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16 Guidelines for the Surgical Management of Traumatic

Brain Injury

Michael Karsy and Gregory W.J Hawryluk

Abstract

Compared with other fields of medicine, there are relatively

few data guiding management of traumatic brain injury (TBI)

Nonetheless, the TBI field has led in the development of

evi-dence-based guidelines with the available literature The TBI

guidelines have become some of the most respected and

adopted recommendations in medicine Numerous guidelines

for TBI have been developed, predominantly by the Brain

Trauma Foundation In addition to Guidelines for the

Manage-ment of Severe TBI, additional guidelines are available

specifi-cally pertaining to pediatrics, prehospital management,

prognosis, combat, penetrating TBI, and surgical management

This chapter aims to review aspects of published guidelines

rel-evant to the surgical treatment of patients with TBI along with

updates from recent key studies Because of the difficulty

inher-ent in studying the emerginher-ent surgical manageminher-ent of TBI,

many of these recommendations are consensus-based

Manage-ment of epidural hematoma, subdural hematoma,

intraparen-chymal hematoma, posterior fossa lesions, skull fractures, and

penetrating brain injury will be discussed here Guidelines

related to decompressive hemicraniectomy will also be

presented

Keywords:traumatic brain injury, epidural hematoma, subdural

hematoma, contusion, posterior fossa lesions, depressed skull

fracture, penetrating brain injury, decompressive

hemicraniec-tomy, guidelines, surgery

16.1 Introduction

Traumatic brain injury (TBI) encompasses a broad,

heterogene-ous constellation of pathoanatomic lesions including

contu-sions, epidural hematoma (EDH), subdural hematoma (SDH),

and others (▶Table 16.1).1These lesions almost always coexist

A broad spectrum of injury severities can be seen ranging from

concussion to mild, moderate, and severe TBI; severe TBI is

syn-onymous with coma

Neurosurgeons play a key role in the management of TBI

Neurosurgery can be lifesaving for many patients with severeTBI, and placement of brain monitors can help optimize recov-ery of the brain Neurosurgeons have led the development ofTBI guidelines, and evidence demonstrates that use of theseguidelines improves patient outcomes.2 This chapter aims toreview key studies and, in particular, published guidelines rele-vant to the surgical management of TBI

16.2 Basics of Traumatic Brain Injury

16.2.1 Definition, Epidemiology, Classification, and Prognostication of Traumatic Brain Injury

TBI is defined as “an alteration in brain function, or other dence of brain pathology, caused by an external force.”3 Thisdefinition was recently ascribed as part of a consensus meeting

evi-to better define TBI for clinical and research purposes tion implies any loss or decrease in consciousness, any amnesiabefore or after the event, neurological deficits, or change inmental status The use of imaging was also discussed as animportant aspect of the modern understanding of TBI Thesedefinitions help clarify the heterogeneous nature of TBI

Altera-TBI is a nationwide and global epidemic, accounting annuallyfor 235,000 hospitalized cases for nonfatal TBI, 1.1 millionpatients treated in emergency departments, and 50,000 deaths

in the United States alone.4,5Approximately 40 to 50% of term survivors demonstrate long-term disability.5,6,7Moreover,the cumulative costs in initial care, long-term comorbidity, andloss in productivity account for $60 billion annually in theUnited States Common causes of head injury are motor vehicleaccidents (MVAs), falls, and assaults, with MVAs common inyounger individuals and falls seen in the elderly.4In addition,TBI has increased in frequency in the elderly and the developingworld as a cause of patient morbidity and mortality.1

long-Table 16.1 Hemorrhage patterns of traumatic brain injury

Epidural hematoma ● Temporal bone fracture and disruption of middle meningeal artery

● Rupture of bridging veins and extra-axial sinuses

● Laceration of cerebral sinuses (e.g., transverse or sagittal sinus)

● Skull fracture bone bleedingSubdural hematoma ● Rupture of bridging veins and intra-axial vessels

● Parenchymal bleeding (e.g., contusions, intracerebral hematomas)Intraparenchymal hematoma Focal: contusion,alaceration, herniation, infarction, intracranial hematoma,bdelayed intracerebral hematoma

Nonfocal: edema, disseminated swelling, diffuse axonal injury

aBruising of the brain most common against bony prominence or dural folds

bHematomas with more than two-thirds of its volume comprising blood They can form from contusions

Because of the challenges inherent to classifying TBI, it is

most frequently classified by severity.1Patients with mild TBI

(postresuscitation Glasgow Coma Scale [GCS] score of 13–15)

can often be managed conservatively with a period of

observa-tion The Canadian CT Head Rules is a decision score that can

aid in identifying patients with mild TBI in whom computed

tomography (CT) imaging is warranted.8 The criteria were

developed from 3,121 patients showing that five high-risk

fac-tors (failure to reach GCS of 15 within 2 hours, suspected open

skull fracture, any sign of basal skull fracture, more than two

episodes of vomiting, or age > 65 years) were 100% sensitive

and two medium-risk factors (amnesia before impact > 30

minutes and dangerous mechanism of injury) were 98.4%

sen-sitive for predicting need for neurological intervention In

addi-tion, only 32% of patients with high-risk factors and 54% of

patients with medium-risk factors would require CT imaging,

suggesting that the clinical examination could be a powerful

method to identify patients with mild TBI that are likely to

deteriorate Moderate TBI (GCS 9–12) and severe TBI (GCS < 9)

require hospital admission, intensive monitoring, and a greater

likelihood for neurosurgical interventions.9,10,11

Prognostication is of critical importance in the management

of TBI patients; it greatly assists communication with families

and helps with resource allocation and level-of-care decisions

Focal neurological deficits commonly seen in head injury

include pupillary changes, focal neurological deficits, signs of

transtentorial herniation, and seizures, which can also be

important predictors of outcome.12,13,14,15,16,17 Moreover,

gen-eral predictors of good outcome include higher GCS on

admis-sion, as well as absence of transtentorial herniation, basal

cistern effacement, additional intracranial lesions (e.g., skull

fractures), or widespread cortical injury

The International Mission for Prognosis and Analysis of

Clini-cal Trials in TBI (IMPACT) study has been a major advance for

the TBI field as it has served to definitively inform prognostic

variables affecting TBI patients Another major achievement of

this effort has been outcome prediction.18 IMPACT started in

2003 and involved merging 11 large data sets of clinical trials

and observational studies from North America and Europe.19

Multiple studies have been published from the data set, and a

prognostic calculator has been developed for use in counseling

patients’ families, evaluating trauma departments and

institu-tions, and serving as a quality metric to improve care of TBI

patients (http://www.tbi-impact.org/)

16.2.2 Guidelines in Traumatic Brain

Injury

The publication of the evidence-based Guidelines for the

Ma-nagement of Severe Traumatic Brain Injury in 1995, 2000, 2007,

and 2016 by the Brain Trauma Foundation (BTF) helped

increase standardization and wider application of best practices

in post–head injury management.17The success of these

guide-lines led to the development of additional guideguide-lines for the

management of TBI patients Guidelines on pediatric TBI,20

combat-related trauma,21 mild head injury,22and prehospital

TBI emergency care23 discuss various medical management

strategies and will not be reviewed here Recent publication of

the 4th version of the BTF guidelines has further added to the

II evidence supports the placement of an intracranial monitor,either an external ventricular drain or an intracranial pressure(ICP) bolt, for patients with GCS 3 to 8 and an abnormal head

CT suggesting mass effect secondary to trauma Level III dence supports placing a monitor in patients with two of thefollowing: > 40 years of age, unilateral or bilateral motor postur-ing, or systolic blood pressure < 90 mm Hg The use of a monitor

evi-in these situations can be critical evi-in determevi-inevi-ing patients whofail medical management and warrant surgical decompression

16.2.4 Preoperative Management

For TBI patients for whom neurosurgery is planned, severalsteps can be important in avoiding complications despite theemergent nature of the procedure.25Protection of the airwayand hemodynamic stabilization are critical as antecedent steps

to surgery as part of the advanced trauma life support (ATLS)guidelines.26Maintenance of adequate blood pressure, oxygen-ation, and ICP (< 22 mm Hg) is essential.25Hyperosmolar ther-apy can be employed to treat ICP elevation, or in the face offocal neurological changes or a declining neurological examina-tion when ICP elevation is presumed Screening for coagulop-athy is very important when considering surgery Patients withTBI exhibit high rates of disseminated intravascular coagulation,and elderly patients commonly present with an iatrogenic coa-gulopathy To screen for a coagulopathy, it is critical to diligentlyseek any history of anticoagulation use and to assess laboratorystudies (which may include complete blood count, prothrombintime, partial thromboplastin time, thromboelastography).Preparation for an emergency craniotomy involves communi-cation between neurosurgical, anesthesia, and operating roomstaff and other team members as well as a system where requi-site resources can be promptly mobilized Blood productsshould be available Two large-bore (> 16 gauge) intravenouscatheters should be placed, laboratory studies reviewed, andradiographic images of the chest and neck reviewed to rule outadditional injury An arterial line, a central line, a Foley catheter,and a secured endotracheal tube are all highly desirable If fam-ily members are not available to provide consent, then emer-gency consent must be employed Lower-extremity sequentialcompression devices should be placed prior to surgery toreduce the risk of deep vein thrombosis Antibiotics (commonly

30 mg/kg of cefazolin) and antiepileptic medications monly 20 mg/kg of levetiracetam or 25 mg/kg of fosphenytoin)should be administered

(com-16.2.5 Anesthesia Considerations

Various strategies for reduction of ICP and maintaining cerebral

perfusion during an emergency craniotomy can be utilized

dur-ing anesthesia.25Patients in whom ICP elevation is suspected

generally receive little to no premedication to avoid causing

hypercapnia and hypoxemia Patient positioning is often

reviewed to ensure adequate decompression of the jugular

veins to prevent ICP elevations Blood pressure is closely

moni-tored, with avoidance of hypotension (systolic < 90 mm Hg)

par-amount, especially in the setting of head elevation where

decreased cerebral perfusion may occur Invasive arterial

moni-toring may be essential for accurate hemodynamic monimoni-toring

Adequate communication between the anesthesiologist and

neurosurgeon is essential during surgery to avoid complications

and aid in reducing ICP by medical treatments until adequate

decompression can be completed

Selection of medications is also crucial during anesthesia Use

of both volume and inotropes/vasopressors, including

dopa-mine and norepinephrine, may be necessary Preferred agents

are etomidate (0.3 mg/kg), thiopental (3–5 mg/kg), propofol (1–

2 mg/kg), and benzodiazepines (e.g., midazolam 2 mg), which

can aid in lowering ICP and cerebral metabolism (CMRO2) but

also lower cerebral perfusion pressure Inhalational anesthetics

(isoflurane, halothane, sevoflurane, enflurane) have the

poten-tial to cause vasodilation and increase ICP but can also lower

CMRO2 Nitric oxide (N2O) may increase cerebral metabolism,

cause vasodilation, and increase ICP, making it an unfavorable

drug for use in neurotrauma Use of succinylcholine (0.6 mg/kg)

for neuromuscular blockade is controversial because the muscle

fasciculations it causes can increase ICP Nondepolarizing agents

are preferred as they avoid this effect Fentanyl (3–5μg/kg) or

lidocaine (1.5 mg/kg) can be useful in blunting the

hemody-namic response to laryngoscopy and intubation Postintubation

sedation is also essential for avoiding coughing and gagging that

can increase ICP Use of propofol, midazolam, or inhalational

gases can be considered for this purpose

The development of surgical guidelines providing direction on

when neurosurgery should be performed on TBI victims has

been a particularly important effort Because of the difficulty in

studying aspects of emergent surgical management, relatively

little literature (and even less of high quality) informs surgical

decisions made for TBI victims The BTF broke new ground in

publishing Guidelines for the Surgical Management of TBI in

2006, which were necessarily based largely on expert

consen-sus opinion This document provides guidance on the surgical

management of EDH,17SDH,16intraparenchymal lesions,13

pos-terior fossa lesions,13 depressed cranial fractures,14and

pene-trating brain injury (PBI),12 which will be discussed in this

chapter The recommendations contained within are generated

from level II or III evidence because randomization and placebocontrol of emergent interventions for TBI patients are oftenimpractical or unethical

16.3.2 Acute Epidural Hematoma

EDH is a relatively rare entity following TBI, representing only2.7 to 4% of all cerebral injuries; the mean age of patients is 20

to 30 years.15,27,28,29,30,31,32,33,34,35,36,37,38EDH commonly occurs

as a result of injury to the middle meningeal artery, middle ningeal vein, diploic veins (especially in children), or venoussinuses, resulting in a hematoma near the pterion In fact, arte-rial bleeding accounts for 36% of adult EDH and 18% of pediatriccases.39 EDHs are often bound by sutures and lentiform inshape (▶Fig 16.1) A classical “lucid interval” in which patientsregain consciousness after losing it at the time of injury, fol-lowed by a subsequent decline as the acute EDH expands, hasbeen described This classic clinical pattern occurs in only 47%

me-of cases.27,34,38,40,41In fact, because limited injury to the brainparenchyma typifies these injuries, these patients can achieveexcellent outcomes after expedient surgical decompression Thegoal of achieving zero mortality with this condition may be fea-sible with widespread access to trauma centers, CT imaging,and improved early recognition

With regard to timing of surgery for EDH, some studies havefailed to support a time–outcome relationship34,42while otherssupport early treatment.29,41,43,44 There are substantial limita-tions inherent to the performance and interpretation of thesestudies, however The overall findings (▶Table 16.2) from theBTF guidelines suggest prompt surgical evacuation for clots > 30

mL, regardless of GCS, or midline shift (MLS) > 5 mm Patientswith EDH < 30 mL, MLS < 5 mm, and GCS > 8 without focal deficitcan be followed with serial imaging and intensive observation

The guidelines additionally and understandably recommendthat patients with acute EDH and GCS < 9 accompanied byanisocoria should also undergo surgical evacuation as soon aspossible

Various factors supported by the literature are used to aid indecisions to proceed to surgical decompression in thesepatients Important prognostic factors in patients with EDHinclude age, pupillary abnormalities, associated intracraniallesions, time between neurological deterioration and surgery,and ICP.15 Blood clot volumes > 30 mL and MLS > 5 mm havebeen supported by level II evidence for evacuation to improvepatient outcome.15One study of 200 patients showed that 24%

of patients with hematoma volumes > 50 mL had an unfavorableoutcome (i.e., Glasgow Outcome Scale [GOS] score > 3), whereas6.2% of patients with hematomas < 50 mL had an unfavorableoutcome.34In addition, mixed-density hematomas (which sug-gest acute bleeding), MLS > 10 mm, and partial or total basal cis-tern obliteration correlated with worse mortality and GOS

Another study of 158 consecutive patients showed that MLS of >

5 mm and hematoma thickness > 15 mm predicted eventualsurgical treatment A multivariate logistic regression study of

33 pediatric patients showed that MLS, hematoma thickness,volume, and temporal location of clot correlated with under-going surgical evacuation It is noteworthy that these findingswere not universally replicated by other studies, however.38,45

Patients with smaller EDH or better GCS on admission can besafely managed conservatively, at least initially.28,46,47,48,49

16.3.3 Acute Subdural Hematoma

Acute SDH is an important and unique injury pattern

com-monly seen following severe head trauma Acute SDH is seen in

12 to 29% of patients admitted for severe TBI50,51,52,53,54and 11%

of patients with mild TB.16,55,56 Acute SDH often arises from

injury to bridging subdural veins (▶Fig 16.2,▶Fig 16.3) Like

EDH, SDH commonly occurs after MVAs and falls, but the

energy required to cause SDH is generally much larger,

result-ing in greater cerebral injury Approximately 37 to 80% of

patients with acute SDH present with a GCS < 8 and are less

likely to demonstrate a lucid interval than patients with EDH.27,

38,55,56,57In addition, 60 to 70% of patients with SDH show other

intracranial and extracranial injuries.55,56Surgical treatment ofSDH can be lifesaving, but the level of recovery varies widelyand is difficult to predict Chronic SDH, related to prior mildTBI, preceding acute SDH, anticoagulant use, and alcohol abuse

as risk factors, represents a distinct entity from acute SDH andwill not be discussed further here.58

Compared with patients with acute EDHs, patients with acuteSDHs have a comparatively poor prognosis Overall mortality is

15 to 60% but varies depending on other factors, including tional systemic injury and comorbidities.29,59,60,61,62,63,64,65,66

addi-These results suggest an often poor outcome with SDH related

to injury to other parts of the brain or organ systems A modernseries of acute traumatic SDH of 1,427 patients between 2005

Fig 16.1 Case of an acute epidural hematoma.This is a 31-year-old man who presented after abicycle accident He initially presented to thetrauma bay with a GCS of 14 with someconfusion but he acutely declined to GCS of 7 CTimaging demonstrates an acute right EDHmeasuring > 30 mL in volume and with > 5 mm inMLS The patient underwent emergent craniot-omy, based on the size of the clot, MLS, GCS onarrival, and declining GCS, for evacuation of theEDH and replacement of the bone flap No ICPmonitor was placed An ICP monitor was con-sidered if the postoperative wake up exam hadnot returned to baseline

Table 16.2 Guidelines for management of epidural hematomas

GuidelineIndications for surgery ● An EDH > 30 mL should be surgically evacuated regardless of the patient’s GCS score

● An EDH < 30 mL and with < 15-mm thickness and with < 5-mm MLS in patients with a GCS score > 8 without focaldeficit can be managed nonoperatively with serial CT scanning and close neurological observation in aneurosurgical center

Timing It is strongly recommended that patients with an acute EDH in coma (GCS score < 9) with anisocoria undergo surgical

evacuation as soon as possibleMethods There are insufficient data to support one surgical treatment method; however, craniotomy provides a more

complete evacuation of the hematomaAbbreviations: CT, computed tomography; EDH, epidural hematoma; GCS, Glasgow Coma Scale; MLS, midline shift

Fig 16.2 Case of an acute subdural hematoma.

This is a 45-year-old man who presented after amotor vehicle collision with ejection Noncontrast

CT imaging demonstrates an acute right frontalSDH measuring 10 mm in maximal dimensionwith associated tSAH There is associated right-to-left MLS of 10 mm On examination, thepatient had a GCS of 7 and had declined from aninitial GCS of 12 Because of the thickness of theclot, MLS, and GCS, this patient underwent anemergent, right-sided decompressive hemicra-niectomy with ICP monitor placement and closeneurocritical care follow-up

Fig 16.3 Case of an acute-on-chronic subduralhematoma This is a 65-year-old woman with ahistory of warfarin use for treatment of atrialfibrillation who presented after a ground-levelfall A noncontrast CT shows an acute SDH withchronic components The SDH measured 13 mm

in maximal dimension with 7 mm of MLS Thepatient’s initial GCS was 7, and the internationalnormalized ratio was 2.3 on arrival Based on clotthickness, MLS, and GCS, she was eligible forcraniectomy; however, she was not yet optimizedfrom a coagulopathy perspective She underwenttreatment with fresh-frozen plasma and vitamin

K prior to decompressive craniectomy

and 2008 demonstrated a mortality rate of 15% in patients who

underwent surgical evacuation and 17% in patients managed

conservatively.62 Furthermore, 94% of patients on discharge

showed GCS > 13, where only 58% of patients showed the same

on presentation This study also demonstrated improvement in

mortality compared with the results of prior studies, which was

60 to 66% in the 1980s to 1990s and 22 to 26% in the 1990s to

2000s, likely owing to the improvement of modern

neurocriti-cal care and implementation of standardized guidelines for

treatment (▶Table 16.3)

An ongoing randomized clinical trial (the HypOthermia for

Patients requiring Evacuation of Subdural Hematoma [HOPES]

trial) aims to evaluate the putative benefit of hypothermia to

33 °C (35 °C prior to dural opening) during the treatment of

SDH in improving outcome (clinicaltrials.gov, #NCT02064959)

It is hoped that studying prophylactic hypothermia in a more

homogeneous subset of TBI patients than has previously been

examined may lead to a positive result

Earlier time to operative treatment of acute SDH has been

supported in a number of studies as improving prognosis.29,44,

53,54,67,68,69This association has not been uniformly seen in

pub-lished studies, however One study showed a 30% mortality rate

in patients operated after 4 hours compared with a 90%

mortal-ity rate in those treated < 4 hours from injury.53This study also

showed a significantly longer operative time in patients who

died (390 vs 170 minutes) A large retrospective study of 522

patients who underwent surgical treatment of traumatic SDH

showed that increased time to surgical treatment yielded a

sig-nificant decrease in mortality, suggesting preoperative

resusci-tation was an important, but poorly characterized, phase in

improving recovery.68Care is required in the interpretation of

these studies, however, as patients surviving to undergo later

surgery likely had less severe injuries Moreover, some studies

have failed to show an impact on timing of surgery and

out-come,55,56,61,70,71,72while others have shown a contrary result

Generally, patients with indications for decompression of SDH

should be expedited to the operating room, but stabilization of

airway and hemodynamic issues should take precedence

Recommendations from the BTF include surgical evacuation

for patients with declining GCS as well as enlarging SDH

thick-ness and cerebral herniation Several studies support these

recommendations Some have demonstrated a significant

correlation of GCS, SDH volume, MLS, and basal cistern ment and overall mortality.56,70One study demonstrated thatpatients with a clot thickness of < 10 mm had a 10% mortalityrate, whereas those with a clot thickness of > 30 mm had a 90%mortality rate.66In addition, MLS > 20 mm also correlated with

efface-a significefface-ant increefface-ase in mortefface-ality Conversely, efface-another studyfailed to show an impact of SDH volume, MLS, or basal cisterneffacement, suggesting additional factors are important forprognosis.38 Cutoffs used for identifying surgical candidateshave been evaluated by some groups, who have suggested evac-uation of clots > 10 mm and MLS > 5 mm and in patients withworsening ICP levels > 22 mm Hg.63,73,74 One recent studyshowed that a difference between MLS and clot thickness of ≥ 3

mm correlated with a worse outcome.75In fact, a good outcomewas seen in 67% of patients in the nonoperative group com-pared with 23% of patients who required eventual surgery TheBTF guidelines (▶Table 16.3) recommend surgery for hemato-mas > 10 mm in thickness or MLS > 5 mm.16Patients with SDHand GCS < 9 should undergo ICP monitoring.16 In addition,patients with SDH < 10 mm in thickness, MLS < 5 mm, and GCS <

