratory symptoms (respiratory
distress [17%] and apnea [13%]).2
Clinical features vary with age. Although fever is
a common nonspecific symptom, it is more often
absent in neonates. Babies are less likely to have
symptoms and signs of meningism, extremity pain
or hemorrhagic rash, whereas older children and
young people are more likely to have meningism,
confusion/altered mental state, hemorrhagic rash,
or extremity pain. The majority of children and
young people with meningococcal disease will
develop a hemorrhagic rash during their illness,
but this may be primarily absent, and may initially
be blanching or macular in nature.
Bacterial and viral causes of meningitis cannot
be di erentiated reliably based on clinical features
alone. However, children with viral meningitis
are less likely to have shock, decreased level of
consciousness, or seizures than are those with bac-
terial meningitis. Symptoms and signs that are
considered typical of meningeal irritation (head-
ache, neck sti ness, or photophobia) occur in a
minority of children and young people before hos-
pital admission, but they are more likely to occur
in older children and young people. Herpes
simplex encephalitis should be considered as an
alternative diagnosis.
53.2.3 Investigations
Laboratory Tests
The diagnosis of m eningitis is established upon
the clinical history, physical examination, and
laboratory investigations. The definitive test for
meningitis is a lum bar puncture, m easuring the
opening pressure, with laboratory exam ination
of the cerebrospinal fluid (CSF). Although per-
form ance of a lum bar puncture is contraindi-
cated if the following are present, this should
not delay com mencem ent of appropriate antibi-
otic treatment:
● Signs suggesting raised intracranial pressure
(ICP).
– Reduced or fluctuating level of consciousness
(Glasgow Coma Score [GCS] <9 or a drop of≥3).
– Relative bradycardia and hypertension.
– Focal neurological signs.
– Abnormal posture or posturing.
– Unequal, dilated, or poorly responsive pupils.
– Papilloedema.
– Abnormal “doll’s eye” movements.
● Shock.
● Extensive or spreading purpura.
● After seizures until stabilized.
● Coagulation abnormalities.
– Coagulation results outside the normal range.
– Platelet count below 100 ×109/L.
– Receiving anticoagulant therapy.
● Local superficial infection at the lumbar
puncture site.
● Respiratory insu ciency (lumbar puncture is
considered to have a high risk of precipitating
respiratory failure in the presence of respiratory
insu ciency).
CSF examination should include white blood cell
count and examination, total protein and glucose
concentrations, Gram stain and microbiological
culture. A corresponding laboratory-determined
blood glucose concentration should be measured.
In bacterial meningitis one might expect to find
raised protein, low glucose levels, and raised white
blood cells with neutrophilic predominance. The
normal values for CSF di er between laboratories
but approximate values are as below:
● Appearance to the naked eye: clear and colorless.
● Total protein concentration: 0.15 to 0.45 g/L.
● Glucose concentration: 2.78 to 4.44 millimole/L
(~ 60% of the plasma value).
● Cell count (per microliter): 0 to 5 white blood
cells (WBCs) (0–20 in neonates), no RBCs.
Evaluation and Management of Pediatric Intracranial Infections
431

(If RBCs are present and the blood WBC count is
within the normal range, more than one WBC per
500–1000 CSF RBCs can be expected in a child or
young person with meningitis and should not be
ignored).
The normal CSF opening pressure should be in
the range of 10 to 100 mm H2O in less than 8 year
olds and between 60 and 200 mm H2O in greater
than 8 year olds. CSF opening pressures above
250 mm H2O indicates raised ICP.
If a child has an unexplained petechial rash and
fever, that is, suspected meningitis, then the fol-
lowing should also be performed:
● Full blood count.
● C-reactive protein (CRP).
● Coagulation screen.
● Blood cultures.
● Advanced molecular testing (including
polymerase chain reaction [PCR]).
● Blood glucose.
● Blood gas.
The finding of a high CRP (>99 mg/L) is specific but
not sensitive for meningococcal disease in children
with fever and a rash. A low CRP does not exclude
meningococcal disease. Be aware that the CRP may
be normal and the WBC count normal or low even
in severe meningococcal disease. Serum CRP levels
of more than 20 mg/L and procalcitonin of more
than 0.5 ng/mL have greater than 83% sensitivity
for di erentiating bacterial meningitis from asep-
tic meningitis.2
Imaging
In children and young people with a reduced or
fluctuating level of consciousness (GCS<9 or a
drop of ≥3) or with focal neurological signs, per-
form a computed tomography (CT) scan to rule out
alternative intracranial pathology. Patients should
be clinically stable before scanning takes place, but
this should not delay appropriate treatment.
Imaging is not performed to make a diagnosis of
meningitis, but it can be used to look for its com-
plications and sequelae including hydrocephalus,
abscess, empyema, and raised ICP. CT alone is
unreliable for identifying raised ICP, therefore clin-
ical assessment should also be used to decide
whether it is safe to perform a lumbar puncture.
In meningitis, a CT scan is often normal. Mild
ventriculomegaly and enlargement of the subar-
achnoid spaces are early abnormalities. Contrast-
enhanced T1-weighted magnetic resonance
imaging (MRI) is the imaging modality of choice,
looking for enhancement of the leptomeninges
over the cerebral convexities, although this can be
di cult as normal meninges enhance. Contrast-
enhanced fluid-attenuated inversion recovery
(FLAIR) imaging increases the specificity over
contrast-enhanced T1-weighted images for this.3
53.2.4 Management
Clinical progress should be monitored via frequent
vital sign measurements of respiratory rate, heart
rate, blood pressure, conscious level (GCS/APVU),
temperature, perfusion (capillary refill time), and
oxygen saturations. It is important to ensure that
appropriate investigation and management of
metabolic disturbances, seizures, raised ICP, respi-
ratory support, and fluid balance is undertaken.
Medical/Antimicrobial
Treat with an intravenous third-generation cepha-
losporin (e.g., ceftriaxone) immediately if the CRP
and/or WBC count (especially neutrophil count) is
raised, as this indicates an increased risk of having
meningococcal disease.
There is not enough evidence in children to
show that CSF WBC, protein, or glucose values
have su cient diagnostic accuracy to confirm or
exclude bacterial meningitis as compared to viral
or “aseptic” meningitis. Therefore, in cases of
suspected bacterial meningitis start antibiotic
treatment—start before CSF result available if there
is a delay in obtaining CSF—if the CSF WBC count
is abnormal:
● In neonates, at least 20 cells/µL (be aware that
even if fewer than 20 cells/µL, bacterial
meningitis should still be considered if other
symptoms and signs are present).
● In older children and young people more than
5 cells/µL or more than 1 neutrophil/µL,
regardless of other CSF variables.
The empirical antibiotic protocols of choice are2 as
below:
● Children older than 3 months—intravenous
ceftriaxone for at least 10 days.
● Children younger than 3 months—intravenous
cefotaxime plus either amoxicillin or ampicillin
for at least 14 days.
● Suspected meningococcal disease—intravenous
ceftriaxone for 7 days.
● Children and young people who have recently
travelled outside the United Kingdom or have
had prolonged or multiple exposure to
Infections
432

antibiotics (within the past 3 months and who
may have penicillin-resistant pneumococcus)—
vancomycin in addition to the above antibiotics.
● In children younger than 3 months, ceftriaxone
may be used as an alternative to cefotaxime
(with or without ampicillin or amoxicillin), but
be aware that ceftriaxone should not be used in
premature babies or in babies with jaundice,
hypoalbuminemia, or acidosis as it may
exacerbate hyperbilirubinemia.
Below are the antibiotic protocols, which should
be employed for confirmed bacterial meningitis
unless directed otherwise by the results of antibi-
otic sensitivities.2
Children and young people older than or equal
to 3 months.
● H. influenzae type b meningitis—intravenous
ceftriaxone for 14 days.
● S. pneumoniae meningitis—intravenous
ceftriaxone for 14 days.
Children younger than 3 months.
● Group B streptococcal meningitis—intravenous
cefotaxime at least 14 days.
● L. monocytogenes meningitis—intravenous
amoxicillin or ampicillin for 21 days, plus
gentamicin for at least the first 7 days.
● Gram-negative bacilli meningitis—intravenous
cefotaxime for at least 21 days.
In children with bacterial meningitis from high-
income settings, there is no evidence from meta-
analyses that corticosteroids reduce mortality or
short-term neurological sequelae, but there is evi-
dence that adjunctive corticosteroids reduce the
risk of severe hearing loss and long-term neurolog-
ical sequelae following bacterial meningitis. Give
dexamethasone (0.15 mg/kg to a maximum dose
of 10 mg, four times daily for 4 days) for suspected
or confirmed bacterial meningitis as soon as possi-
ble, that is, at the same time as the initial dose of
antibiotic (may not have CSF results available) if
lumbar puncture reveals any of the following:
● Frankly purulent CSF.
● CSF WBC count greater than 1,000/µL.
● Raised CSF WBC count with protein
concentration greater than 1 g/L.
● Bacteria on Gram stain.
There is no evidence to support the use of cortico-
steroids in children younger than 3 months with
bacterial meningitis.
Neurosurgical
Neurosurgical intervention is only required in the
event of raised ICP which is not managed by medi-
cal means. In the majority of these cases, external
ventricular drain (EVD) placement allows drainage
of CSF and can act as a conduit for intrathecal anti-
biotic administration.
Burr hole and subdural washouts are sometimes
required for persistent subdural e usions in the
context of ongoing raised CRP and poor clinical re-
sponse to antibiotics alone ( Fig. 53.1). Neurosur-
gical intervention may be required to deal with
complications of meningitis which are discussed
later.
53.2.5 Prognosis
If meningitis is not e ciently and adequately
treated, it can spread via the leptomeningeal
sheaths of the penetrating cortical vessels in the
perivascular spaces resulting in cerebritis and
brain abscess formation. Spread of infection to the
ependymal surface results in ventriculitis and
aqueductal ependymitis causing hydrocephalus.
Fig. 53.1 Coronal T1 MRI of a 16-month old boy,
presenting with meningitis secondary to chicken pox
infection, demonstrating a right-sided subdural em-
pyema. Patient was surgically treated via burr hole
drainage isolating Streptococcus pyogenes.
Evaluation and Management of Pediatric Intracranial Infections
433

