Background

The brain is surrounded by cerebrospinal fluid (CSF), enclosed in meningeal covering, and
protected inside the skull. Furthermore, the fascia and muscles of the scalp provide additional
cushioning to the brain. Test results have shown that 10 times more force is required to
fracture a cadaveric skull with overlaying scalp than the one without.[1] Although these layers
play a protective role, meningeal attachments to the interior of the skull may limit the
movement of the brain, transmitting shearing forces on the brain.
A transverse temporal bone fracture is shown in the image below.

Transverse temporal bone fracture (courtesy of Adam

Flanders, MD, Thomas Jefferson University, Philadelphia, Pennsylvania)
CSF plays a major role in coup and countercoup injuries to the brain. A blow to a stationary
but moveable head causes acceleration, and the brain floating in CSF lags behind, sustaining
an injury directly underneath the point of impact (coup injury). When a moving head hits the
floor, sudden deceleration results in an injury to the brain on the opposite side (countercoup
injury).

Anatomy of fracture
The causative forces and fracture pattern, type, extent, and position are important in assessing
the sustained injury. The skull is thickened at the glabella, external occipital protuberance,
mastoid processes, and external angular process and is joined by 3 arches on either side. The
skull vault is composed of cancellous bone (diplo) sandwiched between 2 tablets, the lamina
externa (1.5 mm), and the lamina interna (0.5 mm). The diplo does not form where the skull
is covered with muscles, leaving the vault thin and prone to fracture.
The skull is prone to fracture at certain anatomic sites that include the thin squamous
temporal and parietal bones over the temples and the sphenoid sinus, the foramen magnum,
the petrous temporal ridge, and the inner parts of the sphenoid wings at the skull base. The
middle cranial fossa is the weakest, with thin bones and multiple foramina. Other places
prone to fracture include the cribriform plate and the roof of orbits in the anterior cranial
fossa and the areas between the mastoid and dural sinuses in the posterior cranial fossa.

History of the Procedure

Skull fracture is described in Edwin Smith's papyrus, the oldest known surgical paper.[2] The
papyrus describes a conservative and expectant approach to skull trauma, with better results

compared with a more aggressive and less favorable approach described in Hippocratic
medicine.[3]
An extensive discussion of skull fractures and their management is available in the eleventh
century manuscript, "Al-Qanun Fil-Tibb" by Ibn-Sina (Avicenna). This book was a
predecessor to the modern medicine literature.[4]
The 15th century management of pediatric skull fractures is illustrated by a Turkish physician
of the Ottoman Empire, Serefeddin Sabuncuolu (1385-1468) in his textbook "Cerrahiyyetu'l
Haniyye" (Imperial Surgery).[5]
Charles Bell first described occipital condylar fracture in 1817 based on an autopsy finding.[6]
The same fracture was described for the first time as a radiograph finding in 1962 and by
computed tomography (CT) in 1983.[7, 8]

Problem
Fractures of the skull can be classified as linear or depressed. Linear fractures are either vault
fractures or skull base fractures.[9] Vault fractures and depressed fractures can be either closed
or open (clean or dirty/contaminated).
Skull fractures are classified in the image below.

Classification of skull fractures

Linear skull fracture

Linear fracture results from low-energy blunt trauma over a wide surface area of the skull. It
runs through the entire thickness of the bone and, by itself, is of little significance except
when it runs through a vascular channel, venous sinus groove, or a suture. In these situations,
it may cause epidural hematoma, venous sinus thrombosis and occlusion, and sutural
diastasis, respectively. Differences between sutures and fractures are summarized in Table 1.
Table 1. Differences Between Skull Fractures and Sutures (Open Table in a new window)

Fractures
Greater than 3 mm in width
Widest at the center and narrow at the ends
Runs through both the outer and the inner
lamina of bone, hence appears darker

Sutures
Less than 2 mm in width
Same width throughout
Lighter on x-rays compared
with fracture lines

Usually over temporoparietal area

Usually runs in a straight line
Angular turns

At specific anatomic sites

Does not run in a straight line
Curvaceous

Basilar skull fracture

In essence, a basilar fracture is a linear fracture at the base of the skull. It is usually associated
with a dural tear and is found at specific points on the skull base.
Temporal fracture
Temporal bone fracture is encountered in 75% of all skull base fractures. The 3 subtypes of
temporal fractures are longitudinal, transverse, and mixed.[10] A transverse temporal bone
fracture and a longitudinal temporal bone fracture are shown below.