9 should undergo evacuation if GCS declines between injuryand hospitalization by ≥ 2 points, if the patient presents withasymmetric or fixed and dilated pupils, or if the patient’s ICP

is > 22 mm Hg.16Patients with acute SDH should be evaluated

as soon as possible, and surgical interventions should involve acraniotomy with or without bone flap removal and duraplasty

16.3.4 Traumatic Intraparenchymal Lesions

Traumatic intraparenchymal lesions account for 13 to 35% ofsevere TBI, with most small lesions not requiring surgical evac-uation.13,76,77,78,79,80,81Primary mechanisms of traumatic paren-chymal lesions can be divided into focal and nonfocal subtypes.Focal subtypes include contusion, laceration, and intracerebralhematoma (ICH), whereas nonfocal lesions include edema, dif-fuse swelling, traumatic subarachnoid hemorrhage (tSAH), anddiffuse axonal injury Lacerations involve significant traumaresulting in skull fracture and penetration of the brain by skullfragments Contusion often involves bruising of the brain due tocapillary damage most prominent at the frontotemporal poles

Table 16.3 Guidelines for management of acute subdural hematomas

GuidelineIndications for surgery ● An acute SDH with a thickness > 10 mm or MLS > 5 mm on CT should be surgically evacuated, regardless of the

patient’s GCS score

● All patients with acute SDH in coma (GCS score < 9) should undergo ICP monitoring

● A comatose patient (GCS score < 9) with an SDH with a thickness < 10 mm and midline shift < 5 mm shouldundergo surgical evacuation of the lesion if any of the following are true:

○The GCS score decreased between the time of injury and hospital admission by ≥ 2 points

○The patient presents with asymmetric or fixed and dilated pupils

○The intracranial pressure exceeds 20 mm HgTiming In patients with acute SDH and indications for surgery, surgical evacuation should be done as soon as possibleMethods If surgical evacuation of an acute SDH in a comatose patient (GCS < 9) is indicated, it should be done using a

craniotomy with or without bone flap removal and duraplastyAbbreviations: CT, computed tomography; GCS, Glasgow Coma Scale; ICP, intracranial pressure; MLS, midline shift; SDH, subdural hematoma

due to coup-contrecoup injury ICH involves focal hemorrhage,

where blood collection makes up more than two-thirds of the

lesion, within the brain parenchyma (▶Fig 16.4, ▶Fig 16.5)

tSAH involves hemorrhage within the subarachnoid space,

out-side of the brain parenchyma In addition, multiple

intraparen-chymal lesions commonly coexist or accompany SDH and EDH

Importantly, ICHs can appear or enlarge in delayed fashion

after initial presentation This phenomenon has been termed

delayed traumatic ICH (DTICH), which is defined as a lesion of

increased attenuation developing after admission with an initial

normal CT scan of the head; it is often seen in areas of cerebral

contusion.82,83The incidence ranges from 3.3 to 7.4% of patients

with moderate-to-severe TBI and 1.6% of evacuated ICH.82,84,85

In addition, DTICH is associated with increased incidence of

sec-ondary systemic insults, incidence after decompressive surgery,

and coagulopathy, along with a mortality ranging from 16 to

72%.83,85,86,87,88These results suggest a underlying pathological

mechanism for DTICH distinct from those of other types of

trau-matic intraparenchymal injury and provide strong rationale for

early invasive monitoring, which can identify the delayed

appearance or expansion of these mass lesions

Multiple studies have sought to improve prognostic accuracy

by combining clinicoradiographic metrics A key study defining

the Marshall classification of intracerebral injury showed that

CT parameters could predict mortality independent from age

and GCS.89This study of 746 patients with severe TBI showed

better favorable outcomes (23 vs 11%) with ICH volumes > 25

mL and led to the development of further studies regarding

predictive metrics in ICH.89Another large study of 218 patientsshowed that SAH, ICH volumes > 40 mL, and compressed cis-terns correlated with a decline in GCS by 2 points or pupillarydilation.90 Furthermore, delayed deterioration was associatedwith hypoxic events Patients with GCS < 6 and ICH volumes of >

20 mL demonstrated better outcome with surgical evacuationcompared with conservatively managed patients Subgroups ofpatients with MLS of ≥ 5 mm, GCS ≥ 10, temporal contusions,MLS, or obliteration of the basal cisterns also benefited fromcraniotomy A retrospective study 202 patients with traumaticICH showed that low GCS and hematoma > 16 mL independ-ently predicted poor outcome.91 Similarly, patients withreduced ICP prior to evacuation demonstrated improved mor-tality and morbidity.92,93 These results supported the recom-mendations of BTF guidelines (▶Table 16.4 and ▶Table 16.5)including surgical decompression of patients with progressiveneurological deterioration, medically refractory intracranialhypertension, or mass effect on CT In addition, patients withGCS > 6 to 8 and frontotemporal contusions > 20 mL, MLS > 5

mm, or cisternal compression should be treated operatively Aswell, patients with lesions > 50 mL in volume should undergodecompression surgery Patients without neurological compro-mise, with controlled ICP, and with no significant mass effectcan be managed nonoperatively with intensive monitoring andserial imaging Surgical evacuation should include a craniotomyfor focal lesions; bifrontal decompressive craniectomy for dif-fuse posttraumatic cerebral edema and medically refractoryintracranial hypertension; or subtemporal decompression,

Fig 16.4 Case of an acute intraparenchymalhemorrhage This is a 54-year-old man whopresented after a motor vehicle collision CTimaging demonstrates an acute right frontalintraparenchymal hemorrhage measuring > 50

mL with marked mass effect, effacement of theright frontal ventricle, and 10 mm of right-to-leftMLS There is associated right frontal pneumo-cephalus from a comminuted fracture Based onthe GCS, MLS, and lesion volume, the patient wasindicated for a decompressive procedure and clotevacuation The patient had a GCS of 8 on arrival,and he underwent decompressive craniectomywith evacuation of the hematoma and repair ofthe skull fracture

temporal lobectomy, and decompressive craniectomy for

evi-dence of impending transtentorial herniation

16.3.5 Posterior Fossa Lesions

Compressive posterior fossa lesions secondary to trauma are

rare entities but can require emergent attention because of

their direct compression of the cerebellum and brainstem as

well as the risk of causing hydrocephalus A location in the

pos-terior fossa is found in 1.2 to 12.9% of EDH, 0.5 to 2.5% of SDH,

and 1.7% of intraparenchymal hemorrhages.13,94,95,96,97,98,99,100

Nonoperative management has also been employed for patientswith no CT evidence of mass effect and intact neurologicalexamination.94,95,101

Studies generally support hematoma evacuation on an gent basis, with improved outcome in patients with early pre-sentation and greater GCS Caution should be noted in thatpatients can rapidly decline with posterior fossa lesions andbrainstem compression In addition, supratentorial ICP moni-toring may not always reflect localized intracranial hyperten-sion in the posterior fossa One study of 81 patients showedfavorable outcome (GOS 4 or 5) in 95% of patients with GCS ≥ 8

emer-Fig 16.5 Case of diffuse traumatic subarachnoidhemorrhage This is a 25-year-old man whopresented after a skiing accident CT imagingshows diffuse tSAH with a right frontal SDH Nosignificant mass effect or MLS is identified Onexamination, the patient had a GCS of 7 Based

on the GCS exam, lack of mass effect, or MLS, thepatient underwent placement of an ICP mon-itoring device and close neurocritical care follow-up

Table 16.4 Guidelines for management of intraparenchymal lesions

GuidelineIndications for surgery ● Patients with parenchymal mass lesions and signs of progressive neurological deterioration referable to the lesion,

medically refractory intracranial hypertension, or signs of mass effect on CT scan should be treated operatively

● Patients with GCS score 6–8 with frontal or temporal contusions > 20 mL in volume with midline shift > 5 mm and/

or cisternal compression on CT scan, and patients with any lesion > 50 mL in volume should be treated operatively

● Patients with parenchymal mass lesions who do not show evidence for neurological compromise, have controlledICP, and show no significant signs of mass effect on CT scan may be managed nonoperatively with intensivemonitoring and serial imaging

Timing and methods ● Craniotomy with evacuation of mass lesion is recommended for those patients with focal lesions and the surgical

indications listed above

● Bifrontal decompressive craniectomy within 48 hours of injury is a treatment option for patients with diffuse,medically refractory posttraumatic cerebral edema and resultant intracranial hypertension

● Decompressive procedures, including subtemporal decompression, temporal lobectomy, and hemisphericdecompressive craniectomy, are treatment options for patients with refractory intracranial hypertension anddiffuse parenchymal injury with clinical and radiographic evidence for impending transtentorial herniationAbbreviations: CT, computed tomography; GCS, Glasgow Coma Scale; ICP, intracranial pressure

but poor outcome (GOS 1–3) in 81% of patients with GCS < 8.95

One study of 25 patients showed that those with EDH

volumes < 10 mL, thickness < 15 mm, and MLS < 5 mm had better

survival.101A study of 73 patients with posterior fossa lesions

showed 14 patients could be managed conservatively and

59 required surgical evacuation.94Furthermore, overall

mortal-ity was 5.4%, but it was confounded by secondary cerebral

hemorrhages and poor preoperative neurological

examina-tion findings The BTF guidelines (▶Table 16.6) recommend

decompression for patients with mass effect or neurological

dysfunction specific to the posterior fossa lesion, including

compression of the fourth ventricle or basal cisterns, and

obstructive hydrocephalus Patients without symptoms or

mass effect on CT can be managed by observation and

imag-ing, while surgical intervention should be performed rapidly

for deteriorating patients Suboccipital craniectomy and

evacuation of posterior fossa mass lesions are the preferred

treatment strategy

16.3.6 Cranial Vault Fractures

Depressed cranial fractures involve discontinuity of the skull

arising from either blunt or sharp trauma to the head Fractures

are described by shape (linear or stellate), location (including

calvarial vs basilar), displacement (diastatic/nondisplaced

vs displaced/depressed), number of bone pieces (hinge door

vs comminuted), and exposure to environment (simple/closed

vs compound/open) Traumatic skull fractures can also be

associated with facial and orbital fractures The traumatic ing skull fracture is a separate entity related to a laceration ofthe dura resulting in spacing of the fracture edges due to cere-brospinal fluid (CSF) pulsations in a growing pediatric cra-nium.102 The AOCMF skull fracture classification system hasbeen one of many approaches in quantifying craniofacial skullfracture patterns and location.103

grow-General indications for surgical treatment of skull fracturesinclude those that are depressed in frontal or other cosmeticallysensitive areas, fractures over vascular sinuses with the pres-ence of intracranial hemorrhage, open/comminuted fractures

or fractures with > 1-cm depression, and when repair of CSFleak is necessary Linear, diastatic, and nondisplaced fracturescan often be managed nonoperatively Additional vascularimaging may be indicated when fractures extend through areaswith vulnerable vessels, such as when skull base fracturesextend through the petrous carotid canal In addition to repair

of skull fragments and wound debridement, removal of loosebone fragments is advocated; however, evidence for surgicaltreatment is at best class III evidence.104 The BTF guidelines(▶Table 16.7) recommend operative repair of open fracturesgreater than the thickness of the skull to prevent infectionunless there is no clinical or radiographic evidence of duralpenetration, intracranial hematoma, depression > 1 cm, frontalsinus involvement, gross cosmetic deformity, wound infection,pneumocephalus, or gross wound contamination Simpledepressed fractures can be managed nonoperatively Surgeryshould be performed early with elevation, debridement, and

Table 16.5 Guidelines for management of intraparenchymal lesions in infants, children, and adolescents

GuidelineIndications for surgery ● Decompressive craniectomy should be considered in pediatric patients with severe TBI, diffuse cerebral swelling,

and intracranial hypertension refractory to intensive medical management

● Decompressive craniectomy should be considered in the treatment of severe TBI and medically refractoryintracranial hypertension in infants and young children with abusive head trauma

● Decompressive craniectomy may be particularly appropriate in children with severe TBI and refractory intracranialhypertension who have a potentially recoverable brain injury Decompressive craniectomy appears to be lesseffective in patients who have experienced extensive secondary brain insults Surgery may be favorable for patientswho experience a secondary deterioration on the GCS and/or evolving cerebral herniation syndrome within the first

48 h after injury may represent a favorable group, whereas surgery may be unfavorable for patients with anunimproved GCS of 3

Abbreviations: GCS, Glasgow Coma Scale; TBI, traumatic brain injury

Table 16.6 Guidelines for management of posterior fossa mass lesions

GuidelineIndications for surgery ● Patients with mass effect on CT scan or with neurological dysfunction or deterioration referable to the lesion

should undergo operative intervention Mass effect on CT scan is defined as distortion, dislocation, or obliteration

of the fourth ventricle, compression or loss of visualization of the basal cisterns, or the presence of obstructivehydrocephalus

● Patients with lesions and no significant mass effect on CT scan and without signs of neurological dysfunction may

be managed by close observation and serial imagingTiming In patients with indications for surgical intervention, evacuation should be performed as soon as possible because

these patients can deteriorate rapidly, thus worsening their prognosisMethods Suboccipital craniectomy is the predominant method reported for evacuation of posterior fossa mass lesions and is

therefore recommendedAbbreviation: CT, computed tomography

antibiotics as well as replacement of the primary bone fragment

if wound infection is absent

Management of open air sinus injury from skull fractures

represents a unique aspect of surgical management because of

the potential for CSF leak and intracranial infection

Oblitera-tion, cranializaOblitera-tion, and exoneration of sinuses may be

neces-sary for fractures through the air sinuses to reduce risk of CSF

leak and cerebral infection Unfortunately, criteria

distinguish-ing sinuses at risk of delayed complications remain elusive

Mucoceles, the accumulation and retention of mucoid within

paranasal sinuses, can occur with fractures that occlude the

nasofrontal ducts and can present in a delayed fashion after

TBI.105Meningitis and encephalitis are risks of CSF leak after

mucocele formation Mucopyoceles involve infection of the

mucoid retention, and complicate clinical management

Fron-tal sinus injuries occur in 5 to 12% of patients with severe

facial trauma, can involve the inner table, outer table, or both,

and can be associated with cerebral infection (although they

heal without intervention in 66% of patients).106 Compound

fractures show a significant rate of infection from 1.9 to

10.6%, most commonly a Streptococcus species, neurological

morbidity of 11%, and incidence of late epilepsy of 15%.107,108,

109,110,111 One series of 33 patients discussed the importance

of surgical cranialization of the frontal sinus after injury and

CSF leak along with obliteration of the nasofrontal outflow

tract.112Management guidelines on the repair of open-sinus

fractures remain limited, with recent reviews recommending

recognition of this potential complication, close posttrauma

follow-up, interdisciplinary specialty management, and

crani-alization of posterior table comminuted fractures or those

with CSF leak.105

Treatment of skull fractures in pediatric patients presents a

unique situation because of the ongoing growth of the patients’

craniums These fractures are almost uniformly associated with

a linear fracture and dural tear with entrapment of the

arach-noid or brain within the fracture in children < 3 years of age

The incidence of growing fractures is 0.05 to 1.6% of patients

with linear fractures of the cranium and usually attributed to

the growth of the brain and skull preventing healing of the

frac-ture.102A series of 180 patients < 1 years of age showed only 8

patients required nonemergent surgical treatment of depressed

skull fracture and overall outcome was uniformly positive,

likely because of the limited traumatic mechanism.113Repair of

the growing fracture involves adequate repair of the dural tear,

with earlier treatment favoring improved outcome.102

Cranial fracture alone or when associated with additionalintracranial lesions can predict a poor outcome.63,114,115,116Onestudy of 1,178 adolescents with intracranial injury showed thatcranial fracture was the only independent factor predictingpoor outcome.114 Another study of 923 pediatric patientsdemonstrated that temporal bone fracture, age ≥ 5 years, MVAmechanism, and concomitant organ injury were associatedwith worse prognosis.117Furthermore, parietal fractures weremore frequent in younger age groups, while frontotemporalfractures were more common in older ages (> 5 years) A study

of 850 patients with cranial fracture found that 71% showed anintracranial lesion compared with only 46% of 533 patientswithout a fracture.116Replacement of bone fragments has beenshown in multiple studies to not increase risk of infectiouscomplications with surgery within 72 hours regardless of thelevel of contamination at the time of surgery.107,111,118A meta-analysis of 5 randomized clinical trials and 17 nonrandomizedclinical trials showed that antibiotic prophylaxis after traumaticskull fracture did not reduce risks of infection or all-cause mor-tality after trauma and was generally not recommended.119,120

16.4 Surgical Techniques for Traumatic Brain Injury

16.4.1 Decompressive Craniectomy

Decompressive hemicraniectomy is a surgical option in patientsrequiring evacuation of large intracranial hematomas and thosewith ICP elevation refractory to less aggressive treatment TheMonro–Kellie doctrine dictates that cerebral tissue, CSF, andblood occupy a fixed intracranial volume Decompressive hemi-craniectomy is designed to expand the intracranial volume insettings of hematoma or edema, in hopes of preventing brainherniation, decreased perfusion, and cerebral ischemia Gener-ally, a minimum diameter of 12 cm has been widely accepted asnecessary for decompression.121,122,123,124,125Unilateral, bifron-tal, or posterior fossa decompressive craniotomies can be per-formed when indicated

Survival advantage after decompressive hemicraniectomygreatly depends on appropriate patient selection during neuro-surgical emergencies In a meta-analysis of 12 studies, including

3 randomized clinical trials, decompressive hemicraniectomywith open dural flaps offered significantly improved mortalityand GOS score.121 Moreover, retrospective studies in this

Table 16.7 Guidelines for management of depressed skull fractures

GuidelineIndications for surgery ● Patients with open (compound) skull fractures depressed greater than the thickness of the skull should undergo

operative intervention to prevent infection

● Patients with open (compound) depressed skull fractures may be treated nonoperatively if there is no clinical orradiographic evidence of dural penetration, significant intracranial hematoma, depression > 1 cm, frontal sinusinvolvement, gross cosmetic deformity, wound infection, pneumocephalus, or gross wound contamination

● Nonoperative management of closed (simple) depressed skull fractures is a treatment optionTiming Early operation is recommended to reduce the incidence of infection

Methods ● Elevation and debridement is recommended as the surgical method of choice

● Primary bone fragment replacement is a surgical option in the absence of wound infection at the time of surgery

● All management strategies for open (compound) depressed fractures should include antibiotics

analysis demonstrated improved outcome after decompressive

hemicraniectomy for patients age < 50 years, operation < 5

hours after TBI incident, and GCS > 5.121 However, recent

randomized clinical trials have failed to show an improvement

in GOS score and mortality The Decompressive Craniectomy in

Diffuse Traumatic Brain Injury (DECRA) trial randomized 155

patients with severe TBI and intracranial hypertension to

bifrontotemporal decompressive hemicraniectomy or

aggres-sive medical management alone.122While the trial showed

sig-nificantly ICP reduction, reduced interventions for ICP, and

fewer intensive care unit days for the decompressed group,

extended GOS score was significantly worse (1.84; 95%

confi-dence interval, 1.05–3.24; p = 0.03) in these patients, and

mor-tality was similar at 6 months (19% decompressed group vs

18% medically managed group) Criticisms of the study include

exclusion of patients with mass lesions as well as use of

bifron-tal decompression without cutting of the falx, which is more

limited in alleviating ICP There were also more patients with

bilaterally unreactive pupils in the surgical group, resulting in

imbalanced comparison groups In fact, the patients with worse

pupillary examination results were more common in the

surgi-cal group, demonstrating unbalanced randomization with

sicker patients undergoing decompression Additional

limita-tions of the study also reflect the heterogeneity of TBI patients

The results of the study suggested harm from decompression

compared with medical management, although the results

became nonsignificant after adjusting for the aforementioned

baseline imbalances A retrospective study of 223 patients with

severe TBI demonstrated that decompressive craniectomy

improved mortality but not long-term prognosis when

com-pared with conservatively managed patients.125Another study

of 74 patients randomized to treatment with decompressive

craniectomy or temporoparietal craniotomy showed lower ICP,

improved 1-month mortality, and good 1-year neurological

outcome in patients who underwent decompression.123

Decom-pressive craniectomy remains a treatment option for TBI

vic-tims, and the recently completed RescueICP study will

undoubtedly bring forth much-needed, high-quality evidence

16.4.2 Surgical Decompressive

Frontotemporoparietal

Hemicraniectomy Technique

The decompressive frontotemporoparietal hemicraniectomy

can be performed with the patient in a supine position using a

horseshoe headrest or Mayfield pin fixation.25 The goals of

decompression include a 15 × 12–15-cm opening to give

ad-equate exposure of the frontal lobe 1 to 2 cm behind the orbital

brow, the middle crania fossa, and anterior temporal lobe with

exposure to the root of the zygoma, the parietal eminence, and

1.5 to 2 cm away from midline to avoid injury to the superior

sagittal sinus or bridging veins

The traditional reverse question-mark incision is outlined

with the inferior point approximately 1 cm anterior to the

tragus to avoid both branches of the superficial temporal artery

and above the zygoma to avoid the exiting facial nerve

branches The incision is carried above the auricle and across

the parietal eminence before crossing to reach midline to allow

adequate exposure Although the incision can be made with the

scalpel all the way to the skull, this should be limited inferior tothe superior temporal line to allow careful dissection and elec-trocautery of the temporalis muscle Hemostasis is achievedwith Raney clips and electrocautery After scalp and galeal inci-sion, the temporal muscle can be mobilized as a myocutaneousflap using electrocautery and periosteal elevators with minimalincision of the inferior-most portion Wide scalp exposure ofthe frontal brow, the root of the zygoma, and keyhole areneeded to ensure an adequate bony decompression Relaxation

of the brain should be initiated prior to bone removal, includinguse of external ventricular drains, mild hyperventilation, man-nitol (0.5–1 g/kg), or hypertonic saline Multiple burr holes can

be placed rapidly above the zygoma, squamosal temporal bone,and along the superficial temporal line usually with a perfora-tor Caution is needed to stay 1.5 to 2 cm away from midline toavoid injury to the superior sagittal sinus and bridging veins