Ventriculitis occurs in 30% of patients and can be
as high as 92% in neonates.3 Necrosis in vessel
walls can result in arterial or venous thrombosis,
and overall cerebral infarctions are seen in up to
30% of neonates.3 Neonatal meningitis is a com-
mon recognized cause of hydrocephalus requiring
ventriculoperitoneal (VP) shunt placement.
Meningitis can result in significant long-term
sequelae including those of hearing loss, orthopedic
complications (damage to bones and joints), skin
complications (including scarring from necrosis),
psychosocial problems, neurological and develop-
mental problems, and renal failure. These need to
be fully appreciated, investigated, and managed
prior to discharge and in follow-up.
Group B Streptococcus appears to have the worst
outcomes, with an average of 29% of survivors
developing moderate or severe disabilities. An
average of 22% of S. pneumoniae survivors develop
moderate or severe disabilities and approximately
5% develop hearing deficits require cochlear
implants. An average of 19% of E. coli su erers
develop moderate or severe disabilities. Nine per-
cent of N. meningitidis survivors develop severe or
moderate disabilities and approximately 0.5%
develop hearing deficits require cochlear implants.
H. influenzae has the least damaging long-term
e ects, with only 1% of survivors developing
severe or moderate disabilities and 3.2% requiring
cochlear implants.2
53.3 Viral Meningitis
53.3.1 Background
Viral meningitis is relatively common although
probably underreported. It occurs at any age but
most commonly in young children. A study of
12,000 children in Finland reported the annual inci-
dence of presumed viral meningitis to be 219 per
100,000 in infants younger than 1 year and 27.8 per
100,000 overall in children younger than 14.4
The most common cause of viral meningitis is the
enteroviruses. Mumps virus infection was the com-
monest cause prior to the introduction of the
mumps, measles, and rubella (MMR) vaccination, as
15% of patients with mumps develop meningitis.5
53.3.2 Evaluation
As described previously, it is di cult to distinguish
viral meningitis from bacterial meningitis as both
are characterized by acute onset of fever and irrita-
bility. There are considerable benefits in making
this distinction swiftly, in terms of both reducing
antibiotic usage and hospital bed occupancy and
reassuring parents. Rapid PCR is available to ena-
ble prompt diagnosis. Children with viral meningi-
tis frequently report nausea, vomiting, headache,
and neck sti ness, while more children with bac-
terial meningitis present with the more serious
symptoms of fever, seizures, lethargic or comatose
state, toxic or moribund state, bulging fontanelle,
Brudzinski’s sign, and Kernig’s sign. Photophobia is
not a predictor of meningitis type.
Untreated patients with bacterial meningitis
show progressive deterioration whereas spontane-
ous recovery is usual in viral cases. Suspected
encephalitis warrants empirical antiviral treat-
ment as discussed below, while viral meningitis
does not. History and examination can yield clues
as to viral causes. The viral causes are the same as
those that cause viral encephalitis. It is important
to elicit in the history recent illness contacts, for-
eign travel, and rodents/tick exposure, HIV risk fac-
tors/immunocompetence, immunization status
(specifically MMR/mumps), and if appropriate,
sexual history. In addition, during examination,
evidence of a rash, lymphadenopathy, pharyngitis,
and parotid swelling should be sought.
53.3.3 Investigations
Laboratory Tests
Investigation is the same as that required for
suspected bacterial meningitis. CSF analysis is
required via a lumbar puncture, unless it is contra-
indicated. A blood glucose concentration is essen-
tial and should be collected immediately before
lumbar puncture. Although characteristically
associated with a mononuclear pleocytosis, neu-
trophils may predominate initially in viral menin-
gitis (Table 53.1).5 In a study of 138 children
with aseptic meningitis, 57% had a CSF polymor-
phonuclear predominance that persisted beyond
24 hours.6
As discussed previously serum CRP concentra-
tion and peripheral blood white cell count can be
helpful markers but do not reliably discriminate
diagnoses.
CSF viral analysis using PCR is the initial investi-
gation of choice. Other tests can be performed spe-
cific to the likely causative agent. If enterovirus is
suspected, then culture and PCR of throat swabs
and stool samples should be performed. If herpes
simplex virus (HSV) or varicella-zoster virus (VZV)
is suspected, then HSV type-specific serum
Infections
434

serology, together with PCR, culture, immuno-
fluorescence, electron microscopy, and Tzanck’s
smear of skin lesion samples/scraping should be
performed. In suspected mumps meningitis serum
serology should be performed together with PCR
of throat swabs, urine samples, blood and oral
fluid. If Epstein–Barr virus (EBV) is suspected, then
EBV-specific serology, viral capsule antigen IgM
and IgG, and Epstein–Barr nuclear antigen IgG
tests should be performed together with CSF PCR
and the Monospot test.5
Imaging
As discussed previously, viral meningitis in itself is
not associated with abnormalities on imaging.
53.3.4 Pathogens
Enteroviruses
The Enterovirus groups (Table 53.2) are small
nonenveloped RNA viruses of the picornavirus
family and are the commonest cause of viral
Table 53.1 Typical CSF findings in bacterial and viral meningitis
Meningitis
cause
WCC
(cells/mm 3/106 cells/L)
Predominant cell

CSF: serum glucose
(normal≥0.5)
Protein
(normal 0.2–0.4)
Viral

50–1,000

Mononuclear (may be neu-
trophilic early in course)
>0.5

0.4–0.8
Bacterial

100–5,000

Neutrophilic (mononuclear
after antibiotics)
<0.5

0.5–2
Source: Adapted from Logan and MacMahon.5
Table 53.2 Causes of viral encephalitis
Sporadic causes of viral encephalitis

Travel-related causes of encephalitis
Herpes viruses

Herpes simplex virus types 1
and 2
The Americas

West Nile
Varicella-zoster virus

La Crosse
Epstein–Barr virus

St Louis
Cytomegalovirus

Dengue
Human herpes virus 6 and 7

Rabies
Enteroviruses

Coxsackieviruses

Europe/Middle East Tick-borne encephalitis
Echoviruses

West Nile
Parechovirus

Africa

West Nile
Poliovirus

Rift Valley fever virus
Paramyxoviruses

Measles virus

Crimean–Congo hemorrhagic
fever
Mumps virus

Dengue
Other (rarer causes)

Flu viruses

Rabies
Adenovirus

Asia

Japanese encephalitis
Parvovirus

West Nile
Lymphocytic choriomeningitis
virus
Dengue
Rubella virus

Murray Valley encephalitis
Rabies
Nipah
Australasia

Murray Valley encephalitis
Japanese encephalitis
Source: Adapted from Thompson et al.7
Evaluation and Management of Pediatric Intracranial Infections
435

meningitis. Infections with these ubiquitous
viruses are mostly asymptomatic, but they have a
tendency to be neuroinvasive giving rise to neuro-
logical manifestations ranging from aseptic menin-
gitis to meningoencephalitis and paralytic polio-
myelitis. Focal neurological signs or seizures are
rare, except in neonates who are mostly at risk of
developing meningoencephalitis and severe
systemic complications such as myocarditis or
necrotizing enterocolitis, which are associated
with substantial mortality.8 Coxsackie B viruses
and echoviruses account for most cases of entero-
virus meningitis.5 Infection may be accompanied
by mucocutaneous manifestations including local-
ized vesicles such as in hand, foot, and mouth dis-
ease (enterovirus 71); herpangina (coxsackie virus
A); and generalized maculopapular rash (echovirus
9).8 Infants and young children with no immunity
are most susceptible to enteroviruses, and the inci-
dence decreases with age. Infection is seasonal in
temperate climates, the highest in summer and
autumn, but high all year round in tropical and
subtropical climates.5,8
Herpes Simplex Viruses
(HSV2, HSV1)
HSV is the second most common cause of viral
meningitis in adolescents. The rate of childhood
infection with HSV1 has declined with a fall in
seropositivity rates among 10- to 14-year olds
from 34 (1986–1987) to 24% (1994–1995).9 It is
important to understand that HSV meningitis and
encephalitis are discrete entities in the immuno-
competent host, rather than part of a continuous
spectrum. HSV meningitis is a self-limiting condi-
tion in patients with normal immunity, whereas
HSV encephalitis is a life-threatening medical
emergency warranting emergent antiviral treat-
ment. See “Encephalitis” section.
Constitutional symptoms of primary herpes
infection may occur, with malaise and clinical fea-
tures of genital HSV infection. One-third of cases
with primary HSV-2 meningitis are complicated
by sacral radiculomyelitis (manifesting as urinary
retention, constipation, paraesthesias, and motor
weakness).5
Mumps
The most common neurological manifestation of
mumps virus infection is meningitis, which is two
to five times more common in male than female
patients.8 Mumps meningitis can precede or follow
the parotid swelling, and 50% of cases occur in the
absence of parotitis. It is a recognized cause of
hydrocephalus.
53.3.5 Management
Treatment is mostly supportive and includes anal-
gesics, antipyretics, antiemetics, maintenance of
fluid balance, and prevention and treatment of
complications. There are no specific treatment rec-
ommendations for enterovirus or VZV meningitis
beyond the usual treatment for zoster, and ma-
nagement is conservative.
Immunoglobulin replacement has a role in
patients with hypogammaglobulinemia, who are
prone to severe and chronic enteroviral disease.
53.3.6 Prognosis
Enterovirus and mumps meningitis in most cases is
self-limiting and carries a good prognosis, although
it can progress to meningoencephalitis resulting in a
sudden deterioration in mental status or seizures as
discussed later. HSV2 meningitis causes neurological
complications more often than most other viral
meningitis: around one-third of all patients in one
study developed complications; however, virtually
all of these had resolved after 6 months.7 There is
some evidence that in children with meningitis
under 1 year of age, subtle neurodevelopmental
problems such as language may later be detected.7
A UK study of children with meningitis in the first
year of life found that 42% of children with echovi-
rus meningitis had mild or moderate neurological
disability by the age of 5 years.10
53.4 Encephalitis
53.4.1 Background
Encephalitis is an uncommon but potentially dev-
astating di use inflammatory process of the brain
parenchyma caused by a variety of infective patho-
gens (with viruses being the commonest) or
inflammatory/immune pathologies ( Table 53.2).
The annual rate of encephalitis in children in the
United Kingdom is 2.8/100,000, with the highest
incidence in infants under 1 year of age, 8.7/
100,000. There is no sex preponderance (2.9 in
boys vs. 2.8/100,000 in girls). Although a prospec-
tive multicenter study found the overall incidence
to be higher at around 10.5/100,000 child-years,
with an incidence of 18.4/100,000 child-years in
children younger than 1 year.11
Infections
436