Transverse temporal bone fracture (courtesy of Adam

Flanders, MD, Thomas Jefferson University, Philadelphia, Pennsylvania)

Longitudinal temporal bone fracture (courtesy of Adam

Flanders, MD, Thomas Jefferson University, Philadelphia, Pennsylvania)
Longitudinal fracture occurs in the temporoparietal region and involves the squamous portion
of the temporal bone, the superior wall of the external auditory canal, and the tegmen
tympani. These fractures may run either anterior or posterior to the cochlea and labyrinthine
capsule, ending in the middle cranial fossa near the foramen spinosum or in the mastoid air
cells, respectively. Longitudinal fracture is the most common of the 3 subtypes (70-90%).
Transverse fractures begin at the foramen magnum and extend through the cochlea and
labyrinth, ending in the middle cranial fossa (5-30%).
Mixed fractures have elements of both longitudinal and transverse fractures.
Yet another classification system of temporal bone fractures has been proposed. This system
divides temporal bone fractures into petrous and nonpetrous fractures; the latter includes

fractures that involve mastoid air cells. These fractures do not present with cranial nerve
deficits.[11]
Occipital condylar fracture
Occipital condylar fracture results from a high-energy blunt trauma with axial compression,
lateral bending, or rotational injury to the alar ligament. These fractures are subdivided into 3
types based on the morphology and mechanism of injury.[12] An alternative classification
divides these fractures into displaced and stable, ie, with and without ligamentous injury.[13]
Type I fracture is secondary to axial compression resulting in comminution of the occipital
condyle. This is a stable injury.
Type II fracture results from a direct blow, and, despite being a more extensive basioccipital
fracture, type II fracture is classified as stable because of the preserved alar ligament and
tectorial membrane.
Type III fracture is an avulsion injury as a result of forced rotation and lateral bending. This
is potentially an unstable fracture.
Clivus fractures
Fractures of the clivus are described as a result of high-energy impact sustained in motor
vehicle accidents. Longitudinal, transverse, and oblique types have been described in the
literature. A longitudinal fracture carries the worst prognosis, especially when it involves the
vertebrobasilar system. Cranial nerves VI and VII deficits are usually coined with this
fracture type.[14]

Depressed skull fracture

Depressed skull fractures, as shown in the image below, result from a high-energy direct
blow to a small surface area of the skull with a blunt object such as a baseball bat.
Comminution of fragments starts from the point of maximum impact and spreads
centrifugally. Most of the depressed fractures are over the frontoparietal region because the
bone is thin and the specific location is prone to an assailant's attack. A free piece of bone
should be depressed greater than the adjacent inner table of the skull to be of clinical
significance and requiring elevation.

Depressed skull fracture (courtesy of Adam Flanders, MD,

Thomas Jefferson University, Philadelphia, Pennsylvania)

A depressed fracture may be open or closed. Open fractures, by definition, have either a skin
laceration over the fracture or the fracture runs through the paranasal sinuses and the middle
ear structures, resulting in communication between the external environment and the cranial
cavity. Open fractures may be clean or contaminated/dirty.

Epidemiology
Frequency
Simple linear fracture is by far the most common type of fracture, especially in children
younger than 5 years. Temporal bone fractures represent 15-48% of all skull fractures.
Basilar skull fractures represent 19-21% of all skull fractures. Depressed fractures are
frontoparietal (75%), temporal (10%), occipital (5%), and other (10%). Most of the depressed
fractures are open fractures (75-90%).