Additional burr holes can be made if the dura tears to helpimprove dural separation from the bone edge, which can bemore difficult in elderly patients Burr holes at the coronalsphenoid suture may be helpful in freeing underlying durabecause dural attachments at sutures commonly occur

After dural stripping, the bone can be removed en bloc using

a high-speed craniotome with footplate Care must be takenduring bony removal in the setting of skull fracture Hemostasis

at the bone edges can be attained with the use of hemostaticagents and dural tack-up sutures Further decompression of thesphenoid wing can be performed with a Leksell rongeur, andbony bleeding can be stopped with wax; however, attention tothe dural opening should be the primary focus after bone isremoved to rapidly decompress the brain A variety of duralopenings are acceptable Some favor a C-shaped dural openingwith base toward the superior sagittal sinus, which can be per-formed with additional cruciate cuts as needed for relaxation

The senior author prefers a stellate dural opening Cottonoidsand thrombin-soaked Gelfoam can be used to protect the brainduring opening Blood clots can be removed by gentle irrigationand debridement; aggressive evacuation of deep clot or clotnear the sagittal sinus should be avoided if possible A duralonlay graft can generally be placed without need for tight duralclosure The galea and scalp can be closed in typical fashion,and the senior author prefers placement of both a deep andsuperficial drain to help prevent a postoperative hematoma

In rare situations, removal of cerebral cortex can be useful formanagement of refractory ICP elevation Temporal or frontallobectomy has been used historically and in some rare caseswith poorly controlled ICPs despite craniotomy; however, incontemporary neurosurgery, decompressive craniectomy haslargely supplanted cerebral resection

16.4.3 Technique for Bifrontal Decompression

In cases with extensive frontal contusion or swelling, a bifrontaldecompression may be preferred.25There are many acceptablevariations in how this decompression is performed Generally,the patient is placed supine with the head in a horseshoe head-rest A bicoronal or Soutar incision is outlined starting 1 cmanterior to the tragus and above the zygoma and running to themidline behind the hairline After the incision is opened, the

frontal scalp flap is advanced forward as a myocutaneous flap

until the orbital brow is exposed The galea can be preserved as

a separate layer if a vascularized patch of tissue is likely to be of

assistance with repair of the frontal sinus or a skull base

frac-ture Burr holes are placed at the coronal suture, generally 1.5

to 2 cm away from midline, to allow stripping of the venous

sinus–containing dura Burr holes are also placed frontally and

temporally A craniotome can be used to remove the bone, with

care to always drill away from the venous sinus Dural tack-up

sutures should be placed, and the dura should be opened in a

C-shaped manner with the base toward the sinus If frontobasal

access is required, the superior sagittal sinus is suture-ligated

close to the crista galli A 3- to 4-cm right frontal pole or 4- to

5-cm right temporal lobectomy can be performed if required

16.4.4 Cranioplasty

Cranioplasty after craniectomy is often carried out 6 to 8 weeks

after the initial procedure, although it can be performed either

earlier or later An autologous bone flap can be initially stored

in a sterile –70 °C freezer, in the abdominal fat pad, or in the

thigh, for many months The native bone can be replaced if

there is no suspicion of infection or hydrocephalus or an

artifi-cial cranioplasty can be performed otherwise

16.4.5 Posterior Fossa Decompression

Technique

Evacuation of mass lesions in the posterior fossa or a

decom-pressive procedure can be a life-saving procedure as even small

lesions in this location can place significant pressure on the

brainstem or cause obstructive hydrocephalus by compression

of the cerebral aqueduct.25 For such surgery, the patient is

placed prone with the head in a horseshoe headrest or Mayfield

pin fixation Here, a ventriculostomy can decrease pressure in

the supratentorial space and avoid downward herniation A

midline incision is created, and burr holes are placed below the

transverse sinuses After dural stripping, a craniotomy or

cra-niectomy can be created, with care to separate the midline dura

from the bone Large hematomas in this area required large

decompressions, whereas focal lesions may be evacuated with

smaller approaches In the posterior fossa, the dura is typically

opened in a Y-shaped manner

16.4.6 Surgical Complication Avoidance

A variety of surgical complications during decompressive

craniectomy should be anticipated in an effort to avoid them

Preoperative evaluation to rule out coagulopathy and

hemody-namic instability can aid in avoiding intraoperative

complica-tions During the procedure, positioning of burr holes and

minding of the midline are important for avoiding damage to

the superior sagittal sinus and bridging veins Similarly,

avoid-ing sacrifice of large, drainavoid-ing cerebral veins is important to

prevent cerebral venous congestion that can result in cerebral

ischemia, infarction, or iatrogenic hemorrhage Only the

ante-rior third of the supeante-rior sagittal sinus and associated draining

veins can be sacrificed if necessary Avoidance of excessive clot

removal around large venous structures should be minded to

avoid removal of tamponading sites Should a large venousinjury occur, large pieces of thrombin-soaked Gelfoam that can-not be lost within the injury site should be used along withcompression Mild elevation of the head can reduce venouspressure and encourage hemostasis, although air embolismmust be avoided Strategies involving the use of rotational duralflap, muscle patch, or venous Gore-Tex patch with or withoutbypass have been described for the repair of sinus injuries

16.5 Management of Penetrating Brain Injury

16.5.1 Penetrating Brain Injury Introduction

After publication of the Guidelines for Management of SevereTraumatic Brain Injury and surgical management guidelines,the International Brain Injury Association, the Brain Injury As-sociation, the American Association of Neurological Surgeons,and the Congress of Neurological Surgeons began development

of Guidelines for Penetrating Brain Injury in 1998, independent

of the BTF These guidelines were ultimately published in 2001(▶Table 16.8).12 Recently, an update of these guidelines wasconsidered, but the relevant literature has seen little changeand so an update was judged unnecessary

PBI occurs from both low-velocity projectiles (120–250 ft/s;e.g., wooden sticks, knives, shrapnel) and higher-velocity pro-jectiles (710–3,150 ft/s; e.g., gunshot wounds) Primary injuryfrom objects and ensuing pressure waves can result in cerebralcontusion, laceration, and hemorrhage well beyond the path ofthe projectile Civilian and military PBI due to gunshot woundsare distinct in energy transmitted, transport time to care facili-ties, and availability of treatment capability Military gunshotwounds often involve high-caliber, high-velocity projectiles,and mortality has been reported to be greater than that fromlow-energy shrapnel.126,127,128 Civilian gunshot wounds aremore often due to handguns and have a mortality rate of 6%,12

whereas mortality from military PBI ranges from 8 to 43%.126, 127,128After initial patient stabilization in accordance with ATLSprotocols, PBI can be evaluated, with attention to neurologicalexamination, skin and scalp wounds, and leakage of CSF, blood,

or brain from the wound Cushing’s own results during WorldWar I showed a reduction of postoperative mortality from 55 to28% with further refinement during each subsequent humanconflict since.129,130 Thus, evidence from early neurosurgicalinvolvement in the management of PBI onward suggestsimprovement in mortality compared with the poor natural his-tory of PBI

16.5.2 Initial Management of Penetrating Brain Injury

It is especially important that ATLS protocol and attention toairway, breathing, and circulation pervade the management ofthose with penetrating TBI These injuries are often dramatic inappearance and can be distracting to those providing care It is

of critical importance that penetrating objects not be removedexcept in a controlled fashion by a surgeon as these are often

providing life-preserving tamponade Imaging is of critical

importance in planning a strategy for removing such an object

CT imaging is recommended as the initial modality for PBI,

although plain X-rays can be valuable because they avoid the

artifact that can be problematic on CT imaging Magnetic

reso-nance imaging (MRI) is, of course, contraindicated for PBI with

bullets and other metallic fragments.131Attention to entry/exit

sites, intracranial fragments, missile trajectory and injury to

intracranial vessels, intracranial air, transventricular injury,

multilobar injury, basal cistern status, MLS, and mass effect is

important for both prognosis and surgical decision-making

Vascular imaging is an important consideration in

penetrat-ing TBI, especially with injuries near the internal carotid artery,

proximal anterior and middle cerebral arteries, sylvian fissure,

or vertebral arteries.132Approximately 0.4 to 0.7% of aneurysms

are due to trauma, with 20% of trauma-related aneurysm

secon-dary to PBI.126,132Distal aneurysms are also possible sequelae of

PBI The incidence of aneurysms due to trauma is between 3

and 33% depending on the type of diagnostic study and

tim-ing133Aneurysm may also present in delayed fashion up to 2

weeks after TBI; these mostly affect the anterior and middle

cerebral arteries The incidence of SAH after trauma-related

aneurysm rupture has been estimated to be 31 to 78% but is

limited by the types of studies evaluated.133,134The guidelines

recommend immediate CT imaging and possible CT

angiogra-phy during the evaluation of PBI

Intracranial monitoring is often used in PBI when there is

potential to affect patient outcome and improve care

Recom-mendations for ICP monitoring in the PBI population have

been reflective of the Guidelines for Management of Severe

Traumatic Brain Injury A variety of studies showed class III dence regarding the helpfulness of ICP monitoring in predictingoutcome after PBI, with values > 20 mm Hg predicting poorprognosis.135,136,137,138,139However, one study showed that ICPmonitoring could not predict poor outcome in this popula-tion.140 The PBI guidelines recommend ICP monitoring andmedical management strategies outlined in the BTF Guidelinesfor Management of Severe Traumatic Brain Injury

evi-16.5.3 Surgical Management of Penetrating Brain Injury

Information about the surgical treatment of PBI is limited toseveral nonrandomized, retrospective studies as well as theprinciples of surgery identified from experience during war-time.129,130,141Smaller wounds with minimal intracranial dam-age and absent mass effect can be managed by wound washoutand primary closure More extensive wounds with intracranialdamage and dural injury require removal of bone fragmentsand watertight dural closure Only in the presence of significantmass effect are wound debridement of necrotic brain, evacua-tion of intracranial hematoma, and safe removal of accessiblebone fragments recommended Early attempts at aggressivewound debridement as seen during the Vietnam War havegiven way to less aggressive, more focused treatments A review

of 148 patients with PBI who underwent local debridement,dural closure, and no attempt to remove deeper fragmentsshowed a mortality rate of 8% and infection rate of 6%.142ThePBI guidelines recommend local wound care and closure with

Table 16.8 Guidelines for management of penetrating brain injury

GuidelineWound size ● Local wound care and closure of small entrance bullet wounds to the head in patients whose scalp is not

devitalized and have no “significant” intracranial pathologic findings is recommended (Note: The term

“significant” has yet to be clearly defined However, the volume and location of the brain injury, evidence of masseffect, displacement of the midline by 5 mm, or compression of basilar cisterns from edema or hematoma, andthe patient’s clinical condition all pertain to significance.)

● More extensive debridement before primary closure or grafting to secure a watertight wound is recommendedfor more extensive wounds with nonviable scalp, bone, or dura

● Debridement of the cranial wound with either craniectomy or craniotomy is recommended in patients withsignificant fragmentation of the skull

Mass effect ● In the presence of significant mass effect, debridement of necrotic brain tissue and safely accessible bone

fragments is recommended Evacuation of intracranial hematomas with significant mass effect is recommended

● In the absence of significant mass effect, surgical debridement of the missile track in the brain is notrecommended based on class III evidence that outcomes are not measurably worse in patients who do not haveaggressive debridement Routine surgical removal of fragments lodged distant from the entry site andreoperation solely to remove retained bone or missile fragments are not recommended

Open-air sinus injury Repair of an open-air sinus injury with watertight closure of the dura is recommended Clinical circumstances

dictate the timing of the repair Any repairs requiring duraplasty can be at the discretion of the surgeon as tomaterial used for closure

CSF leak Surgical correction is recommended for CSF leaks that do not close spontaneously or are refractory to temporary

CSF diversion During the primary surgery, every effort should be made to close the dura and prevent CSF leaksAntibiotics Prophylactic and preoperative broad-spectrum antibiotics are recommended in PBI

Antiseizure medications Antiepileptic medications are recommended to reduce early (≤ 7 days after incident) but not late (> 7 days after

incident) seizuresAbbreviation: CSF, cerebrospinal fluid; PBI, penetrating brain injury

small wounds, nondevitalized scalp tissue, and no significant

intracranial pathology Large wounds are recommended for

extensive debridement of scalp, bone, and dura as well as

watertight wound closure Patients with mass effect are

recom-mended for debridement of necrotic brain tissue and safely

accessible bone fragments, but in the absence of mass effect,

debridement of the projectile track is not recommended

Removal of distal fragments or reoperation solely to remove

bone or missile fragments is not recommended Open air sinus

injuries are recommended for watertight closure

Management of CSF leak has been critical in the management

of PBI because of the high rates of reported associated

infec-tion.141Infection rates after CSF leak are high (49.5–70%) and

confer additional mortality risk.127,137,143,144 In one series of

1,133 patients, CSF leak was seen in 101 patients, and while

44% of leaks closed spontaneously, mortality was significantly

higher after CSF leak (22.8 vs 5.1%).137Moreover, 72% of CSF

leaks appeared within 2 weeks, suggesting that tight dural

clo-sure at time of surgery is critical and close patient surveillance

is required Leaks occurred at the wound site in 50% of cases,

while other sites included areas injured by fractures or dural

rents.141CSF leak occurred in 28% of cases of injury to the

open-air sinuses, and 38% of cases that failed surgical treatment

became infected.145The guidelines suggest meticulous surgical

technique to achieve a watertight closure, repair of open-air

sinuses, and attention to potential sites of CSF leak Secondary

surgeries to repair CSF leak that failed conservative treatment

(e.g., CSF diversion) are also recommended

16.5.4 Complication Management in

Penetrating Brain Injury

Infectious complications after PBI have been substantially

reduced with the use of antibiotics and refined surgical

meth-ods The infection rate has dropped from 58.8% during World

War I to 4 to 11% in recent conflicts.143,146,147,148 Similarly, a

decrease in cerebral abscess rates from 8.5% during World War

II to 1.6 to 3.1% in modern series has been observed Factors

relating to a greater risk of wound infection generally include

combat situations, deep-seated injury, and shrapnel fragments;

however, studies from civilian cases have shown no increased

incidence of infection (4%), epilepsy (13%), or mortality (33%)

despite retained foreign bodies.136 Predominant bacteria

include Staphylococcus aureus and Staphylococcus epidermidis,

but other species have been found in some series, including

Acinetobacter, Streptococcus, Escherichia coli, Klebsiella,

Entero-bacter, and Clostridium.149,150,151Limited class III evidence

sup-ports the use of prophylactic antibiotics in PBI.146Prophylactic

broad-spectrum antibiotics are recommended in light of early

evidence from the military supporting decreased rates of

infec-tion, as well as some studies suggesting benefit in civilians.146

These recommendations are in contrast to the BTF surgical

guidelines, which do not recommend prophylactic antibiotics,

even in the setting of CSF leak or open fractures

Cranioplasty has been employed for cranial repair, and in one

study of 417 patients over 13 years, a morbidity rate of 2% was

seen after delaying cranioplasty for a minimum of 1 year.127The

morbidity in delaying cranioplasty has been similar to those

from later studies, although the morbidity from cranioplasty

procedures has been reported as high as 35%, thus reconfirmingthe role for selective operative treatment as well as the impor-tance of tight dural closure.139,152In another study, an increasedcomplication rate after cranioplasty was seen after infection,CSF leak, or cranioplasty performed in < 1 year.153

While literature evaluating the timing of surgery is limitedwith civilian PBI, one study of 163 patients with air sinus inju-ries from military PBI showed an infection rate of 5% forpatients who underwent surgery within 12 hours comparedwith 38% for patients in whom surgery was delayed longer than

12 hours.145

Seizure rates after PBI range between 30 and 50%, with 4 to10% of patients having a seizure within the first week and 80%within 2 years of injury.154,155These are higher than the overallseizure rates of 4 to 42% observed after blunt TBI.156,157A largedatabase study of 6,111 patients showed a 2.78 times higherrate of rehospitalization for seizure after PBI than closed TBI.158

Epilepsy rates have ranged from 22 to 53% after military PBIand are correlated with location and size of lesions, as well asthe presence of retained metallic fragments but not bone.128,155,

159Another study suggested that GOS score, central nervoussystem infection, and focal motor deficits correlated with riskfor posttraumatic epilepsy.160 Four class I randomized con-trolled trials evaluated the role of prophylactic antiseizuremedications in the treatment of TBI, with a small number oftotal patients having PBI.156,157,161,162 These results suggestedthat anticonvulsants could reduce the incidence of early seiz-ures (those occurring ≤ 7 days after incident) but not late seiz-ures Levetiracetam has gained favor over phenytoin as apreferred first-line anticonvulsant because of multiple studiessuggesting a lower side-effect profile and equivalent effect.163

The guidelines recommend antiseizure prophylaxis for patientswith PBI but caution the limited ability to prevent late seizures

16.6 Relevant Recommendations from Other Guidelines

16.6.1 Pediatric Traumatic Brain Injury

Guidelines for the Acute Medical Management of Severe matic Brain Injury in Infants, Children, and Adolescents werepublished in 2003 and 2012 by the BTF to evaluate TBI litera-ture with a focus on pediatric patients.20 Several sectionsaddress critical care management specifically with attention toliterature on pediatric patients Specific areas on ICP monitor-ing, hyperosmolar therapy, therapeutic hypothermia, hyper-ventilation, corticosteroids, medical management of ICPelevation, nutrition, and prophylactic antiseizure medicationsare discussed However, little information on surgical decision-making is discussed

Trau-16.6.2 Combat-Related Traumatic Brain Injury

The Guidelines for the Field Management of Combat-RelatedHead Trauma was published in 2005 by the BTF to specificallyaddress the medical and surgical management of soldiers dur-ing combat operations.21 The sections discuss the unique

aspects of the combat environment and specifically address

issues related to injuries soldiers are likely to face These

sec-tions include oxygenation and blood pressure, GCS and

pupil-lary assessment, airway management, fluid resuscitation, pain

management, ICP management, triage and transportation, and

a general algorithm for patient management Transfer of

patients to medical facilities with surgical capabilities is

recom-mended for patients with GCS < 13 and unresponsiveness to

noxious stimuli Early ATLS measures (airway management,

monitoring of oxygenation and blood pressure) and

administra-tion of ICP-lowering strategies (3.0–7.5% NaCl) are

recom-mended Patients with GCS 14 to 15 can remain in the forward

area but require close neurological evaluation

16.6.3 Mild Head Injury

Recommendations regarding the management of mild TBI wereexplored in a statement by the American College of EmergencyPhysicians (ACEP) and Centers for Disease Control and Preven-tion (CDC) in a publication titled “Clinical Policy: Neuroimagingand Decisionmaking in Adult Mild Traumatic Brain Injury in theAcute Setting” and warehoused by the BTF.22Many of the sec-tions address guidelines for triage and management of TBI in anemergency setting A recent meta-analysis of 23,079 patientswith minor head trauma demonstrated a 7.1% prevalence ofsevere intracranial injury and 0.9% risk of death or need for neu-rosurgical intervention.164Moreover, this study suggested thatTable 16.9 Overview of international and national guidelines

European Federation of Neurological

Societies guidelines on mild

trau-matic brain injury165

Evidence sus

Management of severe TBI (first

edition) guidelines166

Italian guidelines for management of

patients with minor head injuries167

Consensus/expert ion

European Brain Injury Consortium

guidelines on management of severe

head injury in adults168

Consensus/expert ion

UK guidelines for the initial

manage-ment of head injuries169

Guidelines for management of acute

neurotrauma in rural and remote

locations of Australia170

Management and prognosis of severe

TBI guidelines17,a

Prehospital management

guide-lines23,a

UK guidelines for triage, assessment,

investigation, and management of

TBIb,c

Field management of combat-related

head trauma guidelines21,a

Surgical management of TBI

guide-lines12,13,14,15,16,17

Revised guidelines for management

of severe TBI (3rd edition)172

Abbreviation: TBI, traumatic brain injury

Source: Adapted with permission from Maas et al.173

Note: The grading scheme for level of recommendations was adapted from the Oxford Centre for Evidence Based Medicine levels of evidence as level A–

D; for consistency, we considered grade A as class I, grade B as class II, and grades C and D as class III

awww.braintrauma.org

bwww.nice.org

cPartial update of NICE clinical guideline 4 (June 2003); September 2007 http://www.nice.org.uk/nicemedia/pdf/CG56NICEGuideline.pdf (accessed June

12, 2008)

GCS < 13, clinical examination findings suggestive of skull

frac-ture, two or more episodes of vomiting, decline in GCS, and

injury by motor vehicle were associated with severe

intracra-nial injury The use of the Canadian CT Head Rules may be a

practical method of identifying high-risk patients who initially

present with mild TBI These results suggest the combination of

history and physical examination could be used in the

manage-ment of mild TBI irrespective of CT imaging

16.6.4 Prehospital Traumatic Brain

Injury Emergency Care

Guidelines on Prehospital Emergency Care were produced by

the BTF in 2000 and 2006 with the emphasis on making

recom-mendations for first responders to TBI patients, including

emer-gency medical services and other emeremer-gency providers.23

Sections discussed recommendations for oxygenation and

blood pressure, GCS score, pupil examination, airway

manage-ment, fluid resuscitation, ICP managemanage-ment, and patient triage

These guidelines emphasized early recognition of TBI, transfer

to a designated trauma center, and close monitoring to identify

patients requiring surgical intervention

16.7 Conclusion

The field of TBI has seen a substantial increase in literature

informing best practices (▶Table 16.9), owing to a recognition

of the widespread incidence of TBI, the significant impact on

patient morbidity and disability, and the recognized benefit

that TBI guidelines have had on patient outcomes

References

[1] Hawryluk GW, Manley GT Classification of traumatic brain injury: past,

present, and future Handb Clin Neurol 2015; 127:15–21

[2] Fakhry SM, Trask AL, Waller MA, Watts DD, IRTC Neurotrauma Task Force.