Variations in the geographical distribution of
disease and their vectors exist, but globally the
commonest viruses are HSV (22%), followed by
varicella (21%), adenovirus (4%), mumps virus, and
arbovirus (e.g., Japanese encephalitis virus and
West Nile virus) spread via the hematogenous
route across the blood–brain barrier.3,7 Others in
the United Kingdom include cytomegalovirus
(CMV), EBV, measles virus, and enterovirus. Spread
to the CNS via peripheral nerves occurs in HSV1
and polio virus. Parasites and fungi are rare causes
of encephalitis, and usually a ect only immuno-
compromised patients.
53.4.2 Evaluation
Symptoms are generally nonspecific, which makes
diagnosis di cult, but it is usually associated with
prodromal acute febrile “flu-like” illness followed
by relatively acute onset of severe headaches, nau-
sea, vomiting, and altered consciousness. Symp-
toms can include seizures, meningism, and focal
neurological deficit. Diagnosis can therefore be
confused with that of bacterial meningitis. Presen-
tation may be subtle with personality/behavioral
or language/speech disturbances prior to becom-
ing frankly encephalopathic, or may be more suba-
cute in immunocompromised individuals.
An understanding of the pathogenesis of ence-
phalitis can help with appropriate diagnoses and
treatment as most present as a result of a mixture
of direct viral cytopathology and a parainfectious
or postinfectious inflammatory or immune-
mediated response.
History is important in etiology, as with viral
meningitis. Vaccination, travel history, and social
history (HIV) is important, as is a history of a rash
(chickenpox [VZV], slapped cheek syndrome (par-
vovirus), hand, foot, and mouth disease (enterovi-
rus), and roseola (human herpesvirus 6 [HHV-6]).
Parotitis, abdominal pain (pancreatitis), or testicu-
lar pain (orchitis) may be present in those with
mumps.7
Important examination findings include signs of
meningism (bulging fontanelle in a young infant,
and nuchal rigidity or positive Kernig’s sign in
older children) but these may not always be
present. It is important to assess the conscious
level and monitor for signs of raised ICP, as well as
identifying subtle seizures.
53.4.3 Investigations
Laboratory Tests
The following are recommended to be performed
routinely7:
● Full blood count and film—which may show
lymphocytosis.
● Urea and electrolytes.
● Liver function tests—raised hepatic enzymes
may be seen in EBV & CMV.
● Raised amylase in mumps.
● Capillary glucose, laboratory blood glucose.
● Blood gas (arterial or capillary or venous).
● Lactate.
● Urinalysis (dipstick) for ketones, glucose,
protein, nitrites, and leucocytes.
● Plasma ammonia (taken from a venous or
arterial sample).
● Blood culture—may identify bacteria or fungi.
● Approximately 1 to 2 mL plasma to be separated,
frozen, and saved for later analysis if required.
● Approximately 1 to 2 mL of plain serum to be
saved for later analysis if required.
● Approximately 10 mL of urine to be saved.
Culture, PCR, or immunofluorescence techniques
may be able to identify respiratory viruses, mea-
sles, enteroviruses, Chlamydophila pneumoniae
and Mycoplasma pneumoniae from a throat swab.
Using a nasopharyngeal aspirate, respiratory
viruses (influenza A, parainfluenza, adenoviruses,
and respiratory syncytial virus [RSV]) can be iden-
tified using PCR, antigen detection, or culture.
Stool samples may reveal infection with enterovi-
ruses or measles viruses, and urine samples may
reveal infection with mumps virus, through PCR or
culture. If vesicles are present, a viral swab should
be taken from the vesicle for detection of VZV or
HSV by immunofluorescence or PCR. Urine can be
cultured for CMV, mumps, or measles virus. Serum
and CSF IgM antibodies or a rising IgG concentra-
tion may allow identification of infection with
HSV, VZV, CMV, EBV, RSV, adenovirus, influenza A
and B virus, parainfluenza and enteroviruses, rota-
virus, M. pneumoniae, and arboviruses.7
A lumbar puncture should be performed in all
cases of suspected encephalitis unless contraindi-
cations exist (see “Bacterial meningitis” section).
CSF should be sent for the following investiga-
tions:
Evaluation and Management of Pediatric Intracranial Infections
437

● Microscopy, culture, and sensitivity analysis.
● PCR for HSV types 1 and 2 and VZV (HHV-6 and
HHV-7, CMV, EBV, enteroviruses, respiratory
viruses, HIV, and C. pneumonia).
● Glucose, lactate, and oligoclonal bands (with
paired serum sample).
CSF examination may reveal a mononuclear pleo-
cytosis and moderately elevated protein level, or
the CSF red blood cell count may be raised in hem-
orrhagic encephalitis. The presence of eosinophils
suggests infection with helminths, but is also seen
with toxoplasma infection, Rickettsia rickettsii, and
infection with M. pneumoniae. A decreased CSF
glucose concentration suggests a bacterial, fungal,
or protozoal etiology, but may occur in viral ence-
phalitis. Although up to 10% of patients with viral
encephalitis will have a completely normal CSF, at
least initially, and therefore a second lumbar punc-
ture should be considered if clinical evidence of
encephalitis continues.7
Occasionally pathological diagnosis may have to
be made via tissue/brain biopsy, but this is not
always feasible. Despite use of a wide range of
investigations, the etiology of encephalitis remains
unknown in approximately one-third of cases.7
Therefore, a diagnosis of encephalitis is made in
most patients who have an appropriate history
and clinical presentation together with markers of
brain inflammation (CSF pleocytosis and/or
inflammatory changes on brain MRI).
53.4.4 Pathogens
Herpes Simplex Virus 1
HSV is the commonest cause of sporadic encepha-
litis. HSV1 is the commonest cause of herpes ence-
phalitis in children over the age of 6 months.3
About 30% of all cases of HSV1 infection occur in
patients younger than 20 years. As a consequence
of the increasing incidence of genital herpes,
clinical cases of HSV encephalitis in the United
Kingdom are set to increase.5 The virus penetrates
the oral and nasal mucosa and remains dormant in
the trigeminal ganglion, after initial infection. After
reactivation (70% of all cases of HSV encephalitis
already have antibodies present) the virus spreads
along the branches of the trigeminal nerve in the
anterior and middle cranial fossa.7 It is not under-
stood why the virus reactivates, but two mutations
in children that result in impaired interferon-
production and a predisposition to herpes ence-
phalitis have been identified.7 The disease begins
in the anterior and medial parts of the temporal
lobes, spreads to the insular cortex, inferior parts
of the frontal lobes, and the cingulate gyri.
Bilateral involvement is common. Basal nuclei are
usually spared. In those that survive multifocal
encephalomalacia, cortical gyriform calcification
and ventriculomegaly are seen.
53.4.5 Varicella Virus
Varicella-zoster infection is common in childhood
and results in chickenpox, but fewer than 0.1% have
CNS complications. Symptoms usually develop
within 10 days of the onset of skin rash and include
headache, vomiting, dysarthria, hemiparesis, and
signs of raised ICP. Varicella infection results in a sig-
nificant vasculitis causing infarcts of the basal gan-
glia resulting in focal neurological deficit, which can
be sometimes delayed to between 1 and 4 months
following the initial skin rash.
Measles Virus
Measles involves the CNS as either acute postinfec-
tious encephalitis, progressive infectious encephali-
tis, or as subacute sclerosing panencephalitis (SSPE).
Acute postinfectious encephalitis is an autoimmune
process with perivascular inflammation, which
causes hemorrhage and demyelination resulting in
acute hemorrhagic leukoencephalitis. Progressive
infectious encephalitis is associated with impaired
cell immunity resulting in progressive neurological
deterioration with seizures and altered mental
state. SSPE is caused by reactivation of the measles
virus after many years of latency. This results in
behavioral change, mental deterioration, ataxia,
myoclonus, and visual disturbance. Followed even-
tually by severe dementia, quadriparesis, and auto-
immune instability. Most patients die within 1 to 3
years after the onset of the disease.
Rasmussen’s Encephalitis
First described by Rasmussen in 1958, this chronic
localized encephalitis is one of the common causes
of intractable epilepsy in childhood. A ected chil-
dren usually present between the ages of 2 and 14
years with the mean age of 7 years. Symptoms
include hemiparesis, dysphasia, hemianopia, and
mental deterioration together with progressive
refractory seizures. Surgical resection of the
a ected hemisphere is the only e ective treat-
ment. It is thought to be due to a slow viral infec-
tion like EBVor CMV, or an autoimmune cause.
Infections
438

Acute Demyelinating
Encephalomyelitis
This autoimmune postinfectious encephalitis, with
or without myelitis results in demyelination. It
occurs after a vaccination or late in the course of a
viral infection. Symptoms occur a few days to a
few weeks after a viral event. Presentation is with
seizures, ataxia, and altered mental state. Most
cases are self-limiting, with most patients making
a complete recovery although between 10 and 30%
have some permanent neurological deficit. The
disease can relapse rarely with the chances of a
second attack greater in patients who are more
than 10 years of age at initial presentation. A hem-
orrhagic variant is described in which involved
brain undergoes hemorrhagic necrosis. The prog-
nosis is poor with most patients dying days to
weeks after onset.
Imaging
MRI demonstrates inflammation of the white mat-
ter, and occasionally meninges, with neuronal loss.
Some viruses have predilection to involve certain
brain areas. Di usion-weighted imaging (DWI)
shows abnormalities earlier and more extensively
than the standard T2-weighted imaging. In HSV1,
hemorrhage can occasionally be seen and en-
hancement occurs in the subacute phase involving
the cortex and overlying meninges. In varicella
infection, lesions are often seen in the gray–white
junction, cerebral cortex, basal ganglia, and in the
cerebellum. Angiography can demonstrate associ-
ated vasculitis demonstrating narrowing of the
distal internal carotid artery (ICA) and proximal
anterior and middle cerebral arteries. In acute
postinfectious measles, encephalitis MRI demon-
strates T2 hyperintensity in the thalami, basal gan-
glia, and cortex.
In SSPE, there is di use atrophy with multifocal
areas of T2 hyperintensity in periventricular and
subcortical white matter. There is not usually con-
trast enhancement. There is typical asymmetric
involvement of the temporal and parietal lobes. The
basal ganglia are involved in 20 to 35% of cases and
the brainstem is involved late in the disease. In
Rasmussen’s encephalitis, initial imaging is often
normal. Subsequent imaging demonstrates areas of
T2 signal especially in the frontal and temporal
lobes. Atrophy of the involved regions and subcorti-
cal white matter involvement is seen later. Basal
ganglia involvement is seen in about 65% of cases.3
In acute demyelinating encephalomyelitis
(ADEM), involved areas show low attenuation on
CT and increased T2/FLAIR signal with bilateral
asymmetric involvement. DWI shows increased
water di usion. Periventricular white matter and
deep cerebral nuclei involvement is seen in 50% of
cases. The brainstem, cerebellum, and spinal cord
are involved in about 30 to 50% of cases. Spinal
imaging should be obtained that shows contrast
enhancement in the subacute stages and evidence
of swelling and increased T2 signal within the
cord.3
53.4.6 Management
Children are often inpatients for several weeks due
to prolonged courses of intravenous treatments
often coupled with lengthy recovery and rehabili-
tation. Some children will need management in an
intensive care setting.
Medical/Antimicrobial
At the time of clinical presentation, the pathogen
is uncertain and therefore broad-spectrum intra-
venous antimicrobials and antiviral treatment,
acyclovir, should be initiated pending the results
of diagnostic studies. Suitable broad-spectrum
antimicrobials include a third-generation cephalo-
sporin such as ceftriaxone, to cover S. pneumoniae,
H. influenzae, and N. meningitidis infections in
addition to ampicillin or amoxicillin to cover
L. monocytogenes (although listeriosis in immuno-
competent children is very unusual). Despite treat-
ment with acyclovir, two-thirds of patients with
HSVencephalitis are left with significant neurolog-
ical impairment.7 However, high-dose acyclovir
(60 mg/kg/day intravenously) given for 21 days for
HSV encephalitis in neonates has been shown to
reduce the rates of relapse and improve neurologi-
cal outcome.12 In adults and children older than
12 years, the current recommended treatment
regime is intravenous acyclovir 10 mg/kg every 8
hours (i.e., 30 mg/kg/day) for 21 days. The British
National Formulary for children states that chil-
dren aged 3 months to 12 years should receive
intravenous acyclovir 500 mg/m 2 every 8 hours.
Rates of relapse of herpes encephalitis have been
reported to be as high as 26% but do not occur if
treatment is given for longer than 14 days and at
doses greater than or equal to 30 mg/kg/day.7 A
negative CSF PCR result at the end of treatment is
associated with a better outcome and antiviral
Evaluation and Management of Pediatric Intracranial Infections
439