Etiology
In newborns, "ping-pong" depressed fractures are secondary to the baby's head impinging
against the mother's sacral promontory during uterine contractions.[15] The use of forceps also
may cause injury to the skull, but this is rare.
Skull fractures in infants originate from neglect, fall, or abuse. Most of the fractures seen in
children are a result of falls and bicycle accidents. In adults, fractures typically occur from
motor vehicle accidents or violence.

Presentation
Linear skull fracture
Most patients with linear skull fractures are asymptomatic and present without loss of
consciousness. Swelling occurs at the site of impact, and the skin may or may not be
breached.

Basilar skull fracture

Patients with fractures of the petrous temporal bone present with CSF otorrhea and bruising
over the mastoids, ie, Battle sign. Presentation with anterior cranial fossa fractures is with
CSF rhinorrhea and bruising around the eyes, ie, "raccoon eyes." Loss of consciousness and
Glasgow Coma Score may vary depending on an associated intracranial pathologic condition.
Longitudinal temporal bone fractures result in ossicular chain disruption and conductive
deafness of greater than 30 dB that lasts longer than 6-7 weeks. Temporary deafness that
resolves in less than 3 weeks is due to hemotympanum and mucosal edema in the middle ear
fossa. Facial palsy, nystagmus, and facial numbness are secondary to involvement of the VII,
VI, and V cranial nerves, respectively. Transverse temporal bone fractures involve the VIII
cranial nerve and the labyrinth, resulting in nystagmus, ataxia, and permanent neural hearing
loss.

Occipital condylar fracture is a very rare and serious injury.[16] Most of the patients with
occipital condylar fracture, especially with type III, are in a coma and have other associated
cervical spinal injuries. These patients may also present with other lower cranial nerve
injuries and hemiplegia or quadriplegia.
Vernet syndrome or jugular foramen syndrome is involvement of the IX, X, and XI cranial
nerves with the fracture. Patients present with difficulty in phonation and aspiration and
ipsilateral motor paralysis of the vocal cord, soft palate (curtain sign), superior pharyngeal
constrictor, sternocleidomastoid, and trapezius.
Collet-Sicard syndrome is occipital condylar fracture with IX, X, XI, and XII cranial nerve
involvement.[17, 18, 19]

Depressed skull fracture

Approximately 25% of patients with depressed skull fracture do not report loss of
consciousness, and another 25% lose consciousness for less than an hour. The presentation
may vary depending on other associated intracranial injuries, such as epidural hematoma,
dural tears, and seizures.
http://emedicine.medscape.com/article/248108-overview#showall

Skull fractures
Step-by-step diagnostic approach
Key risk factors for skull fractures include male gender, [3] [5] a fall, [2] [6] a motor vehicle
accident (MVA), [1] [2] [3] [6] assault, [9] and gunshot injury. However, skull fractures can
be found even in patients with minor head trauma, [1] and may feature in 2% to 20% of all
paediatric head trauma presenting to emergency departments, and in 5.8% of minor adult
head trauma. [5] Therefore, in the presence of even minor head injury, a high level of
suspicion must be maintained. With the exception of basilar skull fractures, isolated skull
fractures rarely manifest any clinical signs. In one study, only 2.1% of patients with fractures
had clinical signs of injury; and signs, when present, were non-specific. [5]
It is very important to identify patients with associated intracranial injury early in order to
institute emergency management. The patient's neurological status should be assessed at
initial presentation and subsequently monitored to help guide management decisions. CT scan
of the head and brain should be considered in high-risk patients or those with deteriorating
neurological status. [23] [24] [25]

History
Patients may report a history of trauma. This may include a fall (especially from a height), [2]
[6] MVA, [1] [2] [3] [6] or assault. [9] The trauma may be relatively minor. [5]
Presenting complaints may be due either to the skull fracture itself or to associated injury.