Management of brain-injured patients by an evidence-based medicine

pro-tocol improves outcomes and decreases hospital charges J Trauma 2004; 56

(3):492–499, discussion 499–500

[3] Menon DK, Schwab K, Wright DW, Maas AI, Demographics and Clinical

Assessment Working Group of the International and Interagency Initiative

toward Common Data Elements for Research on Traumatic Brain Injury and

Psychological Health Position statement: definition of traumatic brain

injury Arch Phys Med Rehabil 2010; 91(11):1637–1640

[4] Bruns J, Jr, Hauser WA The epidemiology of traumatic brain injury: a review.

Epilepsia 2003; 44 Suppl 10:2–10

[5] Corrigan JD, Selassie AW, Orman JA The epidemiology of traumatic brain

injury J Head Trauma Rehabil 2010; 25(2):72–80

[6] Langlois JA, Rutland-Brown W, Wald MM The epidemiology and impact of

traumatic brain injury: a brief overview J Head Trauma Rehabil 2006; 21

(5):375–378

[7] Selassie AW, Zaloshnja E, Langlois JA, Miller T, Jones P, Steiner C Incidence of

long-term disability following traumatic brain injury hospitalization, United

States, 2003 J Head Trauma Rehabil 2008; 23(2):123–131

[8] Stiell IG, Wells GA, Vandemheen K, et al The Canadian CT Head Rule for

patients with minor head injury Lancet 2001; 357(9266):1391–1396

[9] Malec JF, Brown AW, Leibson CL, et al The mayo classification system for

traumatic brain injury severity J Neurotrauma 2007; 24(9):1417–1424

[10] Nakase-Richardson R, Sherer M, Seel RT, et al Utility of post-traumatic

amnesia in predicting 1-year productivity following traumatic brain injury:

comparison of the Russell and Mississippi PTA classification intervals J

Neu-rol Neurosurg Psychiatry 2011; 82(5):494–499

[11] Russell WR, Smith A Post-traumatic amnesia in closed head injury Arch

[16] Bullock MR, Chesnut R, Ghajar J, et al Surgical Management of Traumatic Brain Injury Author Group Surgical management of acute subdural hemato- mas Neurosurgery 2006; 58(3) Suppl:S16–S24, discussion Si-iv

[17] Bullock MR, Povlishock JT Guidelines for the management of severe matic brain injury Editor’s Commentary J Neurotrauma 2007; 24 Suppl 1:2

trau-p trau-preceding S1 [18] Maas AI, Murray GD, Roozenbeek B, et al International Mission on Prognosis Analysis of Clinical Trials in Traumatic Brain Injury (IMPACT) Study Group Advancing care for traumatic brain injury: findings from the IMPACT studies and perspectives on future research Lancet Neurol 2013; 12(12):1200– 1210

[19] Marmarou A, Lu J, Butcher I, et al IMPACT database of traumatic brain injury: design and description J Neurotrauma 2007; 24(2):239–250 [20] Kochanek PM, Carney N, Adelson PD, et al American Academy of Pediatrics- Section on Neurological Surgery, American Association of Neurological Sur- geons/Congress of Neurological Surgeons, Child Neurology Society, Euro- pean Society of Pediatric and Neonatal Intensive Care, Neurocritical Care Society, Pediatric Neurocritical Care Research Group, Society of Critical Care Medicine, Paediatric Intensive Care Society UK, Society for Neuroscience in Anesthesiology and Critical Care, World Federation of Pediatric Intensive and Critical Care Societies Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents–second edition Pediatr Crit Care Med 2012; 13 Suppl 1:S1–S82

[21] Guidelines for the Field Management of Combat-Related Head Trauma New York, NY: Brain Trauma Foundation; 2005

[22] Jagoda AS, Bazarian JJ, Bruns JJ, Jr, et al Clinical policy: neuroimaging and decisionmaking in adult mild traumatic brain injury in the acute setting J Emerg Nurs 2009; 35(2):e5–e40

[23] Gabriel E, Ghajar J, Jagoda AS, Pons P, Scalea T, Walters BC Guidelines for Pre-Hospital Management of Traumatic Brain Injury New York, NY: Brain Trauma Foundation; 2000

[24] Carney N, Totten AM, O'Reilly C, et al Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition Neurosurg 2017; 80(1):6–15 [25] Palmer S, Bader MK, Qureshi A, et al Americans Associations for Neurologic Surgeons The impact on outcomes in a community hospital setting of using the AANS traumatic brain injury guidelines J Trauma 2001; 50(4):657–664 [26] Zacko J, Harris L, Bullock MR Surgical management of traumatic brain injury In: Winn H, ed Youman’s Neurological Surgery Philadelphia, PA: Elsevier; 2011:3424–3452

[27] ATLS Subcommittee; American College of Surgeons’ Committee on Trauma; International ATLS working group Advanced trauma life support (ATLS(R)): the ninth edition J Trauma Acute Care Surg 2013; 74(5):1363–1366 [28] Cordobés F, Lobato RD, Rivas JJ, et al Observations on 82 patients with extra- dural hematoma Comparison of results before and after the advent of com- puterized tomography J Neurosurg 1981; 54(2):179–186

[29] Cucciniello B, Martellotta N, Nigro D, Citro E Conservative management of extradural haematomas Acta Neurochir (Wien) 1993; 120(1–2):47–52 [30] Haselsberger K, Pucher R, Auer LM Prognosis after acute subdural or epi- dural haemorrhage Acta Neurochir (Wien) 1988; 90(3–4):111–116 [31] Jamjoom A The influence of concomitant intradural pathology on the pre- sentation and outcome of patients with acute traumatic extradural haema- toma Acta Neurochir (Wien) 1992; 115(3–4):86–89

[32] Jamjoom AB The difference in the outcome of surgery for traumatic dural hematoma between patients who are admitted directly to the neuro- surgical unit and those referred from another hospital Neurosurg Rev 1997; 20(4):227–230

extra-[33] Jones NR, Molloy CJ, Kloeden CN, North JB, Simpson DA Extradural toma: trends in outcome over 35 years Br J Neurosurg 1993; 7(5):465–471 [34] Kuday C, Uzan M, Hanci M Statistical analysis of the factors affecting the outcome of extradural haematomas: 115 cases Acta Neurochir (Wien) 1994; 131(3–4):203–206

haema-[35] Lee EJ, Hung YC, Wang LC, Chung KC, Chen HH Factors influencing the

func-tional outcome of patients with acute epidural hematomas: analysis of 200

patients undergoing surgery J Trauma 1998; 45(5):946–952

[36] Paterniti S, Fiore P, Macrì E, et al Extradural haematoma Report of 37

con-secutive cases with survival Acta Neurochir (Wien) 1994; 131(3–4):207–

210

[37] Rivas JJ, Lobato RD, Sarabia R, Cordobés F, Cabrera A, Gomez P Extradural

hematoma: analysis of factors influencing the courses of 161 patients

Neu-rosurgery 1988; 23(1):44–51

[38] Sullivan TP, Jarvik JG, Cohen WA Follow-up of conservatively managed

epi-dural hematomas: implications for timing of repeat CT AJNR Am J

Neurora-diol 1999; 20(1):107–113

[39] van den Brink WA, Zwienenberg M, Zandee SM, van der Meer L, Maas AI,

Avezaat CJ The prognostic importance of the volume of traumatic epidural

and subdural haematomas revisited Acta Neurochir (Wien) 1999; 141

(5):509–514

[40] Mohanty A, Kolluri VR, Subbakrishna DK, Satish S, Mouli BA, Das BS

Progno-sis of extradural haematomas in children Pediatr Neurosurg 1995; 23

(2):57–63

[41] Ganz JC The lucid interval associated with epidural bleeding: evolving

understanding J Neurosurg 2013; 118(4):739–745

[42] Poon WS, Li AK Comparison of management outcome of primary and

secon-dary referred patients with traumatic extradural haematoma in a

neurosur-gical unit Injury 1991; 22(4):323–325

[43] Bricolo AP, Pasut LM Extradural hematoma: toward zero mortality A

pro-spective study Neurosurgery 1984; 14(1):8–12

[44] Cohen JE, Montero A, Israel ZH Prognosis and clinical relevance of

anisoco-ria-craniotomy latency for epidural hematoma in comatose patients J

Trauma 1996; 41(1):120–122

[45] Sakas DE, Bullock MR, Teasdale GM One-year outcome following

craniot-omy for traumatic hematoma in patients with fixed dilated pupils J

Neuro-surg 1995; 82(6):961–965

[46] Seelig JM, Marshall LF, Toutant SM, et al Traumatic acute epidural

hema-toma: unrecognized high lethality in comatose patients Neurosurgery.

1984; 15(5):617–620

[47] Bullock R, Smith RM, van Dellen JR Nonoperative management of extradural

hematoma Neurosurgery 1985; 16(5):602–606

[48] De Souza M, Moncure M, Lansford T, et al Nonoperative management of

epi-dural hematomas and subepi-dural hematomas: is it safe in lesions measuring

one centimeter or less? J Trauma 2007; 63(2):370–372

[49] Offner PJ, Pham B, Hawkes A Nonoperative management of acute epidural

hematomas: a “no-brainer” Am J Surg 2006; 192(6):801–805

[50] Servadei F, Faccani G, Roccella P, et al Asymptomatic extradural

haemato-mas Results of a multicenter study of 158 cases in minor head injury Acta

Neurochir (Wien) 1989; 96(1–2):39–45

[51] Cagetti B, Cossu M, Pau A, Rivano C, Viale G The outcome from acute

sub-dural and episub-dural intracranial haematomas in very elderly patients Br J

Neurosurg 1992; 6(3):227–231

[52] Farahvar A, Gerber LM, Chiu YL, Carney N, Härtl R, Ghajar J Increased

mor-tality in patients with severe traumatic brain injury treated without

intra-cranial pressure monitoring J Neurosurg 2012; 117(4):729–734

[53] Jamjoom A Justification for evacuating acute subdural haematomas in

patients above the age of 75 years Injury 1992; 23(8):518–520

[54] Seelig JM, Becker DP, Miller JD, Greenberg RP, Ward JD, Choi SC Traumatic

acute subdural hematoma: major mortality reduction in comatose patients

treated within four hours N Engl J Med 1981; 304(25):1511–1518

[55] Wilberger JE, Jr, Harris M, Diamond DL Acute subdural hematoma:

morbid-ity, mortalmorbid-ity, and operative timing J Neurosurg 1991; 74(2):212–218

[56] Massaro F, Lanotte M, Faccani G, Triolo C One hundred and twenty-seven

cases of acute subdural haematoma operated on Correlation between CT

scan findings and outcome Acta Neurochir (Wien) 1996; 138(2):185–191

[57] Servadei F, Nasi MT, Giuliani G, et al CT prognostic factors in acute subdural

haematomas: the value of the ‘worst’ CT scan Br J Neurosurg 2000; 14

(2):110–116

[58] Dent DL, Croce MA, Menke PG, et al Prognostic factors after acute subdural

hematoma J Trauma 1995; 39(1):36–42, discussion 42–43

[59] Ivamoto HS, Lemos HP, Jr, Atallah AN Surgical treatments for chronic

sub-dural hematomas: a comprehensive systematic review World Neurosurg.

2016; 86:399–418

[60] Fell DA, Fitzgerald S, Moiel RH, Caram P Acute subdural hematomas Review

of 144 cases J Neurosurg 1975; 42(1):37–42

[61] Hatashita S, Koga N, Hosaka Y, Takagi S Acute subdural hematoma: severity

of injury, surgical intervention, and mortality Neurol Med Chir (Tokyo).

1993; 33(1):13–18 [62] Koç RK, Akdemir H, Oktem IS, Meral M, Menkü A Acute subdural hema- toma: outcome and outcome prediction Neurosurg Rev 1997; 20(4):239–

244 [63] Ryan CG, Thompson RE, Temkin NR, Crane PK, Ellenbogen RG, Elmore JG.

Acute traumatic subdural hematoma: current mortality and functional comes in adult patients at a Level I trauma center J Trauma Acute Care Surg.

out-2012; 73(5):1348–1354 [64] Servadei F, Nasi MT, Cremonini AM, Giuliani G, Cenni P, Nanni A Importance

of a reliable admission Glasgow Coma Scale score for determining the need for evacuation of posttraumatic subdural hematomas: a prospective study of

65 patients J Trauma 1998; 44(5):868–873 [65] Tallon JM, Ackroyd-Stolarz S, Karim SA, Clarke DB The epidemiology of sur- gically treated acute subdural and epidural hematomas in patients with head injuries: a population-based study Can J Surg 2008; 51(5):339–345 [66] Tian HL, Chen SW, Xu T, et al Risk factors related to hospital mortality in patients with isolated traumatic acute subdural haematoma: analysis of 308 patients undergone surgery Chin Med J (Engl) 2008; 121(12):1080–1084 [67] Zumkeller M, Behrmann R, Heissler HE, Dietz H Computed tomographic cri- teria and survival rate for patients with acute subdural hematoma Neuro- surgery 1996; 39(4):708–712, discussion 712–713

[68] Son S, Yoo CJ, Lee SG, Kim EY, Park CW, Kim WK Natural course of initially non-operated cases of acute subdural hematoma : the risk factors of hema- toma progression J Korean Neurosurg Soc 2013; 54(3):211–219

[69] Walcott BP, Khanna A, Kwon CS, Phillips HW, Nahed BV, Coumans JV Time interval to surgery and outcomes following the surgical treatment of acute traumatic subdural hematoma J Clin Neurosci 2014; 21(12):2107–2111 [70] Zafrullah Arifin M, Gunawan W Analysis of presurgery time as a prognostic factor in traumatic acute subdural hematoma J Neurosurg Sci 2013; 57 (3):277–280

[71] Howard MA, III, Gross AS, Dacey RG, Jr, Winn HR Acute subdural mas: an age-dependent clinical entity J Neurosurg 1989; 71(6):858–863 [72] Kotwica Z, Brzeziński J Acute subdural haematoma in adults: an analysis of outcome in comatose patients Acta Neurochir (Wien) 1993; 121(3–4):95–

hemato-99 [73] Uzan M, Yentür E, Hanci M, et al Is it possible to recover from uncal hernia- tion? Analysis of 71 head injured cases J Neurosurg Sci 1998; 42(2):89–94 [74] Mathew P, Oluoch-Olunya DL, Condon BR, Bullock R Acute subdural haema- toma in the conscious patient: outcome with initial non-operative manage- ment Acta Neurochir (Wien) 1993; 121(3–4):100–108

[75] Wong CW Criteria for conservative treatment of supratentorial acute dural haematomas Acta Neurochir (Wien) 1995; 135(1–2):38–43 [76] Bartels RH, Meijer FJ, van der Hoeven H, Edwards M, Prokop M Midline shift

sub-in relation to thickness of traumatic acute subdural hematoma predicts tality BMC Neurol 2015; 15:220

mor-[77] Bullock R, Golek J, Blake G Traumatic intracerebral hematoma–which patients should undergo surgical evacuation? CT scan features and ICP mon- itoring as a basis for decision making Surg Neurol 1989; 32(3):181–187 [78] Gennarelli TA, Spielman GM, Langfitt TW, et al Influence of the type of intracranial lesion on outcome from severe head injury J Neurosurg 1982;

56(1):26–32 [79] Lobato RD, Cordobes F, Rivas JJ, et al Outcome from severe head injury related to the type of intracranial lesion A computerized tomography study.

J Neurosurg 1983; 59(5):762–774 [80] Mendelow AD, Gregson BA, Rowan EN, et al STITCH(Trauma) Investigators.

Early surgery versus initial conservative treatment in patients with matic intracerebral hemorrhage (STITCH[Trauma]): the first randomized trial J Neurotrauma 2015; 32(17):1312–1323

trau-[81] Miller JD, Butterworth JF, Gudeman SK, et al Further experience in the nagement of severe head injury J Neurosurg 1981; 54(3):289–299 [82] Nordström CH, Messeter K, Sundbärg G, Wåhlander S Severe traumatic brain lesions in Sweden Part I: Aspects of management in non-neurosurgi- cal clinics Brain Inj 1989; 3(3):247–265

ma-[83] Gentleman D, Nath F, Macpherson P Diagnosis and management of delayed traumatic intracerebral haematomas Br J Neurosurg 1989; 3(3):367–372 [84] Miller J, Lieberman L, Nahab B, et al Delayed intracranial hemorrhage in the anticoagulated patient: a systematic review J Trauma Acute Care Surg.

2015; 79(2):310–313 [85] Ditty BJ, Omar NB, Foreman PM, Patel DM, Pritchard PR, Okor MO The non- surgical nature of patients with subarachnoid or intraparenchymal

hemorrhage associated with mild traumatic brain injury J Neurosurg 2015;

123(3):649–653

[86] Zahari M, Mohd Ali AK, Chandrasekharan S Delayed intracranial

haemor-rhage in head injury Singapore Med J 1996; 37(3):285–287

[87] Folkerson LE, Sloan D, Cotton BA, Holcomb JB, Tomasek JS, Wade CE

Predict-ing progressive hemorrhagic injury from isolated traumatic brain injury and

coagulation Surgery 2015; 158(3):655–661

[88] Gudeman SK, Kishore PR, Miller JD, Girevendulis AK, Lipper MH, Becker DP.

The genesis and significance of delayed traumatic intracerebral hematoma.

Neurosurgery 1979; 5(3):309–313

[89] Katayama Y, Tsubokawa T, Miyazaki S Two types of delayed traumatic

intra-cerebral hematoma: differential forms of treatment Neurosurg Rev 1989;

12 Suppl 1:231–236

[90] Marshall LF, Marshall SB, Klauber MR, et al The diagnosis of head injury

requires a classification based on computed axial tomography J

Neuro-trauma 1992; 9 Suppl 1:S287–S292

[91] Mathiesen T, Kakarieka A, Edner G Traumatic intracerebral lesions without

extracerebral haematoma in 218 patients Acta Neurochir (Wien) 1995; 137

(3–4):155–163, discussion 163

[92] Choksey M, Crockard HA, Sandilands M Acute traumatic intracerebral

hae-matomas: determinants of outcome in a retrospective series of 202 cases Br

J Neurosurg 1993; 7(6):611–622

[93] Guerra WK, Gaab MR, Dietz H, Mueller JU, Piek J, Fritsch MJ Surgical

decom-pression for traumatic brain swelling: indications and results J Neurosurg.

1999; 90(2):187–196

[94] Polin RS, Shaffrey ME, Bogaev CA, et al Decompressive bifrontal craniectomy

in the treatment of severe refractory posttraumatic cerebral edema

Neuro-surgery 1997; 41(1):84–92, discussion 92–94

[95] Bozbuğa M, Izgi N, Polat G, Gürel I Posterior fossa epidural hematomas:

observations on a series of 73 cases Neurosurg Rev 1999; 22(1):34–40

[96] d’Avella D, Servadei F, Scerrati M, et al Traumatic intracerebellar

hemor-rhage: clinicoradiological analysis of 81 patients Neurosurgery 2002; 50

(1):16–25, discussion 25–27

[97] de Amorim RL, Stiver SI, Paiva WS, et al Treatment of traumatic acute

poste-rior fossa subdural hematoma: report of four cases with systematic review

and management algorithm Acta Neurochir (Wien) 2014; 156(1):199–206

[98] Roda JM, Giménez D, Pérez-Higueras A, Blázquez MG, Pérez-Alvarez M

Pos-terior fossa epidural hematomas: a review and synthesis Surg Neurol 1983;

19(5):419–424

[99] Sripairojkul B, Saeheng S, Ratanalert S, Pheunpathom N, Sriplung H

Trau-matic hematomas of the posterior cranial fossa J Med Assoc Thai 1998; 81

(3):153–159

[100] Takeuchi S, Wada K, Takasato Y, et al Traumatic hematoma of the posterior

fossa Acta Neurochir Suppl (Wien) 2013; 118:135–138

[101] Tsai FY, Teal JS, Itabashi HH, Huprich JE, Hieshima GB, Segall HD Computed

tomography of posterior fossa trauma J Comput Assist Tomogr 1980; 4

(3):291–305

[102] Wong CW The CT criteria for conservative treatment–but under close

clini-cal observation–of posterior fossa epidural haematomas Acta Neurochir

(Wien) 1994; 126(2–4):124–127

[103] Liu XS, You C, Lu M, Liu JG Growing skull fracture stages and treatment

strategy J Neurosurg Pediatr 2012; 9(6):670–675

[104] Cornelius CP, Kunz C, Neff A, Kellman RM, Prein J, Audigé L The

comprehen-sive AOCMF classification system: fracture case collection, diagnostic

imag-ing work up, AOCOIAC iconography and codimag-ing Craniomaxillofac Trauma

Reconstr 2014; 7 Suppl 1:S131–S135

[105] Bullock MR, Chesnut R, Ghajar J, et al Surgical Management of Traumatic

Brain Injury Author Group Surgical management of depressed cranial

frac-tures Neurosurgery 2006; 58(3) Suppl:S56–S60, discussion Si-iv

[106] Metzinger SE, Metzinger RC Complications of frontal sinus fractures

Cranio-maxillofac Trauma Reconstr 2009; 2(1):27–34

[107] Castro B, Walcott BP, Redjal N, Coumans JV, Nahed BV Cerebrospinal fluid

fistula prevention and treatment following frontal sinus fractures: a review

of initial management and outcomes Neurosurg Focus 2012; 32(6):E1

[108] Jennett B, Miller JD Infection after depressed fracture of skull Implications

for management of nonmissile injuries J Neurosurg 1972; 36(3):333–339

[109] Jennett B, Miller JD, Braakman R Epilepsy after monmissile depressed skull

fracture J Neurosurg 1974; 41(2):208–216

[110] Mendelow AD, Campbell D, Tsementzis SA, et al Prophylactic antimicrobial

management of compound depressed skull fracture J R Coll Surg Edinb.