therapy should be continued in the context of a
positive PCR.7
Steroids are the mainstay of treatment for chil-
dren with ADEM and are usually given as first-line
treatment to children with an antibody-mediated
encephalitis. Treatment with intravenous immu-
noglobulin, plasma exchange, and other immuno-
suppressants, including cyclophosphamide and
azathioprine have been used.7
Neurosurgical
Neurosurgical input may be required to confirm
the diagnosis via biopsy of a ected brain tissue,
where the diagnosis is equivocal or di cult. The
area of brain to biopsy is guided by the MRI char-
acteristics of involvement. Care should be taken to
avoid eloquent areas as much as possible. Biopsy
may be undertaken using a frame-based or frame-
less stereotactic method.
In rare cases of viral encephalitis causing brain
shift and threat to life due to herniation decom-
pressive craniectomy has been described as an
e ective treatment to improve outcome.13
53.4.7 Prognosis
Studies on long-term outcome are limited
although the literature suggests morbidity rates
of up to 67% in children with HSV encephalitis,
with seizures and developmental delay being
most common.7 A Swedish retrospective study
between 2000 and 2004, of 93 children admitted
with acute encephalitis found that 60% of patients
had sequelae at discharge from hospital.14 In 24%
of cases, symptoms included cognitive impair-
ment, motor impairment, ataxia, dysphasia, or epi-
lepsy. Although relatively small numbers of all
children with RSV encephalitis made a full recov-
ery, however, 66% of children with enterovirus
encephalitis had ataxia, fatigue, and personality
change and 60% of children with VZV encephalitis
had ataxia.
Memory impairment was present in both cases
of HSV encephalitis, and of the two children with
EBV encephalitis one su ered from anxiety and
one with ataxia, cognitive problems, and epi-
lepsy.14
In this study, predictors of adverse outcomes
were focal neurology at the time of presentation,
with 84% having symptoms at discharge, and ence-
phalopathy, CSF pleocytosis, and positive neuroi-
maging finding. Seizures or age at presentation
were not predictive of symptoms at discharge.14
Other studies have suggested that predictors of
poor outcome include a GCS of less than 6 and dis-
ease present for more than 4 days prior to starting
treatment.7
53.5 Brain Abscess, Subdural
Empyema, and Extradural
Empyema
53.5.1 Background
Brain abscess and subdural empyemas are rela-
tively uncommon but serious infections. In the
United Kingdom, over a 10-year period between
1999 and 2009, 121 children presented with brain
abscesses to four large pediatric neurosurgical cen-
ters.15
Brain abscesses arise as localized areas of cere-
britis that evolve through four stages of evolution
into a collection of intraparenchymal purulent
material: early cerebritis (3–5 days), late cerebritis
(5–14 days), early capsule formation, and late cap-
sule formation (weeks to months) (Table 53.3).
The infection most commonly is a complication of
bacterial meningitis but can result via direct
spread from contiguous sites such as sinusitis or
mastoiditis ( Fig. 53.2), through hematogenous
seeding, for example, in congenital heart disease,
or via direct inoculation as occurs with penetrat-
ing injury from trauma, or surgery. Neurological
deficit arises as a consequence of mass e ect/
Table 53.3 MRI appearances during evolution of parenchymal abscesses
Abscess evolution Appearance on T1

Appearance on T2

Contrast appearance
Early cerebritis

Heterogeneous hyperintensity Heterogeneous hyperintensity Patchy enhancement
Late cerebritis

Hyperintense rim
Hypointense cavity
Hypointense rim
Hyperintense cavity
Intense wall enhancement
Early capsular

Hyperintense rim
Hypointense cavity
Hypointense rim
Hyperintense cavity
Intense wall enhancement
Late capsular

Isointense capsule

Hypointense capsule

Smooth and intense enhancement
Infections
440

compression of adjacent structures, direct destruc-
tion, or infarction secondary to vasculitis. The loca-
tion tends to vary with age; cerebellar abscesses
are more common in younger children and tempo-
ral lobe abscesses in older children.16 Deep abscess
location, particularly in the parieto-occipital lobes,
has a higher propensity to rupture into the ven-
tricular system causing ventriculitis, which is a
life-threatening event, associated with poor out-
come. This can occur as the collagen abscess cap-
sule is thicker and better developed on the cortical
side than the ventricular side, probably due to the
increased vascularity on the cortical side.3
Subdural empyema is a rare and life-threatening
complication of sinusitis in children. It may also
occur following meningitis in 2% of infants, pene-
trating head injury, cranial osteomyelitis, or via
hematogenous spread. Pott’s pu y tumor is a non-
neoplastic complication of acute sinusitis charac-
terized by osteomyelitis of the frontal bone and
subperiosteal abscess formation and thus forehead
swelling, hence the name. This infection can
spread intracranially causing epidural abscess,
subdural empyema, and brain abscess, and can
be associated with cortical vein thrombosis
(Fig. 53.3). Sinusitis occurs in 5 to 10% of all
respiratory tract infection in children, and only in a
minority of cases, there is an intracranial spread
with involvement of the subdural or extradural
compartment, via bone erosion or more commonly
by indirect hematogenous spread.17 The frontal
sinus is the most common culprit followed by the
ethmoid, sphenoid, and maxillary sinuses. The
overall reported incidence of subdural empyema is
between 10 and 41% of all localized intracranial
infective processes, with a decreasing mortality rate
from 42% in the 1950s to 12% in the 1990s.18 The
supratentorial compartment is more commonly
a ected (90–95% of cases) with a reported inci-
dence of infratentorial subdural empyema in chil-
dren of 0.6 to 1.9%.18 Aggressive management of
these cases with craniotomy evacuation of the sub-
dural or extradural collection, endoscopic or antral
washout of the sinuses, and parenteral antibiotic
therapy has led to a decrease mortality rate,
although delayed diagnosis and recurrent collec-
tions still appear to be problems and contributing
factors in its morbidity or mortality.18
Fig. 53.2 Axial contrast-enhanced T1 MRI of a 10-year
old girl presenting with mastoiditis, demonstrating a
left cerebellar abscess. Patient was surgically treated via
burr hole drainage under electromagnetic image
guidance and S. intermedius was isolated. This patient
went on to develop venous sinus thrombosis and
secondary hydrocephalus requiring insertion of a
ventriculoperitoneal shunt.
Fig. 53.3 Axial contrast-enhanced CT of a 9-year old
girl, presenting generally unwell with frontal sinusitis,
demonstrating Pott’s puffy tumor and a frontal extra-
dural abscess. Patient was surgically treated via a
craniotomy and drainage isolating S. constellatus.
Epidural abscesses are almost always secondary to or
associated with other infections such as a mastoiditis,
sinusitis, or osteomyelitis of the skull. As the abscess
expands, it strips the dura from the skull due to the
pressure of the expanding inflammatory mass. As a
result of its relatively slow-growing nature, symptoms
are often insidious and, depending on its location, focal
neurological signs may develop due to the pressure
e ect of continued expansion.
Evaluation and Management of Pediatric Intracranial Infections
441

53.5.2 Evaluation
A recent UK study demonstrated the male:female
ratio to be 1:1 but with a bimodal age presentation
distribution, with peaks at younger than 2 and
11 years, boys presenting older than girls (median
11 vs. 8 years).15,19,20 The commonest underlying
medical conditions predisposing patients to these
infections include congenital heart disease and
immunodeficiency. The commonest preceding
infection is sinusitis in approximately a third or
more of patients.15,20 The commonest symptoms at
presentation are nonspecific but headache and
abnormal focal neurology and/or altered con-
sciousness are often present, and seizures occur in
up to 30%.18 The classic triad of headache, fever,
and focal neurological findings is highly suggestive
of intracranial abscess formation, although the
percentage of children presenting with this triad
in the literature varies between 13 and 70%.15,20
Brain abscess should be a strong consideration in a
child who presents with new onset of acute head-
aches or first-time seizures, especially when focal
neurological signs are present. In the neonate, a
brain abscess is a potential cause of irritability, a
bulging fontanelle, and a rapid increase in head
circumference16 ( Fig. 53.4).
53.5.3 Investigations
Laboratory Tests
Analysis of blood inflammatory markers such as
white cell count and CRP should be undertaken, as
should blood cultures. Obtaining CSF via a lumbar
puncture in the presence of a brain abscess may be
life threatening due to a risk of herniation. If CSF is
obtained, there may be a mild mononuclear pleo-
cytosis, slight elevation of protein, and a normal
concentration of glucose; however, the culture
tends to be sterile unless the abscess has ruptured
into the ventricular system.16
Samples of pus taken intraoperatively should be
sent for microscopy, culture, and sensitivity. The
use of further molecular diagnostic techniques,
such as PCR and 16/18 s rDNA testing, is often use-
ful in increasing the diagnostic yield from pus
samples.
Imaging
MRI is the cerebral imaging choice as it allows
prompt confirmation of the clinical diagnosis,
abscess location, and number.16 It has been shown
to have a sensitivity of up to 100%.15
Brain abscess in infants and newborns tend to
be located in the periventricular white matter as
opposed to the subcortical white matter seen in
adults. Subdural empyemas are usually shaped in
a crescent and occur along the cerebral convexities
in approximately 50% of cases and along the falx in
20% of cases. On CT, they appear as extra-axial
fluid collections that are isointense or slightly
hyperintense to CSF. On T1-weighted MRI, they
show mild hyperintense signal when compared to
CSF, and on T2-weighted imaging, they are isoin-
tense or hyperintense. There is restricted di usion
on DWI and apparent di usion coe cient (ADC)
imaging, which is useful to distinguish them from
hygromas or chronic hematomas. There is marked
rim enhancement, on contrast administration,
caused by inflammatory changes of the limiting
membrane caused by hypervascularity and
Fig. 53.4 Axial CT scan of a 3-month old girl infant,
presenting with symptoms of sepsis and macrocephaly,
demonstrating a left frontal loculated intracerebral
abscess. Patient was surgically treated via transfonta-
nelle drainage isolating S. pneumoniae. In subdural
empyema, the presentation may be prolonged and
insidious with nonspecific symptoms such as malaise,
fever, rhinorrhea, and cough. The interval of time
between the onset of first symptoms (rhinorrhea,
cellulitis, feeling unwell, pyrexia) and the development
of symptoms indicative of intracranial infection has
been reported to be between 2 and 6 weeks.18 These
nonspecific symptoms can be easily overlooked by the
family physician, leading to the delayed diagnosis often
seen, but this period of time offers a therapeutic
window in which aggressive treatment of sinus infection
may prevent the formation of subdural empyema.
Infections
442

fibrosis. Surrounding parenchyma may have
abnormal signal due to cerebritis and ischemia
secondary to venous thrombosis.
DWI and MR spectroscopy can aid in the di er-
entiation of a brain abscess from tumor. Brain
abscesses show peaks of aliphatic amino acids like
alanine, succinate, acetate, leucine, isoleucine, and
valine,3 whereas tumors generally show increased
choline with reduced N-acetylaspartate on MR
spectroscopy. Pus in abscesses has restricted di u-
sion and appears hyperintense on DWI.21 Serial
scanning should be used for follow-up to compare
abscess size over time to aid treatment protocols
and ensure resolution. Contrast enhancement
should not be used as a guide to treatment res-
ponse as it may persist, presumably due to fibrosis,
following treatment completion.
Susceptibility-weighted imaging (SWI) MRI
exploits the magnetic susceptibility di erences
between di erent tissues and is exquisitely sensi-
tive to blood, iron, and calcification. SWI may
be helpful in the recognition of infective emboli
associated with systemic sepsis22 ( Fig. 53.5).
If an MRI cannot be obtained, a CT scan with
intravenous contrast should be performed, or in
the neonate, bedside cranial ultrasonography is an
alternative.
53.5.4 Pathogens
Historically subdural empyema was a disease of
infancy associated with meningitis and caused by
H. influenzae type b. The incidence of which has
dropped dramatically since the introduction of
national vaccination programs.
The most common pathogens are streptococci
attributed to over 50% of cases, with the commonest
belonging to the Streptococcus milleri group (Strep-
tococcus intermedius, Streptococcus anginosus, and
Streptococcus constellatus).15,20 These are normal
flora in the mouth and gastrointestinal (GI)
tract. Other organisms include Haemophilus sp,
Enterobacter, Citrobacter, and Pseudomonas
(Table 53.4). Children with penetrating trauma
Fig. 53.5 (a) Axial contrast-enhanced
T1 MRI of a 9-year old boy, presenting
with systemic sepsis requiring extrac-
orporeal membrane oxygenation with
a pleural empyema and osteomyelitis,
demonstrating a left occipital abscess.
(b) Susceptibility-weighted imaging
MRI of the same patient demonstrat-
ing microemboli not identified on the
standard T1 with contrast MRI.
Table 53.4 Common causative organisms of brain
abscess in children, organized by predisposing factors
Predisposing factor