Basilar fractures can also affect cranial nerves resulting in hearing deficit, facial paralysis
(VII) or numbness (V), and nystagmus. Facial (VII) nerve injury may cause sensorineural
hearing loss. Conductive hearing loss may also present early (<3 weeks) because of
haemotympanum with temporal bone fractures, or later (>6 weeks) with longitudinal
temporal bone fracture with disruption of ossicular chain.
Less-specific features include cranial pain and swelling, and patients may complain of
headache and/or nausea. They may report loss of consciousness, which may be related to
associated intracranial pathology rather than to fracture itself.
In children, any history of previous hospital attendance for non-accidental injury should be
considered. This and any clinical signs and symptoms inconsistent with history (e.g.,
unexplained bruising, faltering growth for age) should prompt the physicians to consider
child abuse as an underlying aetiology.

Cranial examination
The skull should be manually examined for bony deformity. Laceration (or wound) to
skin/soft tissue with visible exposed fractured bone or bone fragments is suggestive of a skull
fracture. However, palpable changes in the bony cortex contour (step-offs) or palpable
fracture fragments are rare.
The majority of patients present either with no evidence of injury or with non-specific
evidence of trauma, such as soft-tissue swelling, haematomas, crepitus, lacerations, and
tenderness. Altered mental status and loss of consciousness are related to underlying
associated intracranial injury and are rare in isolated skull fractures (present in 25% of
depressed fractures). The presence of cranial haematomas is more suggestive of a skull
fracture in children than in adults. Unexplained dental injury and/or the presence of torn
lingual or labial frenae should prompt consideration of child abuse.
Basilar skull fractures often have specific clinical features. Blood pooling from these
fractures can result in ecchymosis over the mastoid area (e.g., Battle's sign); periorbital
ecchymosis (raccoon eyes), particularly if unilateral; and bloody otorrhoea. CSF leakage can
result in CSF rhinorrhoea or otorrhoea. The positive predictive value in detecting a basilar
skull fracture is 85% for a unilateral raccoon eye, 66% for the Battle's sign, and 46% for
bloody otorrhoea. [26] Furthermore, these signs may assist in localisation of the basilar
fracture: Battle's sign and otorrhoea are most often associated with fractures of the petrous
portion of the temporal bone; periorbital ecchymosis and CSF rhinorrhoea are more often
associated with fractures of the anterior cranial fossa. [26] There are no data to support the
use of the "halo" sign, where CSF may be distinguished from blood/mucus by the formation
of a "halo" when fluid is deposited on filter paper, as a specific or sensitive marker for CSF
leakage. [27]

Neurological examination
The patient's neurological status should be assessed at initial presentation and subsequently
monitored to help guide management decisions. The Glasgow Coma Scale (GCS) is
commonly used to assess any associated traumatic brain injury. [28] It also acts as a guide in
assessing the need for CT imaging. [24] [25]

Pupils should be examined for size, symmetry, direct/consensual light reflexes, and duration
of dilation/fixation. Abnormal pupillary reflexes can suggest herniation or brainstem injury.
GCS has 3 components: best eye response (E), best verbal response (V), and best motor
response (M).

Eye opening: spontaneous (4 points); on verbal stimulation (3 points); on painful

stimulation (2 points); none (1 point)
Verbal response: orientated, fluent, coherent (5 points); disorientated, confused (4
points); incoherent (3 points); incomprehensible (2 points); none (1 point)
Motor response: obeys commands (6 points); localises to stimulus (5 points);
withdraws to stimulus (4 points); decorticate or flexor posturing (3 points);
decerebrate or extensor posturing (2 points); none (1 point).

The total GCS score is the sum of points from eye opening, verbal response, and motor
response scores (ranging from 3 to 15 points):

GCS of 13 to 15 is associated with mild brain injury

GCS of 9 to 12 is associated with moderate brain injury

GCS of <8 is associated with severe brain injury.