1983; 28(2):80–83

[111] van den Heever CM, van der Merwe DJ Management of depressed skull tures Selective conservative management of nonmissile injuries J Neuro- surg 1989; 71(2):186–190

frac-[112] Wylen EL, Willis BK, Nanda A Infection rate with replacement of bone ment in compound depressed skull fractures Surg Neurol 1999; 51(4):452– 457

frag-[113] Ravindra VM, Neil JA, Shah LM, Schmidt RH, Bisson EF Surgical management

of traumatic frontal sinus fractures: case series from a single institution and literature review Surg Neurol Int 2015; 6:141

[114] Addioui A, Saint-Vil D, Crevier L, Beaudin M Management of skull fractures

in children less than 1 year of age J Pediatr Surg 2016; 51(7):1146–1150 [115] Chan KH, Mann KS, Yue CP, Fan YW, Cheung M The significance of skull frac- ture in acute traumatic intracranial hematomas in adolescents: a prospec- tive study J Neurosurg 1990; 72(2):189–194

[116] Hung CC, Chiu WT, Lee LS, Lin LS, Shih CJ Risk factors predicting surgically significant intracranial hematomas in patients with head injuries J Formos Med Assoc 1996; 95(4):294–297

[117] Macpherson BC, MacPherson P, Jennett B CT evidence of intracranial sion and haematoma in relation to the presence, site and type of skull frac- ture Clin Radiol 1990; 42(5):321–326

contu-[118] Adetayo OA, Naran S, Bonfield CM, et al Pediatric cranial vault fractures: analysis of demographics, injury patterns, and factors predictive of mortal- ity J Craniofac Surg 2015; 26(6):1840–1846

[119] Braakman R Depressed skull fracture: data, treatment, and follow-up in 225 consecutive cases J Neurol Neurosurg Psychiatry 1972; 35(3):395–402 [120] Poole D, Chieregato A, Langer M, et al Trauma Update Working Group Sys- tematic review of the literature and evidence-based recommendations for antibiotic prophylaxis in trauma: results from an Italian consensus of experts PLoS One 2014; 9(11):e113676

[121] Ratilal BO, Costa J, Pappamikail L, Sampaio C Antibiotic prophylaxis for venting meningitis in patients with basilar skull fractures Cochrane Data- base Syst Rev 2015; 4(4):CD004884

pre-[122] Barthelemy EJ, Melis M, Gordon E, Ullman JS, Germano I Decompressive niectomy for severe traumatic brain injury: a systematic review World Neu- rosurg 2016; 88:411–420

cra-[123] Cooper DJ, Rosenfeld JV, Murray L, et al DECRA Trial Investigators, Australian and New Zealand Intensive Care Society Clinical Trials Group Decompres- sive craniectomy in diffuse traumatic brain injury N Engl J Med 2011; 364 (16):1493–1502

[124] Qiu W, Guo C, Shen H, et al Effects of unilateral decompressive craniectomy

on patients with unilateral acute post-traumatic brain swelling after severe traumatic brain injury Crit Care 2009; 13(6):R185

[125] Tanrikulu L, Oez-Tanrikulu A, Weiss C, et al The bigger, the better? About the size of decompressive hemicraniectomies Clin Neurol Neurosurg 2015; 135:15–21

[126] Yu P, Tian Q, Wen X, Zhang Z, Jiang R Analysis of long-term prognosis and prognostic predictors in severe brain injury patients undergoing decompres- sive craniectomy and standard care J Craniofac Surg 2015; 26(7):e635– e641

[127] Aarabi B Surgical outcome in 435 patients who sustained missile head wounds during the Iran-Iraq War Neurosurgery 1990; 27(5):692–695, dis- cussion 695

[128] Hammon WM Analysis of 2187 consecutive penetrating wounds of the brain from Vietnam J Neurosurg 1971; 34(2, Pt 1):127–131

[129] Levi L, Borovich B, Guilburd JN, et al Wartime neurosurgical experience in Lebanon, 1982–85 I: Penetrating craniocerebral injuries Isr J Med Sci 1990; 26(10):548–554

[130] Surgical management of penetrating brain injury J Trauma 2001; 51(2) Suppl:S16–S25

[131] Agarwalla PK, Dunn GP, Laws ER An historical context of modern principles

in the management of intracranial injury from projectiles Neurosurg Focus 2010; 28(5):E23

[132] Neuroimaging in the management of penetrating brain injury J Trauma 2001; 51(2) Suppl:S7–S11

[133] Vascular complications of penetrating brain injury J Trauma 2001; 51(2) Suppl:S26–S28

[134] Levy ML, Rezai A, Masri LS, et al The significance of subarachnoid rhage after penetrating craniocerebral injury: correlations with angiography and outcome in a civilian population Neurosurgery 1993; 32(4):532–540 [135] Aldrich EF, Eisenberg HM, Saydjari C, et al Predictors of mortality in severely head-injured patients with civilian gunshot wounds: a report from the NIH Traumatic Coma Data Bank Surg Neurol 1992; 38(6):418–423

hemor-[136] Crockard HA Early intracranial pressure studies in gunshot wounds of the

brain J Trauma 1975; 15(4):339–347

[137] Lillard PL Five years experience with penetrating craniocerebral gunshot

wounds Surg Neurol 1978; 9(2):79–83

[138] Nagib MG, Rockswold GL, Sherman RS, Lagaard MW Civilian gunshot

wounds to the brain: prognosis and management Neurosurgery 1986; 18

(5):533–537

[139] Petridis AK, Doukas A, Barth H, Mehdorn M Outcome of craniocerebral

gun-shot injuries in the civilian population Prognostic factors and treatment

options Cent Eur Neurosurg 2011; 72(1):5–14

[140] Sarnaik AP, Kopec J, Moylan P, Alvarez D, Canady A Role of aggressive

intra-cranial pressure control in management of pediatric craniocerebral gunshot

wounds with unfavorable features J Trauma 1989; 29(10):1434–1437

[141] Siccardi D, Cavaliere R, Pau A, Lubinu F, Turtas S, Viale GL Penetrating

cra-niocerebral missile injuries in civilians: a retrospective analysis of 314 cases.

Surg Neurol 1991; 35(6):455–460

[142] Management of cerebrospinal fluid leaks J Trauma 2001; 51(2) Suppl:S29–

S33

[143] Gönül E, Baysefer A, Kahraman S, et al Causes of infections and management

results in penetrating craniocerebral injuries Neurosurg Rev 1997; 20

(3):177–181

[144] Aarabi B, Taghipour M, Alibaii E, Kamgarpour A Central nervous system

infections after military missile head wounds Neurosurgery 1998; 42

(3):500–507, discussion 507–509

[145] Meirowsky AM, Caveness WF, Dillon JD, et al Cerebrospinal fluid fistulas

complicating missile wounds of the brain J Neurosurg 1981; 54(1):44–48

[146] Arendall RE, Meirowsky AM Air sinus wounds: an analysis of 163

consecu-tive cases incurred in the Korean War, 1950–1952 Neurosurgery 1983; 13

(4):377–380

[147] Antibiotic prophylaxis for penetrating brain injury J Trauma 2001; 51(2)

Suppl:S34–S40

[148] Rish BL, Caveness WF, Dillon JD, Kistler JP, Mohr JP, Weiss GH Analysis of

brain abscess after penetrating craniocerebral injuries in Vietnam

Neuro-surgery 1981; 9(5):535–541

[149] Taha JM, Haddad FS, Brown JA Intracranial infection after missile injuries to

the brain: report of 30 cases from the Lebanese conflict Neurosurgery.

1991; 29(6):864–868

[150] Aarabi B Comparative study of bacteriological contamination between

pri-mary and secondary exploration of missile head wounds Neurosurgery.

1987; 20(4):610–616

[151] Carey ME, Young H, Mathis JL, Forsythe J A bacteriological study of

cranio-cerebral missile wounds from Vietnam J Neurosurg 1971; 34(2 Pt 1):145–

154

[152] Hagan RE Early complications following penetrating wounds of the brain J

Neurosurg 1971; 34(2, Pt 1):132–141

[153] Shoung HM, Sichez JP, Pertuiset B The early prognosis of craniocerebral

gun-shot wounds in civilian practice as an aid to the choice of treatment A series

of 56 cases studied by the computerized tomography Acta Neurochir

(Wien) 1985; 74(1–2):27–30

[154] Rish BL, Dillon JD, Meirowsky AM, et al Cranioplasty: a review of 1030 cases

of penetrating head injury Neurosurgery 1979; 4(5):381–385

[155] Antiseizure prophylaxis for penetrating brain injury J Trauma 2001; 51(2)

Suppl:S41–S43

[156] Salazar AM, Jabbari B, Vance SC, Grafman J, Amin D, Dillon JD Epilepsy after

penetrating head injury I Clinical correlates: a report of the Vietnam Head

Injury Study Neurology 1985; 35(10):1406–1414

[157] Annegers JF, Hauser WA, Coan SP, Rocca WA A population-based study of

seizures after traumatic brain injuries N Engl J Med 1998; 338(1):20–24

[158] Temkin NR, Dikmen SS, Wilensky AJ, Keihm J, Chabal S, Winn HR A ized, double-blind study of phenytoin for the prevention of post-traumatic seizures N Engl J Med 1990; 323(8):497–502

random-[159] Walker WC, Ketchum JS, III, Marwitz JH, Kolakowsky-Hayner SA, McClish

DK, Bushnik T Global outcome and late seizures after penetrating versus closed traumatic brain injury: a NIDRR TBI model systems study J Head Trauma Rehabil 2015; 30(4):231–240

[160] Caveness WF, Walker AE, Ascroft PB Incidence of posttraumatic epilepsy in Korean veterans as compared with those from World War I and World War

II J Neurosurg 1962; 19:122–129 [161] Aarabi B, Taghipour M, Haghnegahdar A, Farokhi M, Mobley L Prognostic factors in the occurrence of posttraumatic epilepsy after penetrating head injury suffered during military service Neurosurg Focus 2000; 8(1):e1 [162] Temkin NR, Dikmen SS, Anderson GD, et al Valproate therapy for prevention

of posttraumatic seizures: a randomized trial J Neurosurg 1999; 91 (4):593–600

[163] Young B, Rapp RP, Norton JA, Haack D, Tibbs PA, Bean JR Failure of lactically administered phenytoin to prevent late posttraumatic seizures J Neurosurg 1983; 58(2):236–241

prophy-[164] Zafar SN, Khan AA, Ghauri AA, Shamim MS Phenytoin versus leviteracetam for seizure prophylaxis after brain injury - a meta analysis BMC Neurol.

2012; 12:30 [165] Easter JS, Haukoos JS, Meehan WP, Novack V, Edlow JA Will neuroimaging reveal a severe intracranial injury in this adult with minor head trauma?:

The rational clinical examination systematic review JAMA 2015; 314 (24):2672–2681

[166] The Study Group on Head Injury of the Italian Society for Neurosurgery.

Guidelines for minor head injured patients’ management in adult age J rosurg Sci 1996; 40(1):11–15

Neu-[167] Bullock R, Chesnut RM, Clifton G, et al Brain Trauma Foundation Guidelines for the management of severe head injury Eur J Emerg Med 1996; 3 (2):109–127

[168] Smits M, Dippel DW, Steyerberg EW, et al Predicting intracranial traumatic findings on computed tomography in patients with minor head injury: the CHIP prediction rule Ann Intern Med 2007; 146(6):397–405

[169] Maas AI, Dearden M, Teasdale GM, et al European Brain Injury Consortium.

EBIC-guidelines for management of severe head injury in adults Acta rochir (Wien) 1997; 139(4):286–294

Neu-[170] Bartlett J, Kett-White R, Mendelow AD, Miller JD, Pickard J, Teasdale G ommendations from the Society of British Neurological Surgeons Br J Neu- rosurg 1998; 12(4):349–352

Rec-[171] Newcombe R, Merry G The management of acute neurotrauma in rural and remote locations: A set of guidelines for the care of head and spinal injuries.

J Clin Neurosci 1999; 6(1):85–93 [172] Adelson PD, Bratton SL, Carney NA, et al American Association for Surgery

of Trauma, Child Neurology Society, International Society for Pediatric rosurgery, International Trauma Anesthesia and Critical Care Society, Society

Neu-of Critical Care Medicine, World Federation Neu-of Pediatric Intensive and ical Care Societies Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents Chapter 1: Intro- duction Pediatr Crit Care Med 2003; 4(3) Suppl:S2–S4

Crit-[173] Carney NA, Ghajar J, Brain Trauma Foundation, American Association of rological Surgeons, Congress of Neurological Surgeons, Joint Section on Neu- rotrauma and Critical Care, AANS/CNS Guidelines for the management of severe traumatic brain injury Introduction J Neurotrauma 2007; 24 Suppl 1:S1–S2

Neu-[174] Maas AI, Stocchetti N, Bullock R Moderate and severe traumatic brain injury

in adults Lancet Neurol 2008; 7(8):728–741

17 Concomitant Injuries in the Brain-injured Patient

Kathryn S Hoes, Ankur R Patel, Vin Shen Ban, and Christopher J Madden

Abstract

Both blunt and penetrating traumas to the head are associated

with significant forces that may lead in certain circumstances to

concomitant injuries to surrounding structures Evaluation of

the brain-injured patient should include assessment for injuries

to the orbit, the face, the vascular supply to the brain, and the

spine This chapter will describe these injuries and discuss their

evaluation and treatment

Keywords:skull base, orbit, cervical spine, fracture

17.1 Introduction

Brain injury is chief among early concerns to those providing

care to patients with head trauma Providers should also be

cognizant of the possibility of injuries to associated structures

and be aware of strategies to recognize, evaluate, and treat

concomitant injuries Multidisciplinary teams composed of

emergency department and trauma providers, neurosurgery,

otolaryngology, ophthalmology, and facial trauma surgeons are

often needed to evaluate and treat these associated injuries This

chapter will describe the spectrum of possible injuries to the

orbit, the face, the vascular supply to the brain, and the spine

17.2 The Orbit

17.2.1 Injuries

Fractures of the Orbit

Orbital and ocular injuries are frequent with between 10 and

17% of patients presenting with these injuries in the setting of

trauma.1 While clinical examination is important, computed

tomography (CT) imaging is the preferred imaging modality for

detection of traumatic fracture and soft-tissue injury.1,2 The

mnemonic BALPINE has been developed to facilitate CT

evalua-tion in the setting of orbital trauma where the acronym stands

for: bones, anterior chamber, lens, posterior to the globe,

intra-conal orbit, neurovascular structures, and extraocular muscles/

extraconal orbit.1An important measurement on CT is orbital

volume A fracture may expand the space available for

intraor-bital contents and an increase in orintraor-bital volume of as little as 5%

may cause enophthalmos.3Rounded morphology of the inferior

rectus muscle may hint at enophthalmos as well.3

Orbital Floor

The orbital floor is the most commonly injured boundary of the

orbit Typically direct anteroposterior trauma to the globe is

transmitted to the orbital floor; this is termed a “blow-out”

fracture as the fragments of the orbital floor displace into the

maxillary sinus.1The sagittal view on CT allows for best

visual-ization of the orbital floor.3An important subset of orbital floor

fractures occurs with the “white eye syndrome.” Common in

children, the orbital floor fracture segment will displace and

recoil with resulting minimal displacement of the fracturedbone.3The globe will appear uninjured; however, the inferiorrectus muscle can herniate downward and become entrapped,leading to restricted ocular motility; this is the “trapdoorphenomenon.”3

Orbital RoofBlunt injury to the forehead and orbital rim may cause isolatedfractures of the orbital roof This is especially common in chil-dren who lack fully pneumatized frontal sinuses In adults, com-plex, high-energy trauma mechanisms can cause similar fracturepatterns Fractures through the orbital roof are highly associatedwith dural tears, cerebrospinal fluid (CSF) leak, and pneumoce-phalus If unrecognized or unrepaired in children, “growingfractures” may occur whereby CSF pulsations and cranial growthallow herniation of brain beyond the fracture line into anencephalocele with ultimate gliosis of the involved brain.1

Medial Wall of the OrbitThe medial wall of the orbit is the second most commonlyinjured segment Its walls are thin but are reinforced by thenumerous septations of the adjacent air cells.1Fractures of themedial wall are best appreciated on axial CT.3These fracturesare often asymptomatic but may present with complaints ofdiplopia Trapdoor fractures are possible with medial wall frac-tures as well.1

Lateral Wall of the OrbitFor the purposes of this chapter, the lateral wall of the orbit will

be discussed as part of the face under the section “Fractures ofthe Zygomaticomaxillary Complex.”

Other Ocular InjuryCompressive neuropathy, superior orbital fissure syndrome, andorbital apex syndrome are rare though potentially devastatingconsequences of fractures to the deep orbit Optic nerve com-pression following trauma to the globe may lead to progressivevision loss secondary to refractory elevated intraocular pressure,retrobulbar hematoma, and perineural edema.4 The superiororbital fissure syndrome may be either complete or partial withparesis of the third, fourth, or sixth cranial nerve causingextraocular muscle impairment and possible ophthalmoplegia.Accompanying parasympathetic disruption may present withptosis as well as mydriasis The orbital apex syndrome can sharemany features of the superior orbital fissure syndrome, but theetiology is usually a mass lesion located at the fundus of theorbital cone that also may impinge the optic nerve.5 Finally,severe direct forces to the globe may result in rupture

17.2.2 Anatomy

The orbit can be conceptualized as a pyramid encompassing theocular contents and the extraocular muscles.1,6See▶Fig 17.1

for an illustration of the skeleton of the orbit The deepest

seg-ment of the pyramid or cone is the orbital apex The skeletal

confines of the orbit are divided into its roof, medial wall,

lat-eral wall, and floor The orbit proper begins latlat-eral to the

naso-orbital-ethmoidal (NOE) region and its roof is the remainder of

the floor of the anterior skull base lateral to the cribriform plate

and anterior to the sphenoid sinus The lesser wing of the

sphe-noid also has a small contribution to the roof of the orbit at its

apex.1The medial wall of the orbit is multifaceted as well; from

superficial to deep, it is composed of the maxilla, lacrimal, and

ethmoid bones terminating into the body of the sphenoid.1The

medial wall of the orbit is adjacent to the ethmoid air cells The

lateral wall of the orbit is composed of the zygoma anteriorly

and the greater wing of the sphenoid at its posteriormost

mar-gin It is the curved strut of the zygomatic arch that is the most

conspicuous component of the lateral orbit.7 The mainstay of

the floor of the orbit is composed of the maxilla with small

seg-ments of the zygoma and palatine bones that contribute as well

The floor of the orbit is the roof of the maxillary sinus

At the apex of the orbit are key foramina: the optic canal and

the superior orbital fissure The optic canal is the passageway

for the optic nerve with the overlying ophthalmic artery

Through the superior orbital fissure, the nerves responsible for

extraocular muscle motility, the divisions of the ophthalmic

veins, and sympathetic fibers of the cavernous plexus transit

The superior orbital fissure can be further organized into thirds:

the lateral third containing the superior ophthalmic vein,

lacri-mal nerve, frontal nerve, trochlear nerve (the fourth cranial

nerve), and the recurrent meningeal branch of the lacrimal

artery The middle third transmits both the inferior and

supe-rior divisions of the oculomotor nerve (the third cranial nerve)

as well as the abducens nerve (the sixth cranial nerve) Finally,

the medial third of the superior orbital fissure contains the

infe-rior ophthalmic veins, sympathetic nerves arising in the

caver-nous sinus

The skeletal anatomy of the orbit serves to protect its

soft-tissue components The globe with components of the

sclera, cornea, anterior chamber, posterior chamber, and

vascular uvea is anteriormost within the orbit The ular muscles and their overlying fasciae comprise a muscularcone posterior to and flanking the globe Within the cone ofthe extraocular muscles lie the fat of the periorbita, vascularchannels, and lymphatics Centrally within the muscularcone are the optic nerve and the ophthalmic artery encircled

extraoc-by a dural sheath.6

17.2.3 Examination

Patient complaints can alert the examiner to look for physicalfindings and help determine imaging strategies Reports of pain,diplopia, and nausea can be subtle cues External examinationfor symmetry, depth of the globe, position of the globe verti-cally or horizontally, and ability to close the eye can be of highyield Signs of orbital injury including enophthalmos, hypoglo-bus, telecanthus, proptosis, hypesthesia of the infraorbital nervedistribution, and subcutaneous emphysema are visualized withexternal examination.2,3,5 Subconjunctival hemorrhage, trau-matic hyphema, and chemosis are also indicative of possibleinjury.3,6

Ocular examination may be challenging especially in cases ofdepressed mental status, use of sedation, or other severe inju-ries.1The complete ocular examination is only possible in theawake, cooperative patient and requires formal ophthalmologicevaluation In the emergent setting, globe integrity must first

be determined It is important that globe integrity is verifiedprior to ocular motility testing.3Signs of globe integrity viola-tion include subconjunctival hemorrhage, pupillary shapeabnormality, and flattening of the anterior chamber In theintact globe, ocular pressure determination is the next step inassessment Complete ocular assessment by ophthalmologyproviders should follow and may include the following: visionassessment, ocular motility, pupil examination, slit-lamp ocularexamination, and retinal examination.3,8Testing color percep-tion can be useful in evaluation of the optic nerve in that loss ofcolor saturation in the red hues may represent early traumaticoptic neuropathy.5

Fig 17.1 A schematized view of the left orbit

Labeled are the skeletal components of theorbital walls, roof, and floor

In the unconscious, or uncooperative patient, forced duction

testing may be used to determine ocular motility, and this may

require sedation as it can involve significant discomfort.5The

optic nerve function is ascertained via ophthalmoscopy

exami-nation, vision acuity, and pupillary response The oculomotor

nerve is also assessed via pupillary response The larger

compo-nent of the oculomotor nerve responsible for extraocular

motil-ity is assessed together with the trochlear and abducens nerves

in voluntary movements of the eye

17.2.4 Classifications

The injuries to the orbit are largely classified by the

topo-graphic skeletal subregions within the pattern of fracture

or to the soft-tissue structure involved.9The most hensive of the classification systems for orbital fractures isthe AOCMF classification system This tiered system withlevels 1 through 3 subdivides the orbit according to its rele-vant anatomy to specifically document the structuresinvolved See▶Table 17.1 for a summary of the orbital ana-

Strengths of this system are its unambiguity and its basis

on CT findings

17.2.5 Treatment

See▶Fig 17.2 for a simplified algorithm for the management oforbital fractures

Table 17.1 Orbital anatomical structure mapping as reported in Kunz et al9

Orbital rims

body

Orbital walls

the lacrimal bone)