Causative organism(s)
Neonate

Proteus spp
Citrobacter spp
Enterobacter spp
Immunocompromised

Nocardia spp
Fungi
Mycobacterium tuberculosis
Congenital heart disease

Streptococcus viridans
Microaerophilic strepto-
cocci Haemophilus spp
Middle ear infection

Streptococci (aerobic and
anaerobic)
Enterobacteriaceae
Pseudomonas spp
Sinusitis

Streptococci (aerobic and
anaerobic)
Staphylococcus aureus
Enterobacteriaceae
Oral cavity infection

Mixed anaerobic flora
Streptococci (aerobic and
anaerobic)
S. aureus
Enterobacteriaceae
Posttraumatic

S. aureus
Streptococcus spp
Enterobacteriaceae
Source: Adapted from Sheehan et al.16
Evaluation and Management of Pediatric Intracranial Infections
443

or postneurosurgery are more likely have Staphy-
lococcus aureus infections. Very few abscesses are
caused by anaerobic bacteria. Fungal and amoebic
abscess are very rare and generally in immuno-
compromised hosts. Multiple pathogens have been
found in up to 25% of cases. In those cases where a
pathogen is not identified from samples taken
intraoperatively, it is important to culture material
from di erent sites that include blood, phlegm,
urine and stool cultures, and CSF as this can often
lead to positive results.
53.5.5 Management
Medical/Antimicrobial
The importance of obtaining a sample for culture
cannot be overemphasized but empirical treat-
ment should be commenced as soon as possible.
● Ceftriaxone/cefotaxime plus metronidazole as
initial treatment.
● If meningitis or cyanotic congenital heart disease
is present, then ceftriaxone alone may be
su cient.
● In penetrating trauma/postneurosurgery,
treatment should cover S. aureus, but there are
insu cient data to support whether
flucloxacillin or a carbapenem should be used or
whether ceftriaxone is su cient.
● Meropenem is the first-line choice in the
severely ill or immunocompromised.
● Vancomycin should be added if the patient is
methicillin-resistant S. aureus (MRSA)-colonized
or is from a high-prevalence area.
The optimal duration of treatment is not known
but the consensus is that brain abscesses should be
treated with a total of 6 weeks of antibiotics, of
which at least 1 to 2 weeks should be intravenous,
guided by improvement in clinical condition, MRI
findings, and blood inflammatory markers.15,16,23
Oral step-down antibiotics would include amoxi-
cillin/clavulanate, although alternatives such as
clindamycin or rifampicin may be suitable, and
treatment should be guided by culture results.15,23
Some studies have suggested shorter courses can
be advocated but at present, there is limited data
to support this.
Seizure Prophylaxis
There are no studies to guide the prophylactic use
of antiepileptic therapy in children with brain
abscesses. Some practitioners favor short-term
prophylactic use of antiepileptic drugs in all chil-
dren with a brain abscess, others commence antie-
pileptic therapy only in patients whose presentation
includes a seizure. If anticonvulsants are started, be
mindful of the possible pharmacological interac-
tions between antibiotics and anticonvulsants in
calculating dosages.
Neurosurgical
Cerebral Abscess
Consideration of treating cerebritis, small solitary
abscesses (<2 cm in diameter), or those in which
the causative agent has been identified by antimi-
crobials alone is possible,16
although thought
should be given to surgical drainage. Surgical
drainage is required if there is (1) deteriorating
neurological deficit or consciousness, (2) marked
mass e ect on imaging, (3) failure of antibiotic
treatment, (4) need to obtain organism samples
for culture.
Surgical drainage can often be performed using
frameless stereotactic burr hole aspiration (CT,
MRI, or ultrasound based), or via neuroendoscopy,
without the need for a craniotomy. The use of int-
raoperative ultrasonography can further help to
ensure abscess evacuation. The majority of chil-
dren only require a single aspiration.16,24 If there is
a progressive neurological deterioration, or nonre-
solution or growth of the abscess despite adequate
and appropriate antimicrobial therapy, then repeat
aspiration or craniotomy should be performed.
Craniotomy allows more complete evacuation and
debridement of the infected parenchyma together
with the abscess wall, but its size should be as
small as possible. Intracranial foreign bodies asso-
ciated with abscesses, such as shunt tubing or deep
brain electrodes, should be removed.
Surgical complications associated with burr hole
aspiration or craniotomy include hemorrhage, CSF
leakage, seizure, stroke, and risk to life. It is impor-
tant when planning a needle trajectory for aspira-
tion that in addition to avoiding eloquent areas
does not penetrate the ventricle due to the risk of
seeding the infection.
Subdural Empyema
This is a neurosurgical emergency that commonly
requires emergency craniotomy. Craniotomy and
evacuation of the pus collection followed by intra-
venous antibiotic treatment is the standard neuro-
surgical treatment in most neurosurgical centers.
Infections
444

It has been reported that wide craniotomy with
pus washout and deloculation of the collection, if
saeptae are present, allows better control of raised
ICP and reduced incidence of reaccumulation.18,25
If sinus disease is the causative insult, then consid-
eration of a sinus washout by the otolaryngology
team during the same operating sitting should
be made. Attempts should not be made to
remove formed adherent pus from the arachnoid
due to risk of damaging underlying parenchyma
(Fig. 53.6).
The empyema may recollect at the site of the
original craniotomy or a de novo focus of infection
may form in a di erent location. The reaccumula-
tion rate requiring reoperation has been reported
to vary between 18 and 33%.18,26 Therefore, post-
operative imaging is an essential tool in the early
detection of possible recollections.
Subdural empyema may present with associated
lesion such as an intra-axial abscess, extradural
collection, bone infection, soft tissue infection,
meningitis, or hydrocephalus. The incidence of
these associated lesions varies with the location
and the severity of the subdural infection, but the
treating team must be mindful to monitor for
these.
Epidural Abscess
Treatment consists of appropriate antibiotic ther-
apy combined with neurosurgical drainage with
thorough irrigation, either through burr holes, cra-
niotomy, or craniectomy. In epidural abscesses,
consideration should be made to removal of
infected bone especially if it is sequestered or pre-
viously devascularized by surgery or trauma. In
suppuration complicating craniofacial reconstruc-
tion where bone loss would create irreparable
defects, the bone may be replaced, and prolonged
antibiotic administration planned. This may be
successful in preserving bone fragments until they
are revascularized or resorbed.
53.5.6 Prognosis
Although relatively rare in children, intracranial
suppuration is associated with significant morbidity
and mortality. The potential long-term sequelae
depend on abscess location and cortical involve-
ment but can include among others seizures,
hemiparesis, cognitive deficits, and cranial nerve
dysfunction. Approximately a third of children will
not return to their predisease state, having focal
neurological deficits, and approximately 6% will
die.15,20 Predisposing factors to a poorer outcome
include age younger than 5 years and a GCS less
than or equal to 8 at admission.15 It is therefore
essential that early diagnosis combined with the
prompt initiation of empirical antimicrobial therapy
and neurosurgical intervention are instigated to try
and minimize long-term sequelae.
53.6 Common Clinical
Questions
1. In neonates what are the common causative
organisms of bacterial meningitis and from
where are they generally acquired?
2. What are the contraindications to performing a
lumbar puncture?
3. What are the commonest global causes of viral
encephalitis?
4. What are the four stages of brain abscesses
evolution?
5. What are the indications for surgical drainage of
brain abscesses?
Fig. 53.6 Axial contrast-enhanced T1 MRI of a 14-year
old adolescent girl, presenting with 2 weeks of headache
and partially treated frontal sinusitis resulting in menin-
gitis, demonstrating a parafalcine subdural empyema.
Patient was surgically treated via a bifrontal craniotomy
and drainage isolating Streptococcus species.
Evaluation and Management of Pediatric Intracranial Infections
445