CT scan head and brain

CT remains the imaging modality of choice and is superior to MRI for detecting skull
fracture in both paediatric and adult patients. [29] All patients with features suggestive of a
skull fracture (e.g., Battle's sign, periorbital ecchymoses, rhinorrhoea, or otorrhoea) should
have cranial CT. Basilar skull fractures are the most difficult to detect; CT scans should be
performed with thin cuts and should include three-dimensional reconstruction of some type.
[30] A study of 3 different reconstructive techniques revealed the best sensitivity with highresolution multiplanar reformations (HRMPR), which are currently the standard of care, in
combination with maximum intensity projection (MIP) reconstructions. [31] MIP
reconstructions increase detection rate by 18% and can detect different types of fractures
compared with HRMPR. [32] Yield of fracture detection is increased if more than one
radiologist reviews the images. [31]
Other adjuncts to conventional CT include use of intrathecal contrast to localise CSF leak
source and CT angiography if there is any suspicion for vascular injury, such as when the
fracture involves the carotid canal or overlies a vessel (e.g., middle meningeal artery, sagittal
sinus).
However, as skull fractures often present with no clinical symptoms or signs on physical
examination, but are significant risk factors for intracranial pathology, the question of whom
to scan is very important. One large study of several head trauma guidelines for imaging
found that increased sensitivity for detecting pathology was also associated with a significant
number of unnecessary CT scans. [5] Of these, the best guidelines for the highest sensitivity
and specificity for traumatic findings and neurosurgical intervention come from the National
Institute for Health and Care Excellence (NICE UK) criteria. [23] These guidelines
recommend that CT scanning should be performed in the following situations:

Any patient with an initial GCS <13

Any patient with a GCS <15 after 2 hours of observation
Any patient with the following: suspected open or depressed skull fracture; any sign
of basilar skull fracture (e.g., haemotympanum, raccoon eyes, CSF leakage from ear
or nose, Battle's sign); post-traumatic seizure; focal neurological deficit; or repeated
emesis
For both adults and children on warfarin who have sustained a head injury and who
have no other indications for a CT head scan, a CT scan of the brain should be
performed within 8 hours of injury
For children, a CT head scan should be performed for: suspicion of non-accidental
injury; a GCS <14 (or a GCS <15 for children aged under 1 year); a GCS <15 after 2
hours; and, for children aged under 1 year, the presence of bruising, swelling, or
laceration of >5 cm on the head
For adults with any of the following risk factors who have experienced some loss of
consciousness or amnesia since the injury, a CT head scan should be performed
within 8 hours of the head injury:
o Age 65 years
o Any history of bleeding or clotting disorders
o Dangerous mechanism of injury (a pedestrian or cyclist struck by a motor
vehicle, an occupant ejected from a motor vehicle, or a fall from a height of >1
metre or 5 stairs)
o >30 minutes retrograde amnesia of events immediately before the head injury.

The predictive value of many of the above NICE UK criteria were confirmed in a metaanalysis of 71 studies published in 2012, which showed seizure, persistent vomiting, and
coagulopathy all significantly predicted positive head CT findings in patients with mild brain
injury. [33]
Other assessment criteria to guide imaging include New Orleans Criteria [24] and the
Canadian CT head rule. [25]
New Orleans criteria: [24]

CT is required for patients with minor head trauma (minor head injury was defined as
a loss of consciousness in patients with normal findings on a brief neurological
examination and a GCS score of 15, as determined by a physician on arrival at the
emergency department), with any one of the following:
o Headache
o Vomiting
o Age >60 years
o Drug or alcohol intoxication
o Persistent anterograde amnesia (deficits in short-term memory)
o Evidence of traumatic soft-tissue or bone injury above clavicles
o Seizure (suspected or witnessed).

Canadian CT head rule: [25]

CT head required for patients with minor head injuries, defined as witnessed loss of
consciousness, definite amnesia, or witnessed disorientation in a patient with a GCS
score of 13 to 15, with any one of the following:

High risk (for neurological intervention):

o GCS <15 at 2 hours after injury
o Suspected open or depressed skull fracture
o Any sign of basal skull fracture: haemotympanum, raccoon eyes (periorbital
ecchymosis), CSF otorrhoea/rhinorrhoea, Battle's sign (ecchymosis of the
mastoids)
o 2 or more episodes of vomiting
o Age 65 years or above.
Medium risk (for brain injury on CT):
o Amnesia for >30 minutes before impact (retrograde amnesia)
o Dangerous mechanism (pedestrian struck by motor vehicle, occupant ejected
from motor vehicle, fall from height of >3 feet or 5 stairs).