Inferior 11 Anterior section of orbit (including

part of zygoma)

su-ture (greater wing of sphenoid)

bone)

Orbital apex

18 Lateral wall (greater wing of noid)

19 Superior wall (lesser wing of noid)

Abbreviations: ICM, intermediate central midface; UCM, upper central midface

Orbital Injuries

There is no consensus in the literature regarding routine use of

antibiotics in isolated orbital injury There is support for use of

intraoperative antibiotic administration during surgical repair.3,

10It has been noted that patients with increased sinus disease

may be at higher risk of orbital cellulitis, however.3

The oculocardiac reflex may occur with orbital fracture

and entrapment of the extraocular muscles Symptoms

including nausea, emesis, syncope, bradycardia, and asystole

can be associated.3 Advanced Cardiac Life Support protocol

algorithms may be necessary, and immediate surgical release

of incarcerated muscle with fracture repair is indicated.3In

general, clinical or CT findings of entrapment support

opera-tive intervention as soon as feasible and ideally within 48

hours.3

In the absence of entrapment, timing of repair for orbital

fractures is the subject of controversy in the literature.2 The

majority of orbital fractures are initially managed with

observa-tion only until about 5 to 14 days from injury to allow for

decreased periorbital edema.2,3Delayed repair may be offered

electively if any of the following are present: enophthalmos

greater than 2 mm, ocular motility dysfunction, persistent

dip-lopia, CT evidence of extraocular muscle entrapment or floor

disruption greater than 50%, worsening infraorbital nerve

dys-esthesia, and abnormal forced duction testing.2,3 Delaying

surgery may also lessen the risk of possible compartment

syndrome, while there is a trade-off risk of fibrosis of impingedorbital tissue and chronic diplopia.3

The main goal of operative intervention is to restore the tours of the bony orbit and hence orbital volume to correct theeffects secondary to the original offending trauma.2,10Surgicalcomplications include vision loss (up to 0.4%), transient diplopia(common but persistent in 8–48%), persistent enophthalmos(7–27%), and postoperative ectropion.3 Depending on thechoice of material used in the reconstruction, late complicationssuch as encapsulation and extrusion of the surgical buttressescan occur.2

con-Orbital FloorFractures displaced greater than 1 cm2or with involvement ofgreater than 50% of the orbital floor likely require nonurgentsurgery.1 While there is no consensus in the literature, mostreports recommend operative intervention within 7 to 10 daysfollowing trauma In the “white eye syndrome” common in chil-dren with this injury, the oculocardiac reflex may manifest,suggesting severe entrapment warranting surgical repairwithin 1 to 2 days

Orbital RoofSee section on “Frontobasilar Fractures” for further discussion

of management strategies

Fig 17.2 An algorithm for treatment of orbitalfractures

Medial Wall of the Orbit

Combined fractures involving the medial wall of the orbit and

the orbital floor are more likely to lead to enophthalmos; 40%

of medial wall fractures will produce this finding.3Repair needs

to assure the stability of the inferomedial bony orbital strut as

this is important to preserve the suspensory ligaments of the

globe and avoid severe ocular motility problems.1

Multiple open and endoscopic techniques have arisen for

repair of medial orbital fractures The most popular open

technique is the transcaruncular incision, which may be

extended to the transconjunctival approach.3 To minimize

eyelid complications, the endoscopic transethmoidal and

sublabial transmaxillary approaches have been used as well.3

Goals of each of these approaches are reduction of the

orbi-tal contents and stabilization of the bony shelves of the

floor A variety of autograft and allograft techniques have

been developed for this purpose

Other Ocular Injury

Immediate administration of high-dose steroids is first-line

therapy for patients with progressive vision loss following

trauma with evidence of optic nerve compression.4Indications

for urgent surgical intervention include medically refractory

elevated intraocular pressure, retrobulbar hematoma,

progres-sive visual loss, and perineural edema.4Decompression of the

optic canal can be accomplished via intranasal transsphenoidal,

transethmoidal, or bifrontal approaches.4

Rupture of the globe is a surgical emergency Ophthalmology

consultation for repair and potential salvage is indicated If

unable to salvage the globe, enucleation is usually completed in

the 24 hours immediately following the injury to prevent

delayed sympathetic ophthalmia.4

17.3 Facial Fractures

17.3.1 Injuries

Frontobasilar Fractures

A substantial amount of energy is required to produce fracture

of the frontal bone given the system of vertical and horizontal

buttresses of the facial skeleton It has been demonstrated that

approximately 800 to 2,200 pounds of pressure are required to

produce fracture at this site.4It is not surprising then that

fron-tobasilar fractures are often found in association with traumatic

brain injuries

CT is the gold standard for evaluation of frontobasilar injury

Cuts 1 to 3 mm in width in all three planes are required to

determine the extent of the injury because the involved bones

are so thin.4

Naso-Orbital-Ethmoidal Fractures

NOE fractures can be seen in conjunction with other facial

frac-tures or more rarely as an isolated fracture (5% of facial

fractures are isolated NOE fractures).11 Plain radiographs

and conventional CT are not of sufficient resolution to

com-pletely examine the bony segment of the medial canthal tendon

(MCT) insertion A CT protocol using 1.5-mm axial cuts is

recommended.11These scans can also be used for tive navigation during reconstructive attempts

intraopera-Fractures of the Zygomaticomaxillary Complex

With ZMC fractures, the anteroposterior dimension of the orbitdecreases, but the lateral wall is pushed out, causing the face towiden and orbital volume to increase.4This leads to enophthal-mos as the globe retracts into the expanded orbital volume.1,2

Fracture planes are frequently tetrapod involving each of thefour sutures.1,3 Multislice axial and coronal CT is needed todetermine fracture displacement and comminution with highfidelity.2

17.3.2 Anatomy

The frontal bone projects anteroinferiorly from the vertexbeginning at the coronal suture The hallmark of the frontalbone is the frontal sinus This sinus forms with the gradualexpansion of the ethmoid air cells during the process of pneu-matization in childhood and early adolescence.12Multiple pat-terns of pneumatization have been noted in the literature with20% of individuals displaying aberrant pneumatization.13

Within the frontal sinus is a bony midline septum At the rior extent of this septum lie conspicuous hourglass-shapedstructures, the frontal sinus outflow tracts (FSOT) There is asmall cleft, the frontal sinus infundibulum, which at its inferiormargin becomes the frontal sinus ostium opening to the frontalsinus recess The size and conformation of the FSOT is impacted

infe-by the agar nasi cells and frontal air cells; note the medial dary of the FSOT is the middle turbinate.7,12,13In the axial plane,the frontal sinus can be viewed as a facial crumple zone, withthe anterior and posterior tables of the sinus serving to absorbmuch of the force of the traumatic blow The anterior table ofthe frontal sinus is the underlying structure giving aestheticform to the face as the contours of the forehead, glabella, andthe orbital rim arise from it.7The posterior table of the frontalsinus separates the sinus contents from the cranial vault andbegins the anterior skull base

boun-At the central anterior skull base, deep to the posterior table

of the frontal sinus, lies the cribriform plate The cribriformplate is the demarcation of the roof of the ethmoid sinusthrough which the olfactory nerves traverse.14Posterior to thecribriform plate is the anterior cranial fossa, composed of theplanum sphenoidale, the roof to the sphenoid sinus, and thebeginning of the sella turcica

The NOE region extends rostrally from the inferior bounds ofthe frontobasilar skull The nasofrontal suture line is prominent

at this location and is the superficial margin of the ethmoid aircells deep to it Inferior to this suture, the nasal bones and thecartilaginous nasal septum arise The nasal bones articulatesuperomedially with the nasal process of the frontal bone andmedially with one another.7Laterally, the nasal bones articulatewith the frontal process of the maxilla

A key component of the NOE region is the MCT, which insertsupon the medial orbital wall This tendon is the insertion of theorbicularis oculus muscle and the lacrimal system upon thebone of the orbit.11The MCT is important for stabilization ofthe tarsal plates as well The MCT represents a fusion of an

anterior limb, which extends to the anterior lacrimal crest on

the frontal process of the maxilla, and a posterior limb

extend-ing to the posterior lacrimal crest of the lacrimal bone.14A third

limb joining the nasofrontal suture is variable.14 These

seg-ments of the MCT surround the lacrimal sac.15

The articulation of the zygoma with the maxilla is the ZMC

The malar eminence of the ZMC is the most forward projection

of the lateral face and hence it is highly vulnerable to blunt

trauma.7 In trauma, the ZMC is most susceptible to fracture

along its suture lines There are four sutures involved in the

ZMC: the zygomaticofacial, zygomaticotemporal,

zygomatico-maxillary, and that with the sphenoid.1,7

17.3.3 Examination

As with examination of the orbit, the patient’s head should be

visually inspected as well as palpated to assess for

subcutane-ous emphysema, edema, and ecchymosis that could signal

underlying injury When possible, if one side of the face is

unin-volved, the two sides of the face should be compared Flattening

of bony prominences, loss of forehead contours, or abnormal

mobility of the midface is highly suspicious for underlying

frac-ture.11,12In particular, ecchymosis inferior to the orbit (racoon’s

eyes) can be indicative of skull base fracture as well

Addition-ally, palpation of the nasal bridge can reveal separation or

ten-derness indicative of possible septal hematoma It is important

to note that the extent of soft-tissue edema in the acute period

may mask underlying fracture, and hence delayed repeat

examination may be necessary

Epiphora is a phenomenon of abnormal tearing from

nasolacrimal duct obstruction, direct injury to the lacrimal

system, or soft-tissue edema.11If epiphora is present,

prob-ing with irrigation of the lacrimal system is necessary to

further evaluate and possibly clear debris In some cases,

epiphora can spontaneously resolve even as remote as 6

months from injury.11

The integrity of the MCT is assessed via the bowstring test

(palpation of the tendon at the medial canthus) and

measure-ments of intercanthal and palpebral fissure distances.12,14,15

Olfaction is often not assessable in the acute setting if blood

or debris obstructs the nares Sensation testing on the face and

ability to masticate assesses the trigeminal nerve The facial

nerve can be assessed with purposeful gestures of expression to

ensure integrity of each of its divisions

17.3.4 Classifications Frontobasilar Fractures

A common classification scheme for these fractures is by Raveh

as shown in▶Table 17.2 In type I injury, the external frame ofthe face buffers most of the traumatic force and gives way pro-tecting the posterior table of the frontal sinus, the anterior cra-nial fossa, and the optic canal Type II fractures representdislocation of the posterior table of the frontal sinus at a mini-mum; however, they may be as severe as to telescope the cribri-form plate, parasellar, and sphenoidal elements.4 This injurypattern is frequently associated with CSF leak, hematoma, andoptic nerve compression

Naso-Orbital-Ethmoidal FracturesFor NOE fractures, various classification systems have arisensince the 1980s The most common classification system in usetoday is that by Markowitz and Manson in 1991 seen in

▶Table 17.3.11Markowitz and colleagues used the MCT and thedegree of comminution to determine three NOE fracture sub-types In the type I fracture, the bone fragment attached to theMCT is larger and may not displace or demonstrate abnormalmobility on physical examination In type II fractures, there iscomminution of the segment of bone bearing the MCT Finally,the type III fractures are highly comminuted and the MCT may

be completely avulsed from its bony insertion

Fractures of the Zygomaticomaxillary Complex

Fractures of the ZMC are the second most common facial ture.16The Zingg classification subdivides the potential compo-nents injured within the ZMC for classification of injuryseverity.16This is depicted in▶Table 17.4 Type A fractures arenot common and are isolated to a singular component of the

frac-Table 17.2 Classification of frontobasilar fractures according to Raveh

Type Structures involved

I Mechanism: external frame neutralizes impact, preserving

deeper structures

Frontonasal-ethmoidal with medial orbit, not involving skull

base

II Mechanism: high-energy force not dissipated by external

frame with disruption of deeper structures

IIa Central, frontal sinus involvement, ± FSOT (frontal sinus

outflow tract) obstruction

IIb Lateral, temporal bone involvement, ± frontal sinus

involve-ment

Table 17.3 Classification of naso-orbital ethmoidal fractures according

to Markowitz and MansonClass Structures involved

I Large medial canthal tendon (MCT) bearing bone segment,

perhaps no perceptible movement on examination

II MCT attached to comminuted central fragment of boneIII Comminuted central fragment, fracture into bone from

which MCT originates, possible complete avulsion of MCT

Table 17.4 Zingg classification of zygomaticomaxillary complex (ZMC)fractures

Type Structures involvedA1 Isolated to zygomatic arch onlyA2 Lateral orbital wall

A3 Inferior orbital wall

B All four sutures of the ZMC involved

C Comminuted injury of entire ZMC

ZMC; hence, there are three subtypes Type B and C fractures

involve all four sutures, with type C being a comminuted

pat-tern of fracture Fractures of the ZMC nearly always involve the

orbital floor as well.16

17.3.5 Treatment

Frontobasilar Fractures

Type I injuries have minimal cosmetic consequences in most

cases and hence repair is optional (▶Fig 17.3) Type II injuries

can be highly disfiguring In the absence of emergent surgical

need, delayed intervention for cosmesis may be desired by the

patient Goals of surgery would include re-establishment of the

facial projection with reduction, stabilization, and fixation of

fracture segments Many type II fractures need surgery at the

time of initial hospitalization either to treat underlying

hema-tomas or to repair a CSF leak If there is a displacement of the

posterior wall of the frontal sinus, there is a possibility of

delayed mucocele development if FSOT obstruction occurs

Many surgeons opt to exenterate the frontal sinus to prevent

this complication in the process of cranialization of the frontal

sinus.10 Newer more conservative strategies to re-create the

FSOT using endoscopic techniques are gaining popularity as

well.10There is no role for prophylactic antibiotics with

fronto-basilar fractures with or without CSF leak Use of intraoperative

antibiotics is supported.10

Naso-Orbital-Ethmoidal Fractures

The degree of displacement and comminution of fracture

seg-ments in NOE fractures indicate whether an injury should be

observed or surgically treated (▶Fig 17.4).1If there is no

move-ment of the fracture segmove-ment on physical examination or no

evidence of displacement on CT, no intervention may be

neces-sary.11Conversely, as in type II and III fractures, fractures with

demonstrable displacement on CT, movement upon palpation,

or noteworthy comminution require open reduction and

internal fixation.4,11A variety of incisions can be used Commontechniques for fixation include screw-and-plate fixation, trans-nasal wiring, or cantilever calvarial bone grafting.11In cases ofMCT avulsion, transnasal canthopexy is required.4,11 Surgicalgoals include restoration of the position of the canthus andintercanthal distance For aesthetics, nasal contour, nasal pro-jection, and symmetry of the bilateral medial canthi are alsotargeted.11

Failure to recognize NOE or to reconstruct type II or III tures can lead to complications with persistent telecanthus andepiphora being most common.11The higher the degree of com-minution, the greater the likelihood of nasolacrimal duct involve-ment; 20% of patients with NOE type II and III fractures go on todevelop epiphora in the absence of surgical intervention.1

frac-Fractures of the Zygomaticomaxillary Complex

Type A injuries that do not cause deformity or diplopia do notrequire surgical correction (▶Fig 17.5).17With involvement ofthe suture or comminution of the fragments, it is more likelythat surgical correction with open reduction and internal fixa-tion is necessary The initial step in correction of ZMC type Band C fractures is an attempt at reduction, usually closed atfirst.7Goals of correction are to stabilize the ZMC against thepull of the masseter and to correct the features of the malarcontours.16Critical additional considerations in ZMC fracturemanagement rely on an interplay with potential orbital struc-tures involved in the injury, that is, attempting to restore thepretrauma orbital volume

17.4 Vascular InjuryThe internal carotid artery (ICA) and vertebral artery areexposed to substantial forces during trauma and are at risk ofinjury The presence of certain fractures suggests significanttrauma and should lead the treating physician to assess for

Fig 17.3 Timeline for treatment of frontobasilarfractures by Raveh type

vascular injury Moreover, when there is a neurologic disability

that cannot be explained on the noncontrast CT scan of the

head, vascular injury should be suspected as a potential

etiol-ogy for ischemic stroke The cerebral venous sinuses are also at

risk for injury in traumatic brain injury patients

17.4.1 Injuries

Injury to the cerebral vasculature can result from a number of

mechanisms including acceleration or deceleration shearing of

the vessel wall during stretching or tearing caused by excessive

movement at the neck with impingement of the vessel wall by

bony structures or fracture fragments Certain fractures shouldheighten suspicion for injury to certain vessels based on theiranatomic course For example, injuries at the skull base throughthe petrous bone or carotid canal are at high risk for injury tothe carotid arteries Fractures through the transverse foramen

of the cervical spine place the vertebral arteries at risk cavernous fistulas (CCFs) form when there is an abnormal(either direct or indirect) connection from the ICA to the caver-nous sinus In addition to the mechanisms discussed earlier,traumatic CCFs are also thought to form due to the suddenincrease in ICA intraluminal pressure with concurrent distalimpingement following blunt trauma.18

Carotid-Fig 17.4 Decision tree for naso-orbital ethmoidal(NOE) fracture treatment

Fig 17.5 Decision tree for zygomaticomaxillarycomplex (ZMC) fracture treatment

The most significant possible morbidity from blunt injury to

the ICA and vertebral artery is an ischemic stroke The

patho-physiology is explained by thrombus formation secondary to

the intimal tear The thrombus could then lead to vessel

occlu-sion or dislodge emboli to cause distal infarcts

The superficial cerebral venous sinuses are also at risk of

damage during a traumatic brain injury, particularly in the

set-ting of depressed skull fractures The presence of a depressed

skull fracture over the known course of the superior sagittal,

transverse, or sigmoid sinuses places these structures at risk of

being torn or occluded This can lead to hematoma formation or

sinus obstruction Obstruction of the cerebral venous sinuses

leads to venous congestion and places patients at risk of venous

infarcts and increased intracranial pressure

17.4.2 Anatomy

The ICA and vertebral artery are responsible for the intradural

blood supply as their position in the neck and skull base

sub-jects them to the many forces responsible for traumatic brain

injury An understanding of the anatomic course that each

ves-sel takes and the osseous structures they are associated with

can help physicians determine whether an injury is likely

The ICA, which branches off the common carotid artery (CCA)

at the level of C4, ascends anterior to the transverse processes

of C3–C1 and then travels toward the carotid canal (cervical

segment) The vessel then travels in the carotid canal of the

pet-rous bone up to the foramen lacerum (petpet-rous segment) The

ICA then passes over the foramen lacerum and pierces the dura

toward the cavernous sinus (lacerum segment) where it then

enters the cavernous sinus (cavernous segment) After exiting

the cavernous sinus, the ICA enters the proximal dural ring and

then courses through the distal dural ring (clinoid segment)

where it finally enters the dura The ophthalmic segment

encompasses the portion of the ICA from the distal dural ring to

the posterior communicating artery The communicating

seg-ment is the last segseg-ment and includes the area from the

poste-rior communicating artery to the ICA bifurcation.19

The vertebral artery branches off the subclavian artery to

ascend in the neck (V1 segment) It most commonly enters the

foramen transversarium at the level of C6 and travels through

the foramen transversarium until C2 (V2 segment), turns

later-ally upon exiting the C2 foramen transversarium before

ascend-ing into the C1 foramen transversarium (V3 segment), and

pierces the dura before entering the skull through the foramen

magnum (V4 segment)

17.4.3 Examination

As with every other injury described in this chapter, assessment

of these patients begins with a thorough neurologic

examina-tion Screening for blunt cervical vascular injury (BCVI) occurs

through a screening protocol such as the Denver criteria or

modifications of the same.20,21 CT angiography (CTA) of the

head and neck is generally performed on all patients found to

have cervical spine fractures of the vertebral body or pedicle,

basilar skull fractures involving the carotid canal or petrous

bone, Le Fort II or III fractures, Glasgow Coma Scale (GCS) score

lower than 7 without obvious cerebral injury on head CT, and/

or near hanging or strangulation with a ligature mark or

contusion Patients with traumatic CCFs can present acutelywith orbital bruit, pulsatility, exophthalmos, chemosis, head-aches, and visual disturbances.22,23,24Despite a lack of definitiveevidence, a combination of these symptoms and radiographicfindings such as cavernous sinus enlargement and superiorophthalmic vein dilatation should prompt further investigationwith catheter angiography.25In patients where there is a con-cern for cerebral venous sinus injury, CT venography or mag-netic resonance venography may be performed

17.4.4 Classifications

The most commonly used classification system for BCVI to theICA and vertebral artery is the Denver criteria.21 Injuries aregrouped into five categories: grade I—with luminal irregularity

or dissection with less than 25% luminal stenosis; grade section or intramural hematoma with ≥ 25% luminal stenosis,intraluminal thrombus, or raised intimal flap; grade III—pseu-doaneurysm; grade IV—occlusion; and grade V—transection.Stroke rates originally reported for each grade were the follow-ing: grade I—3%; grade II—11%; grade III—33%; grade IV—44%;and grade 5—100% Subsequent literature has suggested lowerrates with grade III and IV injuries.21

II—dis-17.4.5 Treatment

Treatment of cerebrovascular injuries can involve observation,antiplatelet therapy, anticoagulation, endovascular interven-tion, or surgical intervention (▶Fig 17.6) The goal of therapy is

to minimize ischemic or hemorrhagic complications that canlead to further brain injury and worse neurologic outcome.BCVI treatment is directed primarily at reduction of ische-mic stroke risk and is largely determined based on grade.Grade I and II injuries have low risk of stroke and can bemanaged conservatively either with observation alone orantiplatelet therapy with aspirin.26,27Grade III and IV lesionshave traditionally been treated under the assumption thatthey are associated with high ischemic stroke rates.21 Morerecent data have suggested that the rates may not be as high

as previously thought.26,27 At our institution, these highergrade lesions are treated with antiplatelet therapy usingaspirin and followed with serial imaging For patients whodevelop strokes on aspirin, consideration is made to switch

to dual antiplatelet therapy with the addition of clopidogrel

or transition to anticoagulation Another option, particularlyfor pseudoaneurysms (grade III), is endovascular treatmentwith stenting