53.7 Answers to Common
Clinical Questions
1. In neonates (<28 days old), the most common
causative organisms are likely to be acquired
around the time of birth from the maternal
genital and GI tract, and are S. agalactiae
(Group B Streptococcus), E. coli, S. pneumoniae,
and L. monocytogenes.
2. Performance of a lumbar puncture is
contraindicated if the following signs are
present:
● Signs suggesting raised ICP:
– Reduced or fluctuating level of
consciousness (GCS<9 or a drop of ≥3)
– Relative bradycardia and hypertension
– Focal neurological signs
– Abnormal posture or posturing
– Unequal, dilated, or poorly responsive
pupils
– Papilloedema
– Abnormal “doll’s eye” movements
● Shock
● Extensive or spreading purpura
● After seizures until stabilized
● Coagulation abnormalities:
– Coagulation results outside the normal
range
– Platelet count below 100 ×109/L
– Receiving anticoagulant therapy
● Local superficial infection at the lumbar
puncture site.
● Respiratory insu ciency (lumbar puncture is
considered to have a high risk of precipitating
respiratory failure in the presence of
respiratory insu ciency).
3. Globally the commonest causes of viral
encephalitis are herpes simplex virus (22%),
followed by varicella (21%), adenovirus (4%),
and mumps virus.
4. The four stages of evolution of brain abscesses
are early cerebritis (3–5 days), late cerebritis
(5–14 days), early capsule formation, and late
capsule formation (weeks to months).
5. Surgical drainage is required if there is:
● Deteriorating neurological deficit or
consciousness.
● Marked mass e ect on imaging.
● Failure of antibiotic treatment.
● Need to obtain organism samples for
culture.
References
[1] Brouwer MC, Tunkel AR, van de Beek D. Epidemiology,
diagnosis, and antimicrobial treatment of acute bacterial
meningitis. Clin Microbiol Rev. 2010; 23(3):467–492
[2] National Collaborating Centre for Women’s and Children’s
Health. Bacterial Meningitis and Meningococcal Septicaemia
in Children. London, UK: RCOG Press; 2010
[3] Parmar H, Ibrahim M. Pediatric intracranial infections.
Neuroimaging Clin N Am. 2012; 22(4):707–725
[4] Rantakallio P, Leskinen M, von Wendt L. Incidence and
prognosis of central nervous system infections in a birth
cohort of 12,000 children. Scand J Infect Dis. 1986; 18(4):
287–294
[5] Logan SA, MacMahon E. Viral meningitis. BMJ. 2008; 336
(7634):36–40
[6] Negrini B, Kelleher KJ, Wald ER. Cerebrospinal fluid findings
in aseptic versus bacterial meningitis. Pediatrics. 2000; 105
(2):316–319
[7] Thompson C, Kneen R, Riordan A, Kelly D, Pollard AJ.
Encephalitis in children. Arch Dis Child. 2012; 97(2):150–161
[8] Chadwick DR. Viral meningitis. Br Med Bull. 2006; 75–76:1–
14
[9] Vyse AJ, Gay NJ, Slomka MJ, et al. The burden of infection
with HSV-1 and HSV-2 in England and Wales: implications
for the changing epidemiology of genital herpes. Sex Transm
Infect. 2000; 76(3):183–187
[10] Bedford H, de Louvois J, Halket S, Peckham C, Hurley R,
Harvey D. Meningitis in infancy in England and Wales: follow
up at age 5 years. BMJ. 2001; 323(7312):533–536
[11] Koskiniemi M, Korppi M, Mustonen K, et al. Epidemiology of
encephalitis in children. A prospective multicentre study. Eur
J Pediatr. 1997; 156(7):541–545
[12] Kimberlin DW, Lin CY, Jacobs RF, et al. National Institute of
Allergy and Infectious Diseases Collaborative Antiviral Study
Group. Safety and e cacy of high-dose intravenous acyclovir
in the management of neonatal herpes simplex virus
infections. Pediatrics. 2001; 108(2):230–238
[13] Pérez-Bovet J, Garcia-Armengol R, Buxó-Pujolràs M, et al.
Decompressive craniectomy for encephalitis with brain
herniation: case report and review of the literature. Acta
Neurochir (Wien). 2012; 154(9):1717–1724
[14] Fowler A, Stödberg T, Eriksson M, Wickström R. Childhood
encephalitis in Sweden: etiology, clinical presentation and
outcome. Eur J Paediatr Neurol. 2008; 12(6):484–490
[15] Felsenstein S, Williams B, Shingadia D, et al. Clinical and
microbiologic features guiding treatment recommendations
for brain abscesses in children. Pediatr Infect Dis J. 2013; 32
(2):129–135
[16] Sheehan JP, Jane JA, Ray DK, Goodkin HP. Brain abscess in
children. Neurosurg Focus. 2008; 24(6):E6
[17] Waseem M, Khan S, Bomann S. Subdural empyema
complicating sinusitis. J Emerg Med. 2008; 35(3):277–281
[18] Osman Farah J, Kandasamy J, May P, Buxton N, Mallucci C.
Subdural empyema secondary to sinus infection in children.
Childs Nerv Syst. 2009; 25(2):199–205
[19] Wong TT, Lee LS, Wang HS, et al. Brain abscesses in children—
a cooperative study of 83 cases. Childs Nerv Syst. 1989; 5(1):
19–24
[20] Leotta N, Chaseling R, Duncan G, Isaacs D. Intracranial
suppuration. J Paediatr Child Health. 2005; 41(9–10):
508–512
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[21] Nickerson JP, Richner B, Santy K, et al. Neuroim aging of
pediatric intracranial infection–part 1: techniques and
bacterial infections. J Neuroim aging. 2012; 22(2):
e42–e51
[22] Lai PH, Chang HC, Chuang TC, et al. Susceptibility-weighted
imaging in patients with pyogenic brain abscesses at 1.5T:
characteristics of the abscess capsule. AJNR Am J
Neuroradiol. 2012; 33(5):910–914
[23] Infection in Neurosurgery Working Party of the British
Society for Antimicrobial Chemotherapy. The rational use of
antibiotics in the treatment of brain abscess. Br J Neurosurg.
2000; 14(6):525–530
[24] Goodkin HP, Harper MB, Pomeroy SL. Intracerebral abscess in
children: historical trends at Children’s Hospital Boston.
Pediatrics. 2004; 113(6):1765–1770
[25] Hendaus MA, Corporation HM. Subdural empyema in
children. Glob J Health Sci. 2013; 5(6):54–59
[26] Glickstein JS, Chandra RK, Thompson JW. Intracranial
complications of pediatric sinusitis. Otolaryngol Head Neck
Surg. 2006; 134(5):733–736
Evaluation and Management of Pediatric Intracranial Infections
447

54 Evaluation and Management of Pediatric
Spinal Infections
Lydia J. Liang, Mari L. Groves
54.1 Introduction
Spinal infections have been recognized throughout
history.1
Regional variability in socioeconomic
changes and endemic microbial flora has led to dif-
ferences in the epidemiology of spinal infections
worldwide. While advances in medical technology
have enhanced the ease of detection and options for
definitive treatment of these infections, they have
also promoted the development of spinal infections
by increasing the number of patients on iatrogenic
immunosuppression and incidence of iatrogenic
infections. Infections of the spine are relatively rare,
yet often present with variable, nonspecific symp-
toms, requiring a high index of suspicion from clini-
cians. Spinal infections in the pediatric population
are generally less common and less completely char-
acterized than those in adults.1,2
From a neurosurgical perspective, spinal infec-
tions can be broadly divided into three categories
by location—(1) infections of the spinal cord; (2)
infections of the nerve roots and meninges; and
(3) infections of the spinal axis, including the ver-
tebrae, disks, and epidural space. Infections of the
spinal axis can be further subdivided into sponta-
neous pyogenic infections, iatrogenic infections,
and granulomatous infections caused by mycobac-
terium, fungi, unusual bacteria, and parasites. This
chapter will focus on infections of the spinal cord
and spinal axis. The severity of spinal infections
relates to the number of structures involved, verte-
bral level of involvement, presence or absence of
neurological symptoms, delay in diagnosis, viru-
lence of the organisms involved, and immunologi-
cal status of the host.
Risk factors for children and adults include
intravenous (IV) drug abuse, AIDS, and chronic
conditions such as diabetes. Medical interventions
such as immunosuppression, chronic indwelling
catheters for venous access, or chemotherapy also
increase the risk for spinal infections.
The vertebral end plate is the most commonly
reported focus of vertebral infection, followed by
the disk space itself, epidural abscess formation,
and paraspinal abscess formation.3
Spinal axis infections:
● Average delay in diagnosis is 3 months, average
recovery period is 12 months.3
● Pyogenic spinal infections (PSIs)—neutrophil
predominant:
– More frequent in males (55–75%).3
– Annual incidence now estimated at between 5
and 10 cases per million 1 (17–19).
– Diskitis—infection of the intervertebral disk.4,5,6
○ A ects children of all ages, but its prevalence
is highest in children younger than 5 years,
and adolescents.7,8
○ Lumbosacral (78%) >thoracic >cervical
disease.3,9
– Pyogenic vertebral osteomyelitis (PVO)
(Fig. 54.1)—infection of the vertebral body/
pyogenic spondylodiskitis—infection of the
vertebral body and adjacent disk.10
○ A ects older children past the age of 8 years,
incidence peaks in adolescence and again in
later adult years.
○ About 2 to 7% of all cases of osteomyelitis
involve the spine.
○ In persons younger than 20 years, the
incidence is 0.3 per 100,000, but rises
sharply in late adulthood to 6.5 per 100,000.
– Spinal epidural abscess (SEA) ( Fig. 54.1)
purulent collection between the bone and
dura mater:11,12
○ Majority of cases of SEA in children are
individual case reports. Overall incidence of
SEA ranges from 2 to 20 per 100,000.
○ Less common than cranial epidural
abscesses. Commonly secondary to
pyogenic or tubercular diskitis and
osteomyelitis.
○ More common in girls than in boys.
● Granulomatous spinal infections:
– Tuberculosis (TB) of the spine (Pott’s disease;
tuberculosis spondylodiskitis [TS])—caused by
Mycobacterium Tuberculosis.
○ More common in developing world with
higher rates of TB.
○ Spinal TB occurs in 1 to 3% of people infected
with TB.
○ Predilection for anterior vertebral body
involvement of the thoracolumbar spine,
although posterior vertebral body can be
involved.
○ Axial skeleton accounts for about 60% of all
cases of TB osteomyelitis.13
448

○ Up to 10% of patients have multiple involved
levels with intervening normal “skip”
regions. Unlike in adult patients, children
rarely present with paraplegia.
○ Neurological loss observed in 10 to 60% of
patients.2,14
– Brucellosis:
○ Most common zoonosis in humans. About 20
to 25% of systemic brucellosis cases involve
children. In children, transmission occurs
from infected animals to humans via
consumption of raw milk or milk products.
○ Cutaneous, hematological, and respiratory
complications are most common in children.
○ May be present focally or di usely.2
● Iatrogenic infections:
– Rates of surgical site infections (SSIs) following
pediatric spine surgery range from 3.7 to
8.5%.15,16
– Reported risk factors include inappropriate
timing of antibiotics, previous spine surgery,
complex medical comorbidities, age, more
than 10 vertebrae fused, increase
intraoperative blood loss, obesity, infection
prophylaxis with clindamycin, and prolonged
intraoperative hypothermia.17,18,19 Skin
preparation before surgery, wound irrigation
before closure, nutritional status, and
preoperative antibiotic administration have
also been hypothesized as major factors
influencing infection.
– Financial costs range from $26,977 to $961,722
secondary to hospital readmissions and repeat
surgeries.20
● Intramedury spinal cord abscess (ISCA)—
suppurative infection of the central nervous
system (CNS) similar to pyogenic brain
abscesses21:
– Isolated infection of the spinal cord is
uncommon overall, with only 96 cases published
between 1830 and 2011,22 yet over 40% of ISCA
presents in patients younger than 20 years, with
25 to 27% of patients younger than 10 years.23,24
– Male predilection—60 to 70% of cases occur in
men.23,24
– Most frequently found in the thoracic region
(32%) >cervical (17%) >lumbar (12%).
– About 69% of all abscesses involved some
portion of the thoracic cord.23
– Causative organisms include Schistosoma
(particularly common children), Candida
infection, Aspergillus, and nocardiosis.14
– Predisposing conditions include congenital
heart disease, disorders of the immune system,
underlying spinal cord tumors, and dermal
sinuses, which may give rise to intraspinal
abscesses outside and inside the cord.14
– Higher incidence in IV drug users.25
Infective organisms can be carried to the spine by
direct inoculation through surgical manipulation
or a penetrating injury, by local spread from
Fig. 54.1 (a) Sagittal fat-suppressed T2-weighted imaging demonstrating vertebral osteomyelitis at the L4–L5 level, seen as
poorly defined zones with high signal in the marrow of the vertebral bodies (arrows) and corresponding gadolinium contrast
enhancement on (b) sagittal and (c) axial fat-suppressed T1-weighted imaging (arrows). Abnormal high signal on T2-
weighted imaging is seen involving the L4–L5 disk as well as irregularities at the end plates of the adjacent vertebral bodies.
The infection extends posteriorly to involve the epidural soft tissues, and there is an epidural abscess at the L5 level (arrow in
b). (Reproduced with permission from Differential Diagnosis in Neuroimaging: Spine, 2017. Meyers, Steven. Fig. 1.193)
Evaluation and Management of Pediatric Spinal Infections
449