American College of Radiology Appropriateness Criteria [34]

Patients identified as having moderate or high risk for intracranial injury should
undergo early postinjury noncontrast CT for evidence of intracerebral hematoma,
midline shift, or increased intracranial pressure. Patients with minor head injuries can
use the New Orleans criteria or similar criteria to identify when CT is appropriate.
Appropriateness ratings for imaging modalities for skull fracture:
o 9: CT head without contrast
o 7: CTA head and neck (if vascular injury is suspected)
o 6: MRI head without contrast
o 6: X-ray and/or CT cervical spine without contrast
o 5: X-ray head (for selected cases)
o 4: MRI head without and with contrast (useful if infection suspected)
o 4: CT head without and with contrast
o 4: MRA head and neck without contrast
o 4: MRA head and neck without and with contrast
Where 4,5,6 = may be appropriate and 7,8,9 = usually appropriate.

Additional imaging
X-ray skull

Plain films were previously used to help screen which patients would benefit from CT
scanning. However, they offer no additional information and are associated with poor
sensitivity and failure to detect any associated intracranial pathology. [29] With the
widespread availability of CT scans to help detect intracranial pathology, plain skull
x-rays are no longer recommended as a first-line investigation in either children or
adults. However, they may be used as an interim aid if CT scanning is not available.

MRI brain

MRI is not recommended for initial or routine evaluation of skull fractures. However,
it can be a useful adjunct or a secondary imaging modality. Its main benefit is
increased detection of associated intracranial pathology. MRI can detect diffuse
axonal injury not seen on CT scan, and can increase detection of intracranial
haemorrhage (extradural/subdural) by up to 30%. [2] [30] [35] MRI may therefore be

considered if there is continuing concern of intracranial pathology in the absence of

CT findings.
MRI and MR angiography may also be useful if the fracture involves major
vasculature structures (e.g., the carotid canal or superior sagittal sinus), to assess
underlying vascular injury/pathology. [30] [36] [37] [38]

Cervical spine imaging

Historically, skull fractures (in particular, occipital condylar fractures) were

associated with a high risk of cervical spine injury. However, several studies have
found no such association. [39] [40] Cervical spinal imaging should be at the
discretion of the attending physician, based on clinical examination, level of
suspicion, age of the patient, and mechanism of injury.

Ultrasound brain

May be a useful adjunct to CT brain following confirmation of a fracture in the

paediatric population, to detect dural tears, brain herniation, or a growing skull
fracture. There may also be a role for ultrasound to screen for skull fractures in
paediatric patients with minor head trauma. [41] [42]

Skeletal survey

Should be considered if child abuse is a suspected underlying aetiology. Imaging of

hands, feet, long bones, skull, spine, and ribs (including oblique ribs) should be
performed, with high-definition imaging (CT/MRI of evident fractures) if possible. If
the initial skeletal survey is negative or equivocal, a repeat skeletal survey or selected
images performed between 10 and 14 days after the initial investigation will give
further information about ambiguous findings, identify further fractures, and add
information about the age of a fracture.

Laboratory investigations
For any patient with head trauma and otorrhoea/rhinorrhoea, an immunoassay (beta-2
transferrin assay) of the suspect fluid can stain positive in the presence of the protein.
The test should be performed if clear or blood-tinged drainage is present from the nose or
ears.
If positive, it indicates CSF leakage and is reliable even in the presence of blood or mucus. It
has a sensitivity of nearly 100% and a specificity of 95%. [43]
Click to view diagnostic guideline references.
http://bestpractice.bmj.com/best-practice/monograph/398/diagnosis/step-by-step.html