When considering traumatic CCFs, conservative managementhas no role Ocular symptoms typically resolve with successfultreatment of the CCF Visual deficits may be permanentdepending on the delay to treatment, arguing for prompt diag-nosis, and definitive management of CCFs Left untreated, CCFscould also lead to intracranial hemorrhage Fortunately, endo-vascular treatment of these lesions offers a high cure rate andgood prognosis.18,23,28,29

On the other hand, cerebral venous sinus injuries are bestmanaged conservatively Surgical repair of the sinus is difficultand may lead to vessel sacrifice due to inability to controlbleeding Unless there is a strong indication for operative inter-vention such as an expanding epidural hematoma with

significant mass effect or open depressed skull fracture, surgical

intervention is generally avoided

17.5 Spine Fractures

Patients who sustain a traumatic brain injury are at high risk

for a concomitant spine injury When taking into account all

segments of the spine (cervical, thoracic, lumbar, and sacral),

rates as high as 19.4% have been reported.30Within the cervical

spine, fracture rates of 6.6% and dislocation rates of 2.8% have

been observed in all patients with an acute head injury The

cervical spine fracture rate increases to 9.3% in those patients

with an acute traumatic intracranial lesion.31As a result, it is of

paramount importance to perform a thorough evaluation of the

spine and in particular the cervical spine when treating

patients with a traumatic brain injury

17.5.1 Injuries

When considering injuries to the cervical spine, one must sider fractures as well as ligamentous strain or tearing Ulti-mately, the treating physician is most concerned with whetherthe injury is classified as stable or unstable and whether it pla-ces the spinal cord and nerve roots at risk of damage that wouldlead to neurologic disability To qualify as a stable injury, thespine should be able to maintain structural integrity and pre-vent neurologic injury without any intervention Unstable inju-ries indicate loss of biomechanical integrity and necessitatesome form of support, which may range from bracing to surgi-cal fixation

con-Working from the craniocervical junction down, the first area

at risk of injury is the atlanto-occipital segment Injuries at thislevel of the spine include occipital condylar fractures A large

Fig 17.6 An algorithm for treatment of vascularinjuries based on grade

proportion of patients with occipital condylar fractures also

have other concomitant injuries including additional cervical

fractures and ligament or cord injuries.32,33,34,35 Cranial nerve

deficits, particularly cranial nerves IX through XII, were found

in 31% of patients from one series.36These patients are

chal-lenging to manage in the intensive care unit and beyond due to

resulting postural hypotension, dysphagia, severe upper

gastro-intestinal dysmotility, oropharyngeal secretions, airway

protec-tion, and respiratory control issues The other major injury at

this segment of the spine is atlanto-occipital dislocation (AOD),

which is a result of injury to the craniocervical ligaments This

is a highly unstable injury that is characterized by the

dissocia-tion of the occipital condyles from the articuladissocia-tion at the C1

articular pillars While advances in prehospital care have

increased survival, morbidity and mortality remain high from

bulbar–cervical dissociation.37

The atlas, or C1 vertebrae, is the next segment of the spine

that must be evaluated for injury C1 fractures account for 3 to

13% of cervical spine fractures In one series, 21% had associated

head injuries.38The most common fracture of C1 is a Jefferson

fracture, which is a result of axial loading It describes a fracture

through the ring of C1 at more than two points and classically

at four points Neurologic deficits are uncommon due to the

large canal diameter at this level and the tendency for fracture

fragments to be displaced outward.3 Other fractures of C1

include those involving a single arch or the lateral masses

Fractures of the axis, or C2 vertebrae, represent 20% of

cervical spine fractures.39The two most frequent types of C2

fractures are odontoid fractures and hangman’s fracture

Flexion is the most common mechanism of injury for

odon-toid fractures, and neurologic injury varies with fracture

type A hangman’s fracture is characterized by bilateral

frac-tures through the pars interarticularis with traumatic

sub-luxation of C2 on C3

Injuries of the subaxial cervical spine involve the C3–C7

ver-tebrae Injuries can be further subdivided based on the

biome-chanical forces causing the injury Flexion injuries include

teardrop fractures, quadrangular fractures, subluxation, and

locked or perched facets Teardrop fractures are characterized

by a triangular fragment of the anteroinferior vertebral body

with posterior displacement of the fractured vertebrae.40

Quad-rangular fractures involve an oblique fracture through the

ver-tebral body with posterior subluxation of the superior verver-tebral

body on the inferior vertebral body and disruption of the disk,

anterior ligaments, and posterior ligaments Locked facets are

caused by hyperflexion and result in the inferior facet of the

level above positioned anterior to the superior facet of the level

below Locked facets have high rates of spinal cord injury with

less than 10% having an intact neurologic examination.41

Exten-sion injuries include those without osseous injury such as

cen-tral cord syndrome from pre-existing cervical stenosis as well

as fractures of the lateral mass and facets Injuries related to

axial load often display a burst pattern involving the anterior

and posterior vertebral walls

17.5.2 Anatomy

A thorough understanding of the anatomy of the spine and itsvarious segments is essential to the evaluation of injuries anddetermination of the most appropriate treatment modality Theoccipital condyles, atlas, and axis are the primary osseous struc-tures that make up the craniocervical junction The occipitalcondyles are protuberances of bone at the lateral extent of theforamen magnum bilaterally The atlas is a ring with an anteriorportion and a posterior portion, which are divided by the trans-verse atlantal ligament (TAL) The axis is characterized by thedens, which is a prominent toothlike process that extends rostralfrom the body of C2 through the ring of C1 C1 and C2 are theonly vertebrae with no intervening disk until the sacrum.The articulation between the occipital condyles and the atlas

is shallow and provides some stability This joint is responsiblefor a significant amount of an individual’s neck flexion and ex-tension The dens of the axis extends upward and forms a syno-vial articulation with the posterior aspect of the anterior arch ofthe atlas The atlantoaxial articulation provides nearly all of anindividual’s head rotation Bilateral arthrodial synovial jointsbetween C1 and C2 complete their osseous articulation Despitethese osseous articulations, the primary stability of the cranio-cervical junction is provided by the ligaments, which are dividedinto intrinsic and extrinsic Intrinsic ligaments include the tecto-rial membrane, the cruciate ligament, and the alar ligament aswell as the joint capsules Within the cruciate ligament is theTAL, which is arguably the most important ligament for main-taining the structural integrity of the craniocervical junction.The TAL extends between the lateral tubercles of the atlas and issolely responsible for maintaining the articulation of the dens tothe atlas Further stabilization of the axis is provided by the api-cal ligament that extends from the dens to the basion and thealar ligaments, which extend from the dens to the occipitalcondyles bilaterally The extrinsic ligaments are made up of theligamentum nuchae and the fibroelastic continuations of theanterior longitudinal ligaments and the ligamentum flavum.2,37

The subaxial cervical vertebrae are more uniform in phology Each is made up of a vertebral body, paired pedicles,transverse processes with foramina, lamina, and a spinousprocess Anteriorly, each vertebral body is separated from thenext by an intervertebral disk, while posteriorly, the facets pro-vide synovial articulation bilaterally The subaxial spine primar-ily provides flexion and extension movements Of note, thevertebral arteries course through the transverse foramen of thecervical vertebrae bilaterally Most frequently, the arteries enterthe transverse foramen at C6 and exit at C2 before entering intothe skull base, but this anatomy can vary.2,5

mor-17.5.3 Examination

As with most clinical situations, evaluation of a patient withspine injuries begins with a thorough history and physicalexam This can be challenging in patients with traumatic brain

injury given diminished altered mental status If history cannot

be obtained from the patient, information from first responders

is critical All patients with traumatic brain injury and

particu-larly those with depressed mental status should be fully

immo-bilized and kept flat on a backboard The neck should be

immobilized in the midline position in a rigid cervical collar

A full neurologic examination should be performed when

possible and is critical for determining the appropriate

inter-ventions as well as timing of treatment If the patient is alert

and cooperative, obtaining a detailed motor and sensory

exami-nation of the upper and lower extremities is essential Deep

tendon reflexes and rectal tone are also critical for determining

varying degrees of spinal cord injury Palpation of the midline

spine to assess for step-offs and pain can help determine

seg-ments of the spine that would require further evaluation with

radiographic imaging

While performing the most thorough neurologic examination

possible is important, most traumatic brain injury patients will

require radiographic imaging of the spine to rule out significant

injuries CT imaging is now the modality of choice for initial

workup A CT scan of the cervical spine should be performed on

all patients with traumatic brain injury The thoracic and lumbar

spine should also be imaged in patients with the examination

findings concerning for a thoracolumbar injury (i.e., pain or

step-offs upon palpation or lower extremity deficits) or in those

patients who cannot fully participate in a thorough physical

examination If ligamentous injury of spinal cord injury is

sus-pected, then further workup with magnetic resonance imaging

(MRI) may be warranted once the patient is stabilized

17.5.4 Classifications

For each segment of the cervical spine, various classificationshave been developed These classifications are aimed to helpassess the stability of the fracture

AOD has been classified into three types based on the tion of distraction Type I AOD is characterized by anterior dis-location of the occiput relative to the atlas Type II AODdescribes longitudinal distraction Type III describes posteriordislocation of the occiput.42 ▶Table 17.5 describes objectivemeasurements used to determine if various AOD types arepresent based on imaging All AOD types are highly unstable

direc-Anderson and Montesano proposed a classification systemfor occipital condyle fractures Type I describes an impactedcondyle with comminution as a result of axial loading In type IIfractures, there is extension of a linear skull base fracture intothe occipital condyle Type III is an avulsion fracture of the occi-pital condyle by the alar ligament Type I and II fractures of theoccipital condyle are generally stable, while type III fracturesare unstable.43

C1 fractures can be classified into three types Type I fracturesinvolve either the anterior or posterior arch, type II classifiesfractures through both the anterior and posterior arches (Jeffer-son’s fracture), and type III is a lateral mass fracture.44The mostimportant factor in the classification of C1 fractures is the integ-rity of the TAL The TAL integrity can be evaluated using therule of Spence, which states that disruption is present when theoverhang of both C1 lateral masses on C2 is ≥ 7 mm on an openmouth odontoid X-ray

There are two main classification systems for C2 fractures,one for odontoid fractures and another for hangman’s fractures

There are three types of odontoid fractures described by son and D’Alonzo.45Type I describes fractures through the tip ofthe dens, type II fractures are those through the base of thedens, and type III fractures involve the vertebral body The Lev-ine classification (or modified Effendi system) of hangman’sfractures divides them into five types, which are described in

Ander-▶Table 17.6.46,47

The subaxial injury classification (SLIC) was developed toguide decision making in the treatment of subaxial cervicalspine injuries Points are given for various examination andimaging findings with the total score differentiating surgicaland nonsurgical management (▶Table 17.7).48

Given the highly unstable nature of all types of AOD, ate immobilization in a halo orthosis is recommended Thesepatients most frequently require subsequent operative fixationvia a posterior occipitocervical fusion.49

immedi-Table 17.5 Measurements used to determine the presence of

atlanto-occipital dislocation (AOD)

Method Dislocation type Measurement Interpretation

Powers’ ratio Anterior AOD

(type I)

BC/AO

●BC = basion toposterior arch

0.9–1Abnormal: ≥ 1

Normal: ≤ 12mm

Basion–axial

interval (BAI)a

Anterior or

posterior AOD

(types I and III)

Distance from thebasion to therostral extension

of the posterioraxial line (posteri-

or cortical margin

of the body ofC2)

Normal: –4 to

12 mm onlateral

aMeasured on lateral X-ray with target-film distance of 1 mm

Occipital condyle fractures are most frequently treated with

external immobilization via a rigid cervical collar regardless of

type A single institution retrospective review of 100 patients

determined that of the 80 patients managed either in a rigid

cervical collar or with no brace, none developed delayed

neuro-logic deficit or craniocervical instability.34

C1 fractures are frequently managed nonoperatively through

external immobilization For type I and III fractures, external

immobilization via a rigid cervical collar is frequently sufficient

for 6 to 8 weeks For type II fractures, or Jefferson’s fractures,

treatment is based on the integrity of the TAL If the TAL is

intact, a rigid cervical collar is sufficient On the other hand, if

the TAL is disrupted, then operative fixation via a C1–C2 fusion

is performed.50 Use of halo immobilization can be associated

with high morbidity, especially with prolonged use in the

eld-erly population.21,51

Management of odontoid fractures of the C2 vertebrae is

var-iable, and patient age and comorbidities are important

consid-erations For all three types of odontoid fractures, external

immobilization via a rigid cervical collar or halo is

recom-mended at the minimum for 10 to 12 weeks For type II and III

fractures, surgical fixation can be considered in younger

patients with comminution of the fracture or significant

dis-placement (≥ 5 mm) Stable hangman’s fractures (type I) are

managed nonoperatively in a rigid cervical collar Type II and III

fractures are at risk of needing surgical fixation Indications for

operative intervention include inability to reduce the fracture,

failure of external immobilization, traumatic C2–C3 disk with

neural compression, and established nonunion.52

Treatment of injuries of subaxial cervical spine should take into

account dislocation, fracture comminution and displacement,

neural compression, and ligamentous injury In patients withnoncomminuted fractures, minimal displacement, no dislocation,

no neural compression, and minimal ligamentous injury mined by MRI), external immobilization is sufficient If all thesefeatures are not present, operative stabilization should be consid-ered as guided by the SLIC score Regardless of the treatmentapproach selected, these patients should be followed closely dur-ing the first 3 months both clinically and radiographically toensure appropriate healing For patients with a locked facet,operative stabilization is indicated Attempts should be made toexpeditiously reduce the dislocation, particularly when the neu-rologic injury is incomplete This can be performed throughclosed reduction using cervical traction in the awake and cooper-ative patient, followed by operative fixation Alternatively, openreduction in the operating room may be performed along withsurgical stabilization in the same setting.53

(deter-Table 17.7 Subaxial injury classification

● Indeterminate (e.g., isolated terspinous widening, MRI [mag-netic resonance imaging] signalchange only)

in-1

● Disrupted (e.g., widening of diskspace, facet perch, or disloca-tion)

2

Neurological status

● Incomplete cord injury 3

● Continuous cord compression insetting of neurological deficit

Axial loadingand extension

Axial loadingand extensionwith reboundflexion

Unstable

IIA Oblique fracture

through the pars

Severe tion but slight or

angula-no subluxation

Flexion tion

angula-at C2–C3

Maybe flexionfollowed bycompression

Unstable

[1] Betts AM, O’Brien WT, Davies BW, Youssef OH A systematic approach to CT

evaluation of orbital trauma Emerg Radiol 2014; 21(5):511–531

[2] Cruz AA, Eichenberger GC Epidemiology and management of orbital

frac-tures Curr Opin Ophthalmol 2004; 15(5):416–421

[3] Boyette JR, Pemberton JD, Bonilla-Velez J Management of orbital fractures:

challenges and solutions Clin Ophthalmol 2015; 9:2127–2137

[4] Bell RB, Chen J Frontobasilar fractures: contemporary management Atlas

Oral Maxillofac Surg Clin North Am 2010; 18(2):181–196

[5] Gart MS, Gosain AK Evidence-based medicine: orbital floor fractures Plast

Reconstr Surg 2014; 134(6):1345–1355

[6] Kubal WS Imaging of orbital trauma Radiographics 2008; 28(6):1729–1739

[7] Fraioli RE, Branstetter BF, IV, Deleyiannis FW Facial fractures: beyond Le Fort.

Otolaryngol Clin North Am 2008; 41(1):51–76, vi

[8] Ellis E, III Orbital trauma Oral Maxillofac Surg Clin North Am 2012; 24

(4):629–648

[9] Kunz C, Audigé L, Cornelius CP, Buitrago-Téllez CH, Rudderman R, Prein J The

Comprehensive AOCMF Classification System: Orbital Fractures - Level 3

Tutorial Craniomaxillofac Trauma Reconstr 2014; 7 Suppl 1:S092–S102

[10] Doerr TD Evidence-based facial fracture management Facial Plast Surg Clin

Curr Opin Otolaryngol Head Neck Surg 2013; 21(4):410–416 [16] Kochhar A, Byrne PJ Surgical management of complex midfacial fractures.

Otolaryngol Clin North Am 2013; 46(5):759–778 [17] Uzelac A, Gean AD Orbital and facial fractures Neuroimaging Clin N Am.

2014; 24(3):407–424, vii [18] Higashida RT, Halbach VV, Tsai FY, et al Interventional neurovascular treat- ment of traumatic carotid and vertebral artery lesions: results in 234 cases.

AJR Am J Roentgenol 1989; 153(3):577–582 [19] Bouthillier A, van Loveren HR, Keller JT Segments of the internal carotid artery: a new classification Neurosurgery 1996; 38(3):425–432, discussion 432–433

[20] Scott WW, Sharp S, Figueroa SA, et al Clinical and radiological outcomes lowing traumatic grade 3 and 4 vertebral artery injuries: a 10-year

fol-Fig 17.7 Initial treatment guidelines for spinefractures

retrospective analysis from a level I trauma center The Parkland Carotid and

Vertebral Artery Injury Survey J Neurosurg 2015; 122(5):1202–1207

[21] Biffl WL, Moore EE, Offner PJ, Brega KE, Franciose RJ, Burch JM Blunt carotid

arterial injuries: implications of a new grading scale J Trauma 1999; 47

(5):845–853

[22] de Keizer R Carotid-cavernous and orbital arteriovenous fistulas: ocular

fea-tures, diagnostic and hemodynamic considerations in relation to visual

impairment and morbidity Orbit 2003; 22(2):121–142

[23] Lewis AI, Tomsick TA, Tew JM, Jr Management of 100 consecutive direct

car-otid-cavernous fistulas: results of treatment with detachable balloons

Neu-rosurgery 1995; 36(2):239–244, discussion 244–245

[24] Gupta AK, Purkayastha S, Krishnamoorthy T, et al Endovascular treatment of

direct carotid cavernous fistulae: a pictorial review Neuroradiology 2006; 48

(11):831–839

[25] Ellis JA, Goldstein H, Connolly ES, Jr, Meyers PM Carotid-cavernous fistulas.

Neurosurg Focus 2012; 32(5):E9

[26] Scott WW, Sharp S, Figueroa SA, et al Clinical and radiographic outcomes

fol-lowing traumatic Grade 1 and 2 carotid artery injuries: a 10-year

retrospec-tive analysis from a Level I trauma center The Parkland Carotid and Vertebral

Artery Injury Survey J Neurosurg 2015; 122(5):1196–1201

[27] Scott WW, Sharp S, Figueroa SA, Madden CJ, Rickert KL Clinical and

radiolog-ical outcomes following traumatic grade 1 and 2 vertebral artery injuries: a

10-year retrospective analysis from a level 1 trauma center J Neurosurg.

2014; 121(2):450–456

[28] Yoshida K, Melake M, Oishi H, Yamamoto M, Arai H Transvenous

emboliza-tion of dural carotid cavernous fistulas: a series of 44 consecutive patients.

AJNR Am J Neuroradiol 2010; 31(4):651–655

[29] Meyers PM, Halbach VV, Dowd CF, et al Dural carotid cavernous fistula:

definitive endovascular management and long-term follow-up Am J

Oph-thalmol 2002; 134(1):85–92

[30] Rosi Junior J, Figueiredo EG, Rocha EP, Andrade AF, Rasslan S, Teixeira MJ.

Whole-body computerized tomography and concomitant spine and head

injuries: a study of 355 cases Neurosurg Rev 2012; 35(3):437–444,

discus-sion 444–445

[31] Thesleff T, Kataja A, Ohman J, Luoto TM Head injuries and the risk of

concur-rent cervical spine fractures Acta Neurochir (Wien) 2017; 159(5):907–914

[32] Aulino JM, Tutt LK, Kaye JJ, Smith PW, Morris JA, Jr Occipital condyle

frac-tures: clinical presentation and imaging findings in 76 patients Emerg

Radiol 2005; 11(6):342–347

[33] White A, Panjabi M Clinical Biomechanics of the Spine 2nd ed Philadelphia,

PA: J.B Lippincott; 1990

[34] Pang D, Nemzek WR, Zovickian J Atlanto-occipital dislocation–part 2: The

clin-ical use of (occipital) condyle-C1 interval, comparison with other diagnostic

methods, and the manifestation, management, and outcome of atlanto-occipital

dislocation in children Neurosurgery 2007; 61(5):995–1015, discussion 1015

[35] Lehn AC, Lettieri J, Grimley R A case of bilateral lower cranial nerve palsies

after base of skull trauma with complex management issues: case report and

review of the literature Neurologist 2012; 18(3):152–154

[36] Maserati MB, Stephens B, Zohny Z, et al Occipital condyle fractures: clinical decision rule and surgical management J Neurosurg Spine 2009; 11(4):388– 395

[37] DeAngelis AF, Barrowman RA, Harrod R, Nastri AL Review article: cial emergencies: Maxillofacial trauma Emerg Med Australas 2014; 26 (6):530–537

maxillofa-[38] Hadley MN, Dickman CA, Browner CM, Sonntag VK Acute traumatic atlas fractures: management and long term outcome Neurosurgery 1988; 23 (1):31–35

[39] Daniels AH, Arthur M, Esmende SM, Vigneswaran H, Palumbo MA Incidence and cost of treating axis fractures in the United States from 2000 to 2010 Spine 2014; 39(18):1498–1505

[40] Harris JH, Jr, Edeiken-Monroe B, Kopaniky DR A practical classification of acute cervical spine injuries Orthop Clin North Am 1986; 17(1):15–30 [41] Andreshak JL, Dekutoski MB Management of unilateral facet dislocations: a review of the literature Orthopedics 1997; 20(10):917–926

[42] Traynelis VC, Marano GD, Dunker RO, Kaufman HH Traumatic tal dislocation Case report J Neurosurg 1986; 65(6):863–870

atlanto-occipi-[43] Maddox JJ, Rodriguez-Feo JA, III, Maddox GE, Gullung G, McGwin G, Theiss

SM Nonoperative treatment of occipital condyle fractures: an outcomes review of 32 fractures Spine 2012; 37(16):E964–E968

[44] Landells C, Peteghem K Fractures of the atlas: classification, treatment and morbidity Spine 1988; 13(5):450–452

[45] Anderson LD, D’Alonzo RT Fractures of the odontoid process of the axis J Bone Joint Surg Am 1974; 56(8):1663–1674

[46] Effendi B, Roy D, Cornish B, Dussault RG, Laurin CA Fractures of the ring of the axis A classification based on the analysis of 131 cases J Bone Joint Surg

Br 1981; 63-B(3):319–327 [47] Levine AM, Edwards CC The management of traumatic spondylolisthesis of the axis J Bone Joint Surg Am 1985; 67(2):217–226

[48] Vaccaro AR, Hulbert RJ, Patel AA, et al Spine Trauma Study Group The ial cervical spine injury classification system: a novel approach to recognize the importance of morphology, neurology, and integrity of the disco-liga- mentous complex Spine 2007; 32(21):2365–2374

subax-[49] Horn EM, Feiz-Erfan I, Lekovic GP, Dickman CA, Sonntag VK, Theodore N vivors of occipitoatlantal dislocation injuries: imaging and clinical correlates.