continuous structures, or hematogenously from a
distant site of infection.1,3 Infections tend to be
localized in a single region (i.e., vertebral body,
disk, and epidural space), but may involve multiple
regions concurrently. For pyogenic and nonpyo-
genic infections that spread hematogenously from
a primary source of infection other than the spine,
a proposed mechanism of spread begins with bac-
teria lodging in the capillary loop or postcapillary
venous channels in the end plate. The infection
can extend anteriorly to create a paravertebral
abscess, longitudinally along the spinal axis to
cause diskitis, or posteriorly to cause myelitis or an
epidural abscess. In most cases, infection of the
vertebral body is limited by the cartilage-capped
end plates. As the infection progresses, suppura-
tive inflammation and tissue necrosis eventually
result in end plate erosions and infection of the
vertebral body. The bone softens and may collapse
under the body’s weight, leading to deformity or
kyphosis. Neurological deficits are caused by direct
extension of the infection to the neural elements,
or secondary compression from pathological frac-
ture as a result of bone softening.3
Tuberculous infections, on the other hand, typi-
cally feature a slow inflammatory response initiated
by bacteria, with the formation of a tuberculous
granuloma in the vertebral end plate.26 It caseates
centrally and forms an abscess, which may extend
in any direction. The abscess grows “cold” and large
and may compress adjacent structures, extend into
the spinal canal, or develop into a sinus.2,27 Patho-
logical fracture of the vertebral body following the
development of a fibrous ankylosis most commonly
in the thoracic spine may eventually result in
angular kyphosis and compromise of the spinal
canal by sequestration of vertebra and disk or by
dislocation of one spinal segment.28
54.2 Anatomy
The vertebral body is composed of a central zone
and a peripheral zone, with an epiphyseal ring
surrounding the outer rim of the vertebral body sur-
face. It is slightly raised, externally overlapping the
outer surface of the vertebral body, and internally
slopes to meet the peripheral zone of the bony end
plate. The bony end plate is separated from the
intervertebral disk by a central cartilaginous end
plate, which consists of hyaline cartilage. The annu-
lus fibrosis of the intervertebral disk is firmly adher-
ent to the epiphyseal ring, where the central portion
is less firmly attached29,30 (Fig. 54.2).
At the level of each vertebra, the vertebral
artery, intercostal artery, or lumbar arteries pro-
vide nutrient vessels that enter the vertebral body,
form anastomoses at each level, and join with a
posterior nutrient and venous network. Vascular
loops and channels formed by these anastomoses
in the bony end plate supply nutrients to the inter-
vertebral disk via di usion through the cartilagi-
nous end plate, as the disk is avascular even in
infants.28,31,32 These loops are more prominent
in children than adults, and diminish with age. In
children younger than 8 years, this vasculature
extends beyond the ossification center into the
surrounding cartilage directly in close proximity
to the border of the intervertebral disk.33,34 This
provides a more direct route of infectious spread
Fig. 54.2 Structure of intervertebral
disk. Anterosuperior view with the
anterior half of the disk and the right
half of the end plate removed. The
intervertebral disk consists of an ex-
ternal fibrous ring (annulus fibrosus)
and a gelatinous core (nucleus pulpo-
sus). (Reproduced with permission
from Thieme. Atlas of Anatomy,
2nd ed. Chapter 1 Bones, Ligaments
& Joints, Fig 1.18.)
Infections
450

to the intervertebral disk and may explain the
distinctly higher incidence of diskitis in children
compared to adults. Notably, a high proportion of
cultures in diskitis are negative.28
The extensive venous drainage of the spine pro-
vides an opportunity for retrograde spread of
infection. The external and internal venous plex-
uses run the length of the spine, and communicate
with venous systems throughout the body, includ-
ing the pelvic, prostatic, sacral, pulmonary, caval,
thoracoabdominal, scalp, skull, and facial venous
systems ( Fig. 54.3 and Fig. 54.4).26,30
Fig. 54.3 Veins of the back. Vertebral
venous plexus, posterior view with
vertebral canal windowed in the lum-
bar and sacral spine. (Reproduced with
permission from Thieme. Atlas of
Anatomy, 2nd ed. Fig. 4.2 B.)
Evaluation and Management of Pediatric Spinal Infections
451

54.3 Examination
54.3.1 History and Physical
Examination
The history of patients with spinal infection is rela-
tively nondiagnostic. One series found 85% of
patients presented with pain.9 Pain occurs primar-
ily in the infected area with changes in position,
ambulation, and other forms of activity, and may
be referred to the abdomen, hips, or genitals. The
intensity of the pain varies from mild to extreme.
Particularly sharp or lancinating pain and the pres-
ence of a rapidly progressing neurological deficit
implicates SEA over PVO or diskitis.35 Young chil-
dren or toddlers may present with a limp or
refusal to walk, and may hold their spine erect to
minimize pain. The pediatric assessment can be
di cult because young children in pain are often
agitated, fearful, and marginally cooperative, and
they may not be able to relate the character or
localization of their pain clearly. A useful diagnos-
tic examination in children involves requesting the
patient to pick up an object from the floor. The
child will generally be unwilling to flex the spine
and instead will squat to lower the body.2 In older
children and young athletes, the prevalence of
back pain increases (24–36%) and back pain from
diskitis or osteomyelitis may be mistaken for a
sports injury.36
Constitutional symptoms include anorexia,
malaise, night sweats, intermittent fever, and
weight loss, but patients only rarely appear sys-
temically ill. Other symptoms include dysphagia or
neck sti ness. Temperature elevation, if present,
usually is minimal, and more suggestive of spon-
dylodiskitis over diskitis. Tenderness to palpation
over the a ected level is the most common physi-
cal sign. Sustained paraspinal spasm, torticollis,
bizarre posturing, severe sti ness of the ham-
string, and generalized weakness may be present
also and are indicative of the acute process. A his-
tory of an immune-suppressing disease or a recent
infection, or both, is common. A history of epidural
catheters for regional anesthesia and spinal instru-
mentation strongly suggest SEA. Spinal deformity
and paralysis are serious, late complications of the
disease.2,3,14,28
Fig. 54.4 Spinal cord in situ: transverse section. Spinal cord at level of C4 vertebra. (Reproduced with permission from
Thieme. Atlas of Anatomy, 2nd ed. Fig. 2.20.)
Infections
452

Because of the depth of the spine, abscess for-
mation is di cult to identify, unless it points
superficially. Children with tuberculosis disease of
the spine often present with large paraspinal
abscesses (62%). A paraspinal abscess commonly
presents as a swelling in the groin below the ingui-
nal because of extension along the psoas muscle.
Straight leg raising examination usually is not
helpful because it may be negative or may elicit
back or rarely leg pain.37
Neurological findings rarely are radicular and
more frequently involve multiple nerve groups.
Deficits such as weakness, numbness, or inconti-
nence suggest a compressive lesion, epidural
empyema, or intradural infection, over diskitis.
ISCAs almost always involve motor (83–94%) or
sensory (60–78%) deficits, and roughly half (51–
56%) of patients will have loss of sphincter control
at the time of diagnosis.21,22,25 Central cord syndro-
me has been reported in two-thirds of patients
with paralysis from cord compression, and ante-
rior cord syndrome was found in one-third.
Neurological symptoms are most frequent with
infections in the cervical and thoracic areas and
are least common with infections in the thoraco-
lumbar region. The development of neurological
signs should suggest the possibility of neural com-
pression from abscess formation, bone collapse, or
direct neural infection. Severe kyphosis from bony
collapse develops in a significant proportion of
children with tuberculosis of the spine (3%). When
neurological symptoms appear, they may progress
rapidly unless active decompression or drainage is
undertaken.
Overall, a high index of clinical suspicion for spi-
nal infection in any child presenting with back
pain and nonspecific constitutional symptoms
expedites the diagnosis and prevents the neuro-
logical morbidity that may accompany diagnostic
delays. This suspicion increases for patients pre-
senting with worsening nonmechanical back pain
(e.g., worse at night, not relieved with rest) in
immunocompromised patients, patients with
travel history to endemic areas, and other risk
factors that also apply to adults mentioned
previously.
54.3.2 Laboratory
The goals of the laboratory work-up are to identify
and isolate the causative organism to guide ther-
apy and monitor the course of treatment. The
standard work-up includes a complete blood count
(CBC) with di erential, measurement of the
erythrocyte sedimentation rate (ESR), and C-
reactive protein (CRP), and blood cultures, ideally
taken during the initial febrile phase of the illness
before antibiotics have been administered. Tempo-
rarily withholding antibiotics may be considered
in patients who are not declining clinically, if anti-
biotic therapy has already been initiated and blood
cultures are unrevealing.38
Blood culture is positive in approximately 50% of
spinal infections.2,3 The most common organism
causing PSI is Staphylococcus aureus.27 S. aureus
with other gram-positive organisms such as Staph-
ylococcus epidermidis, Streptococcus viridans,
Streptococcus pneumoniae, Streptococcus faecalis,
Propionibacterium, and diphtheroids account for
the vast majority of PSIs. Gram-negative organisms
causing PSIs are less frequent and may be associ-
ated with gastrointestinal or genitourinary sources
of infection. Organisms responsible for ISCA
include Staphylococcus, Streptococcus, Actinomyces,
Proteus mirabilis, Pneumococcus, Listeria monocy-
togenes, Haemophilus, and Escherichia coli. These
may arise from contiguous spread from a dermal
sinus tract, postoperatively, or secondary to odon-
togenic bacteremia.22
If the blood cultures are negative, an image-
guided or open biopsy may be indicated in
patients who do not respond to empirical therapy
and who are not in need of immediate surgical
debridement (see Biopsy section below). In diag-
nosing tuberculosis disease of the spine, the Man-
toux (tuberculin skin) test is nearly always positive
secondary to BCG immunization which is widely
conducted in the developing world. Definitive
diagnosis only follows positive culture of a biopsy,
but acid-fast bacilli culture may take 6 to 8 weeks.
Advances in polymerase chain reaction (PCR) tech-
niques specific for Mycobacterium DNA have has-
tened diagnosis.2,28 Positive serology is helpful for
diagnosing brucellosis (sensitivity is 65–95%), but
the specificity is low because of the presence of
antibodies in the bloodstream in regions of
endemic flora.
The ESR and CRP are used to identify and clini-
cally monitor the treatment spinal infections. They
are not diagnostic tests and only indicate an
inflammatory process. The ESR and CRP levels are
normal to mildly elevated in diskitis, elevated in
71 to 97% of children with vertebral osteomyelitis,3
and uniformly increased in SEA.35 Both the ESR
and CRP are elevated after surgery, but the CRP
level tends to peak within the first 2 postoperative
days and then declines rapidly to normal within
14 days given no postoperative infection,
Evaluation and Management of Pediatric Spinal Infections
453

compared to the ESR which may be elevated for up
to 4 weeks after surgery with no postoperative
infection. The CRP level thus serves as a more sen-
sitive marker for early detection of postoperative
spine infections when compared with ESR, and
can also be used to monitor the antibiotic treat-
ment of an infection in the same way.3
Leukocytosis is not especially helpful in diagnos-
ing spinal infection. White blood cell counts may
decrease in infants. High white blood cell counts
may indicate areas of infection other than the
spine. CD4 counts are not helpful in determining
the presence of infection in HIV patients but can
help in determining the location and course of
infection. Patients with CD4 count greater than
200/mL tend to have spinal infections that respond
to antibiotics. Patients with CD4 counts less than
200/mL are more susceptible to osteoarticular and
soft tissue infections.
54.3.3 Radiology
Imaging techniques are used to confirm the clini-
cal impression.3 Plain radiographs of the involved
area are the most common initial study in patients
with spinal infection. Radiographic findings, which
appear 2 weeks to 3 months after the onset of the
infection, include disk space narrowing, vertebral
end plate irregularity or loss of the normal contour
of the end plate, loss of normal lordosis in the cer-
vical or lumbar spine, defects in the subchondral
portion of the end plate, and hypertrophic (scle-
rotic) bone formation in pyogenic and nonpyo-
genic infections. Occasionally, paravertebral soft
tissue masses may be noted with involvement of
nearby areas of the spine. Late radiographic find-
ings may include vertebral collapse, segmental
kyphosis, and bony ankylosis, particularly in late
tuberculosis infections. The sequence of events
may range from 2 to 8 weeks for early findings to
more than 2 years for later findings. The only
definable abnormality on plain radiographs and
computed tomography (CT) scans related specifi-
cally to early tuberculosis is fine calcification in
the paravertebral soft tissue space. In brucellosis,
the vertebral body is characteristically spared,
without deformity.
CT identifies paravertebral soft tissue swelling
and abscesses much more readily and can monitor
changes in the size of the spinal canal. CT also
o ers a more detailed demonstration of the nature
of destruction of the bone, end plate, disk, and soft
tissue densities. Postmyelogram CT more clearly
defines compression of the neural elements by
abscess or bone impingement and helps determine
whether the infection extends to the neural struc-
tures themselves.
Magnetic resonance imaging (MRI) is the gold
standard for diagnosing infectious disorders of the
spine in the pediatric age group.14,39,40 MRI distin-
guishes infected from normal tissues, but does not
di erentiate between pyogenic and nonpyogenic
infections and cannot eliminate the need for diag-
nostic biopsy. MRI may be di cult to attain in chil-
dren without sedation. It is often performed in
emergencies because of the often aspecific clinical
presentation that may raise the suspicion of spinal
cord compression. Intravenous administration of
contrast (i.e., gadolinium) greatly enhances the
identification and delineation of spinal infection.
Spinal infections in the vertebral bodies and disks
demonstrate decreased signal intensity on T1-
weighted images, representing subchondral fibrosis
and bone sclerosis. In T2-weighted images, the signal
intensity is increased in the vertebral disk, represent-
ing tissue edema, and markedly decreased in the
vertebral body. The granulation tissue associated
with diskitis and vertebral osteomyelitis often resem-
bles an abscess on MRI, appearing as areas of
increased uptake. Intramedullary infections demon-
strate hyperintensity on T2-weighted images, irregu-
lar ring enhancement, cord expansion, and restricted
di usion.25,41
The imaging of ISCAs follows the same progres-
sion as brain abscesses. MRI reveals early and
late myelitis. Early myelitis appears as hyperin-
tense on T2-weighted and proton density-
weighted sequences. T1-weighted sequences show
isointense to hypointense signal changes with a
widened spinal cord. Late myelitis, about 7 days
after the initial presentation, corresponds to the
pathological stage of capsular formation, with
more clearly defined marginal enhancement on
contrast-enhanced T1-weighted images, while T2-
weighted hyperintense signal changes become less
di use.22,42 MRI is not a reliable method of docu-
menting resolution of spinal infections. Clinical
findings, such as decreased pain and improved
neurological function, seem to be better indicators
than improvement seen on MRI.
Radionuclide studies are relatively e ective in
identifying spinal infection. These techniques
include technetium-99 m (99 m Tc) bone scan,
gallium-67 (67 Ga) scan, and indium-111-labeled
leukocyte (111 In WBC) scan. In infection, di use
activity is seen on the blood pool images of the
99 m Tc bone scan, and becomes focal on delayed
views. This marked reactivity may persist for
Infections
454

months. The 67 Ga scan is a good adjunct to bone
scanning for the detection of osteomyelitis and it
may be useful to document clinical improvement
because it changes rapidly with the resolution of
the acute active infection.26 The 111 In WBC scan
is useful in detecting abscesses and di erentiating
between noninfectious lesions, but it does not dif-
ferentiate between acute and chronic infections.28
54.3.4 Biopsy
Invasive procedures for diagnosis are recommended
only for failure of conservative management or for
immunocompromised or immunosuppressed patients.
If an invasive procedure is required, image-guided
biopsy typically o ers the least morbid option for
directly obtaining a tissue sample. Time, host resist-
ance, bacterial virulence, prior antibiotic exposure,
and culture of the proper anatomical part all are
factors in successful isolation of the o ending
organism. An exception is diskitis in children
younger than 6 years, which may be viral in origin.
Needle biopsy is rarely performed in these cases,
and these patients may be the only group in whom
careful monitoring without antibiotics is reasonable.
An open surgical biopsy has a higher yield for the
confirmation of a positive bacterial culture and is
obligated if image-guided aspiration fails to grow
an organism and the patient does not respond to
medical management.
54.4 Nonsurgical Management
Identification of a causative organism through
blood cultures or biopsy allows appropriate antibi-
otic therapy in concordance with consideration of
surgical management. Treatment goals are aimed
at resolving the infection, eliminating pain, and
preventing the development of more serious infec-
tion or neurological compromise. CRP profiles are
useful to monitor the activity of most infections,
especially pyogenic infections. Serial MRI is not
recommended to guide duration of antibiotic ther-
apy, because improvements in the appearance on
MRI tend to lag significantly behind clinical
improvement.
Recommendations vary considerably for child-
hood diskitis. Nonoperative therapy, consisting of
analgesia and immobilization for pain control, can
resolve diskitis in almost all pediatric cases and is
particularly appropriate for immunocompetent
patients.2,3,28 In the past, no di erence in the
outcome was reported in children who receive bed
rest or antibiotic therapy. A course of antibiotics is
now recommended for initial treatment, because
prolonged or recurrent symptoms can occur in
children not receiving antibiotics.28 The standard
course is 7 to 10 days of intravenous antibiotics
with a follow-up period of 2 to 3 days of oral anti-
biotics that can be extended up to 6 weeks based
on clinical findings. Patients should be followed up
for at least 12 to 18 months and reassessed if
symptoms recur or ESR and CRP fail to return to
normal.
For osteomyelitis, long-term antimicrobial ther-
apy with immobilization is the optimal treat-
ment.18 The recommended course is 6 weeks of
appropriate intravenous antibiotic therapy with
possibility of extension to 8 to 12 weeks, depend-
ing on the clinical and laboratory findings.43
In SEA acquired postoperatively, Staphylococcus
species resistant to methicillin are seen (methicillin-
resistant S. aureus [MRSA]), whereas community-
acquired infections are most commonly broadly
sensitive to methicillin (methicillin-sensitive S. aureus
[MSSA]). However, surgical intervention is almost
always indicated once a SEA is diagnosed.
Treatment for tuberculosis disease of the spine
(TS) is medical only if TS is diagnosed early, the
neurological examination is intact, and there is no
bony destruction. A common regimen consists of
rifampin, isoniazid, ethambutol, and pyrazinamide
for 2 months, followed by rifampin and isoniazid
for a variable period of 7 to 9 additional months.
This has a success rate of 93% in neurologically
intact patients.3,28 Whether or not to immobilize
patients is controversial, given the risks of bed rest
balanced against the concern for vertebral col-
lapse. Brucellosis requires at least two antibiotics
(tetracycline, doxycycline, or rifampin) over 6
weeks.
54.5 Surgical Indications
Surgical treatment is indicated when there is clini-
cally significant instability of the spine, neurological
deterioration, or severe infection, including septice-
mia or persistent infection after nonoperative treat-
ment (day). Sampling of infectious tissue to provide
diagnostic cultures can also be performed during
surgery. For a diagnosed spinal epidural abscess and
other frank abscesses on imaging, surgical interven-
tion is virtually always indicated due to the possibil-
ity of sudden and irreversible neurological decline
despite antibiotic treatments.2,14 Prompt surgery is
Evaluation and Management of Pediatric Spinal Infections
455

also indicated for all intramedullary spinal cord
abscesses.
For tuberculosis disease of the spine, reports
have demonstrated up to 94% improvement when
surgery is performed as early as possible, followed
by chemotherapy. Long-term results from surgery
with postoperative chemotherapy are superior to
nonoperative management in terms of spinal
stability and alignment, with less angular kypho-
sis. The involvement of multiple vertebrae signifi-
cantly increases the risk of kyphosis and collapse
and may prompt surgical intervention in the
absence of neurological symptoms. Children have
a greater potential to develop kyphosis with
growth over time.2 Indications for surgery in TS
parallel those for pyogenic infections—neurologi-
cal compromise that may be arrested, progressive
or severe kyphosis or angulation, severe pain asso-
ciated with kyphosis or collapse, evidence of pro-
gression of disease while the patient on optimized
medical therapy, and a diagnosis in doubt.2
Situations in which surgical intervention might
not be appropriate include: (1) the presence of a
very small amount of fluid in the epidural space
(particularly if it extends over multiple levels) and
no evidence of neurological impairment, (2) the
presence of complete neurological deficit for lon-
ger than 3 days, (3) profound and overwhelming
comorbidity adversely a ecting the likelihood that
the patient will survive an operation, and (4)
refusal of the patient to consent to operative inter-
vention.2
54.6 Surgical Technique
For pyogenic infections, surgical goals include the
evacuation of free pus from the epidural space, the
sampling of infectious tissue to provide diagnostic
cultures, and the maintenance and protection of
spinal stability. For granulomatous infections, sur-
gical goals include the decompression of neural
elements, stabilization of columnar spinal stability,
and correction of any kyphosis that may be
present.26,28
In a patient with an epidural abscess, surgical
goals can most often be accomplished with a
decompressive laminectomy over the length of the
abscess.28,37 The purulent collection is almost uni-
formly posterior in all reported pediatric cases of
SEA, but even when the collection is anterior, a
laminectomy will often su ce to provide drainage
and allow the sampling of material for diagnostic
culture. An initial strategy of alternating hemila-
minotomies for multilevel abscesses allows vigo-
rous irrigation of the epidural space while still
retaining the posterior tension band to prevent
later spinal instability. Posterior instrumentation
and fusion provides spinal stability during the
postoperative healing process.
Surgical approaches for tuberculosis disease of
the spine have been debated in the medical litera-
ture. Limited surgery consists of laminectomy,
which is the preferred procedure when the
primary problem is a dorsal epidural collection
of granulation material without kyphosis. Lami-
nectomy is insu cient when the patient has
significant vertebral body disease because of the
potential for delayed kyphosis and the inability to
address any ventral spinal cord compression that
may be present. Posterior instrumented fusion can
meaningfully augment stabilization but can do
little to correct kyphosis.26
When vertebral body involvement has produced
wedging and kyphosis, a more radical operation for
TS involves an anterior approach with complete
resection of infected and compromised vertebral
bodies and secondary reconstruction with a bone
graft (the Hong Kong procedure).44,45 Radical sur-
gery in TS is superior to nonsurgical management in
terms of long-term spinal stability and alignment
with less angular kyphosis. Recent reports have
emphasized the addition of anterior stabilizing
instrumentation for better outcomes, although
posterior instrumentation is equally e ective.2,28
Vertebrectomy is associated with better long-term
correction of kyphosis and angulation compared to
laminectomy. Posterior instrumented fusion can be
done at same time or in a staged manner 1 to 2
weeks after the initial surgical debridement in order
to allow for an interval of IV antibiotics.26 Single-
stage anterior–posterior reconstruction is viable
when su cient debridement and stabilization can
be achieved. More extensive surgery appears to be
more e ective in correcting the degree of deformity
in children, but only a very limited experience in
young children has been reported to date.2
Best practice guidelines on minimizing surgical
site infections in high-risk pediatric spinal
surgery were compiled by consensus and include
preoperative, perioperative, and postoperative rec-
ommendations. Preoperative recommendations
include a chlorhexidine skin wash at home the
night before surgery, urine cultures, a Patient
Education sheet, and a nutritional assessment.
Perioperative guidance includes clipping over
shaving if removing hair, IV cefazolin and prophy-
laxis for gram-negative bacilli, limited OR access,
Infections
456