Sur-J Neurosurg Spine 2007; 6(2):113–120 [50] Ryken TC, Aarabi B, Dhall SS, et al Management of isolated fractures of the atlas in adults Neurosurgery 2013; 72 Suppl 2:127–131

[51] Delcourt T, Bégué T, Saintyves G, Mebtouche N, Cottin P Management of upper cervical spine fractures in elderly patients: current trends and out- comes Injury 2015; 46 Suppl 1:S24–S27

[52] Ryken TC, Hadley MN, Aarabi B, et al Management of isolated fractures of the axis in adults Neurosurgery 2013; 72 Suppl 2:132–150

[53] Gelb DE, Aarabi B, Dhall SS, et al Treatment of subaxial cervical spinal ries Neurosurgery 2013; 72 Suppl 2:187–194

inju-18 Pediatric Brain Injury

Andrew Vivas, Aysha Alsahlawi, Nir Shimony, and George Jallo

Abstract

Pediatric traumatic brain injury is the leading cause of death

among children and is a significant cause for morbidity in the

United States and around the globe, with significant burden on

the families and society Yet, the majority of the injuries are

mild without any need for neurosurgical intervention Brain

injury biomechanism is a complex process derived from

pri-mary injury and a secondary injury related to brain vasculature,

parenchymal metabolic demands, and oxygenation Hence, the

injury to the nervous system is gradual with first very short but

significant impact of the intracranial components with

subse-quent possible secondary brain injury that potentially can be

prevented and treated Different injuries can comprise the

pediatric brain including skull fractures and intracranial

bleed-ing, with some age-specific more common injuries The

diag-nostic tools are mainly clinical assessment and imaging

modalities that sometime need to be repeated in order to better

assess the impact severity The treatment relies on medical

measurement to immediately treat the primary injury if needed

and prevent the secondary injury mechanism Careful attention

to control the influence of systemic factors including hypoxia,

hypotension, intracranial pressure, cerebral perfusion pressure,

and the use of anticonvulsants can help prevent secondary

injury In some cases, intractable intracranial hypertension

evolved and the treatment is done in a tiered fashion with

sur-gery reserved as final resource In recent years, more resources

are being invested in prevention of head injuries in children,

including legislation and education of kids and parents

Keywords:brain injury, skull fracture, hematoma, intracranial

pressure, seizure, prevention

18.1 Introduction

Pediatric traumatic brain injury (TBI) is a significant cause of

morbidity and mortality throughout the developed world

Severe brain injuries often leave children with significant

life-long deficits While the vast majority of head injuries are

described as “mild,” these injuries may lead to subtle, profound

learning difficulties and behavioral problems that will have a

lifelong impact on the child The financial and societal costs of

childhood traumatic injuries on the families, health care

sys-tem, and society as a whole are astronomical.1In total, mild TBI

in pediatric patients was reported to cost $695 million in the

first 3 months after injury.2

18.2 Epidemiology

Traumatic injuries are the leading cause of death in children,

exceeding all other causes combined in those younger than 18

years In a recent estimate by the World Health Organization,

TBI is expected to be the major cause of death and disability by

2020 with 10 million people affected annually.3Head injuries

are quite common and are responsible for a significant

proportion of illnesses affecting children in their early years oflife (▶Table 18.1) Approximately 475,000 children youngerthan 14 years sustain a TBI every year.4Recent years have seen

an increasing incidence, with more than 50% increase in TBIfrom 2008 to 2010 Most of these are evaluated and sent home(or never seek medical attention); however, pediatric TBIresulted in 80.8 admissions and 6.2 deaths per 100,000 in 2010alone Children younger than 4 years have the highest rate ofemergency room visits, while adolescents have a higher rate ofadmission The mortality rates from TBI are highest in childrenyounger than 4 years and in 15- to 19-year-olds.5

While 55% of TBIs in children younger than 14 years arecaused by fall, the precise mechanisms of injury leading to TBIvary with age Inflicted injuries remain the leading cause of TBI-related hospitalization and death in children aged 2 years andyounger The median age of inflicted TBI is approximately 3months.6,7 The precise incidence of inflicted injuries remainsuncertain, as 2.6% of maternal caregivers admit to shaking a child

at some stage as a method for enforcing discipline In general,children who suffer nonaccidental trauma are five times morelikely to die than children who suffer accidental head injuries.8

With increasing age, the incidence of inflicted injuriesdeclines as falls and transportation-related accidents become

an increasing problem A report from California found that 21

of 100,000 child injuries occurred as occupants of a motorvehicle; 28 of 100,000 were pedestrians struck by motorvehicles.9TBIs result in direct medical and indirect costs related

to lost productivity and potential, which may reach an mated $60 billion in the United States.10

esti-The majority of TBIs in children are mild esti-The annual dence is likely to be greater than 200 per 100,000 children

inci-Although there is no standard definition of mild TBI, the ity of studies refer to the Glasgow Coma Scale (GCS) score of 13

major-to 15 or an injury major-to the head with a posttraumatic amnesia ing less than 30 minutes While less than 1% of mild TBIs requireneurosurgical intervention, the subsequent cognitive and behav-ioral symptoms may be significant The consequences of mildTBI on the developing child are poorly understood, incompletelycharacterized, and when present may take time to resolve

last-18.3 Classification of Pediatric Head Injury

Injuries to the central nervous system are typically ized as either primary or secondary injuries.11 The primaryinjury represents the immediate effects of impact andTable 18.1 Epidemiology of pediatric traumatic brain injury (TBI)

character-● TBIs are common in children, estimated at 200/100,000 per year

Most are mild

● Mortality is highest in infants and teens

● Most children who die from a traumatic injury die with or because oftheir brain injury

dissipation of energy within the neuraxis These injuries

include direct neuronal and glial disruption, laceration of the

brain, shearing of axons, and vascular injuries While the

pri-mary injury is complete in the matter of a few milliseconds,

there is strong evidence that a whole host of secondary factors

can amplify the ultimate extent of neurological injury, leading

to a delayed deterioration days after injury These include

hypo-xia, hypotension, systemic trauma, fluid and electrolyte

distur-bances, infections, etc (▶Table 18.2) This “secondary injury” is

thought to be caused by changes to the extracellular

environ-ment that ultimately lead to influxes of calcium and sodium

into neuronal and glial cells, resulting in apoptosis and neuronal

death Though the primary effects of injury cannot be reversed,

the control of systemic factors can theoretically reduce the

extent of further injury Understanding the effect that focal

injuries have on cellular processes may one day lead to

neuro-protective treatments.12

Primary pediatric TBI can be further subcategorized as either

focal or diffuse injuries Focal injuries are localized

anatomi-cally, clinianatomi-cally, or radiographianatomi-cally, and include contusions,

lac-erations, and intraparenchymal hematomas (▶Table 18.3)

These injuries may lead to mass effect, resulting in brain shift

with secondary consequences Direct or “coup” injuries most

often occur near bony prominences in the cranial vault such as

the sphenoidal ridge, temporal base, orbital roof, rigid falx, or

underlying fracture sites Contrecoup injuries occur more quently in older children and are the result of the brain strikingthe skull opposite the point of impact As opposed to focal TBI,diffuse TBI results in multilobar damage and may have worseclinical outcomes Recently, the coding and classification ofpediatric TBI has been updated in an effort to better define andgroup these injuries.13

fre-18.4 Intracranial Pathologies 18.4.1 Extradural Hematoma

Extradural hematoma (epidural hematoma) is a life-threateningcondition in pediatric patients The majority of these hemato-mas are associated with an overlying skull fracture, and arefound in the temporal, parietal, and temporoparietal regions(▶Fig 18.1) Posterior fossa epidural hematomas comprise 10%

of all epidural hematomas Contusions may also be associatedwith extradural hematomas, and may be an independent riskfactor for the development of epilepsy.14,15The most commoncause of extradural hematomas is falls

While small, supratentorial epidural hematomas may beobserved if the patient is fully conscious, the majority of poste-rior fossa extra-axial hematomas are evacuated Small epiduralhematomas may require no intervention; however, close obser-vation and watchful waiting is critical Hematomas may becomequite large, especially in young children and infants, and canoccasionally result in anemia It is vital to have blood available inthe operating room for emergent transfusion, as young infantsmay go into shock due to loss of blood into the epidural space

18.4.2 Subdural Hematoma

Subdural hematomas may also be located in the supratentorialspace or the posterior fossa Supratentorial subdural hemato-mas are typically found near the convexity of the skull, and maycause substantial midline shifts They may be associated withcerebral contusion or laceration, and can require evacuationand removal of devitalized brain Posterior fossa subdural hem-atomas are usually adjacent to the tentorium, and often resolvespontaneously

Subdural hematomas are less common in children than inadults, and when present are usually resultant of high-velocityinjuries or nonaccidental trauma.16Nonaccidental trauma is themost common cause of subdural bleeding in children youngerthan 1 year, and as many as 80% of “shaken babies” will haveevidence of subdural hemorrhages at the time of presentation.17

Table 18.2 Classification of Pediatric Head Injury

●Diffuse

●Diffuse axonal injury

●Diffuse brain swelling

Table 18.3 Pediatric focal injuries and hemorrhage

● Epidural hematomas are common in children and many do not requireevacuation On occasion, these hematomas may become very largeand result in anemia, potentially requiring transfusion prior to orduring surgery

● Subdural hematomas are less common in children than adults, and areoften related to high-velocity injuries or abusive head injury

● Massive diffuse hemispheric brain swelling in children can occurassociated with relatively small subdural hemorrhages, abusive headinjury, or the second impact syndrome

18.4.3 Intracerebral Hematoma

Intracerebral hematomas are frequently caused by acceleration/

deceleration injuries and occur most commonly in the

basifron-tal and basitemporal regions Some of these may be in the deep

parenchyma of the brain The majority can be treated tively; however, those with significant mass effect or shift mayrequire evacuation if clinically indicated (▶Fig 18.2)

conserva-18.4.4 Diffuse Axonal Injury

Diffuse axonal injury (DAI) is characterized by disturbance inneuronal function despite admission of computed tomography(CT) that is normal or with minimal abnormality Diffuse inju-ries have a wide spectrum of severity and occur as a result ofenergy distribution throughout the brain DAI is thought to rep-resent a shearing injury at the gray-white matter junction, cor-pus callosum, and brain stem that results in the disconnection

or disruption of axonal tracts (▶Fig 18.3).18 These injuriesresult from angular acceleration/deceleration, with the extent

of injury proportional to the change in the angular velocity ofthe brain The clinical presentation depends on the extent ofaxonal dysfunction, and can range from a minor concussion toprofound and prolonged impairment of neurological function

Patients may demonstrate posturing, abnormal gaze palsy,pupillary changes, and autonomic disturbances

CT findings in DAI may be relatively modest.19 It is morereadily characterized on magnetic resonance imaging (MRI),which has become the modality of choice for assessingsuspected DAI Advanced sequences such as susceptibility-weighted sequences or gradient echo sequences that are sensi-tive to blood products may demonstrate multiple small regions

of susceptibility artifact at the gray–white matter junction, pus callosum, or brain stem DAI is a clinical diagnosis, however,and the absence of radiographic changes does not necessarilyexclude the diagnosis.20,21 In the study by Skandsen et al in

cor-2010, DAI was detected in half the cases of patients with sions and lacerations, suggesting many TBIs have some degree

contu-of concomitant axonal injury.22Children with diffuse injuriestend to have a worse prognosis than adults.23

18.4.5 Diffuse Brain Swelling

Diffuse brain swelling is a reactive posttraumatic phenomenoncharacterized by raised intracranial pressure (ICP) More

Fig 18.2 (a,b) Axial computed tomography (CT)images of a toddler who fell climbing out of thecrib on to a tile floor Note the basal frontalhemorrhagic contusion and intracerebral hema-toma in the left frontal lobe and the smallcontrecoup contusion at the opposite pterion

She did not have any evidence of coagulopathyand her contusion resolved without the need forevacuation of the hematoma

Fig 18.1 This axial computed tomography (CT) image of a child shows

a large epidural hematoma with acute hydrocephalus caused by a fall

from the trunk of a moving vehicle This child’s fracture crossed the

transverse sinus and therefore requires a craniotomy both above and

below the sinus to evacuate the clot safely and control the transverse

sinus injury

common in children, this reactive increase in ICP is thought to

be due to an increase in cerebral blood volume and loss of

cere-bral autoregulation Bruce et al first described this phenomenon

in 1981, demonstrating that delayed deterioration after a lucid

interval was associated with a global increase in cerebral blood

flow, vascular engorgement, and an increase in cerebral blood

volume.24Muizelaar et al later showed that 41% of children with

severe TBI had impaired autoregulatory capacity.25While other

authors have disputed these findings26; recent studies by

Vavi-lala et al seem to reaffirm the idea that there is a loss of

autore-gulation in children, even in the absence of a focal pathology.27

This may explain why children with diffuse brain swelling tend

to have a worse outcome than adults Compared to adults,

chil-dren are known to have a more fragile blood–brain barrier

(BBB) with higher brain water content This may contribute to

the rapid development of brain swelling as a secondary insult.28

The exact pathophysiology of this entity is poorly understood

and may be driven by hyponatremia, hyperemia, hypoxia,

ischemia, loss of blood flow autoregulation, or hyperglycolysis

Whatever the underlying cause, it can be a major cause of

seri-ous deterioration after a minor head injury Aggressive control

of ICP results in a good neurological outcome

18.4.6 Skull Fractures

Skull fractures account for 10 to 30% of pediatric head injuries

in the United States.29As toddlers and infants learn to stand,

walk, and explore their surroundings, low-impact falls and

associated skull fractures ensue In fact, the majority of linear

fractures in young children are caused by falls Although CT

scanning is the test of choice to identify intracranial

hemor-rhage and fracture, occasionally axially oriented fractures may

be missed These can be detected on a careful inspection of the

CT scan scout image Three-dimensional (3D) reconstruction

may also be helpful in identifying suspected skull fractures

Most fractures are not associated with intracranial bleeding

and have a relatively benign prognosis Uncomplicated linear

fractures will generally heal without intervention, and may not

require admission to the hospital if the child has a normal

neuro-logical examination, no intracranial injury, and can be monitored

at home for signs of neurological deterioration (▶Table 18.4) All

other children are best monitored in the hospital, and specificcare should be given to ruling out the possibility of childabuse in young infants and toddlers Fractures with an asso-ciated dural laceration may require repair or exploration toprevent the occurrence of a leptomeningeal cyst Fracturesthat cross venous sinuses may be associated with eitherextradural or subdural hemorrhages and require special cau-tion if repaired.30

18.4.7 Depressed Skull Fractures

Depressed skull fractures are relatively common in children andaccount for approximately 10% of all skull fractures.31 Mostdepressed fractures are small and remodel over time under theinfluence of the underlying developing brain; however, somemay be large and require surgical intervention Closeddepressed fractures usually do not require any surgical inter-vention unless associated with a suspected dural laceration orfor the purposes of cosmesis (▶Fig 18.4)

A unique variant of depressed fractures seen in infants is theping-pong or pond fracture These are usually a consequence ofmalpositioned forceps during delivery or short-distance falls.These fractures are easily repaired by placing a small burr hole

at the edge of the fracture and elevating the bone from beneaththe defect with a Penfield or periosteal elevator Smaller ping-pong fractures may not require surgical intervention, and willremodel over time (▶Fig 18.5)

Compound depressed fractures with an overlying scalp ation may require irrigation and debridement if the wound isgrossly contaminated or a dural laceration is suspected These

lacer-Fig 18.3 Axial fluid attenuated inversion ery magnetic resonance image of a child whosuffered a severe traumatic brain injury in amotor vehicle crash Note the areas of brightsignal in the corpus callosum and at the gray–white matter junction

recov-Table 18.4 Pediatric skull fractures

● Linear skull fractures are common findings after falls in children.Children with uncomplicated skull fractures that can be clinically andreliably observed at home do not require hospital admission

● Many minor depressed fractures, particularly ping-pong-type fractures

in infants, do not require operative intervention and will remodelspontaneously

● Fractures with a suspected dural laceration must be explored to avoidthe subsequent development of a leptomeningeal cyst

fractures may be returned to the site after debridement if

con-tamination is limited, obviating the need for a future

cranio-plasty Frontal depressed skull fractures that violate the

paranasal sinuses are associated with complications such as

meningitis, chronic sinusitis, mucocele cyst, and cerebrospinal

fluid (CSF) leak that may require surgical intervention.32

Growing Skull Fractures

A growing skull fracture, or leptomeningeal cyst, is a rare

com-plication usually seen with skull fractures in young children.33,

34Fractures with an associated underlying dural laceration and

brain injury are the essential precursor of a growing skull

frac-ture (▶Fig 18.6) The fracture edges are often split by the

energy of the injury, and the pulsations of the brain allow tissue

to herniate through the dural tear Over time, the fractured

edges are further eroded, becoming wide and smooth Driven

by the growing cortex and/or the normal cerebral pulsation, the

brain herniates through the bony and dural defects, widening

both over time (▶Fig 18.7) Brain pulsations along the edges of

the dura and bone can cause progressive injury to adjacent

cor-tex The dural defect often becomes much wider than the bony

defect over time—an important consideration if surgical repair

is attempted

These fractures are often located in the parietal region, butmay be present in the occipital region, posterior fossa, or theroof of the orbit Children present with a focal, pulsatile swel-ling consisting of CSF and the herniating brain (i.e., the leptome-ningeal cyst), as well as progressive neurological deficit andseizures The diagnosis can be easily confirmed with a CT scan

or MRI The treatment consists of a wide craniotomy, duralrepair after minimal resection of gliotic, herniated brain, andcranioplasty A cranioplasty should be performed with autolo-gous bone whenever possible to allow for continued skullgrowth and prosthetic materials should always be avoided

Associated hydrocephalus may require CSF diversion, but CSFshunting should never be used as a primary method of treat-ment for a growing skull fracture

18.4.8 Basilar Skull Fractures

Basilar skull fractures account for 15 to 19% of skull fractures inchildren, and are associated with CSF leak, meningitis, andrarely with vascular injury.35If the fracture is associated with a

Fig 18.4 (a,b) Small depressed fracture in a childcaused by an errant golf club as seen on axialcomputed tomography (CT), soft tissue, andbone windows The overlying laceration wascleansed and closed in the emergency depart-ment and the fracture was above the hairline

This fracture will remodel without the need forsurgical intervention

Fig 18.5 (a) Axial computed tomography image of a “ping-pong”-type depressed fracture noted after a cesarean section delivery (b,c) The child was

observed and the fracture remodeled; at 3 months of age, the visible cosmetic deformity had resolved completely

dural laceration, a CSF may egress into the nasopharynx or

mid-dle ear, leading to a CSF leak These may occur despite the fact

that the frontal and sphenoid sinuses are not typically

pneuma-tized in children younger than 5 years.36Leaks will stop

sponta-neously in the vast majority of cases without surgical

intervention.37 The head should be kept elevated and any

straining or vigorous manipulation of the ear or nose should beavoided Examination of the middle ear and a hearing evalua-tion should be pursued in a delayed fashion once the CSF leakhas abated In rare instances where CSF leaks persist, treatmentmay entail repair of the dural laceration or temporary CSFdiversion There is no role for prophylactic antibiotics to pre-vent meningitis, as their use may increase the risk of unusual ordrug-resistant organisms Basilar skull fractures (▶Fig 18.8)may be associated with injury to the middle ear, carotid artery,venous sinuses, and cranial nerves as they exit the foramina

18.4.9 Nonaccidental Trauma

Nonaccidental trauma comprises a sizable source of morbidityand mortality in pediatric patients, and is recognized as a majorhealth care problem In 2012, an estimated 1,640 children (2.2per 100,000) died as a result of abuse or neglect in the UnitedStates alone.38The true incidence of child abuse may be under-estimated by government studies Outside reports have esti-mated that the lifetime rate of maltreatment in the UnitedStates may approach one in four children.39The total lifetimeeconomic burden from child maltreatment in the United States

is thought to be approximately $100 billion.40

As it is defined by the mechanism of injury, nonaccidentaltrauma can result in a combination of the above-listed patho-logies They are frequently associated with thin subduralhemorrhages, DAI, and diffuse swelling Infants appear to beparticularly susceptible to diffuse swelling (malignant edema),and 70% of child fatalities occur in children younger than 3years Children younger than 1 year have the highest rate of vic-timization, at 21.9 per 1,000 children Most victims are younger

Fig 18.6 Complex stellate fractures as seen on this lateral plain

radiograph are commonly associated with an underlying dural and

brain injury

Fig 18.7 Axial, soft-tissue, and bone window computed tomography (CT) images of an infant who suffered an inflicted head injury She wasdischarged into the foster care system and did not return for several months after the injury (a,b) Upon her return, she was noted to have a softswelling of the right scalp and a left hemiparesis Her CT scan, scout, brain, and bone window images revealed widening of her parietal fracture, boneerosion, and underlying encephalomalacia (c–e) Axial and coronal CT images of a child who fell from a shopping cart and suffered a longitudinalfracture of the right petrous bone (f–g)