ORIGINAL ARTICLE

Contemporary Management of Penetrating Brain Injury

Domenic P. Esposito, MD, FACS and James B. Walker, MD

Abstract: Penetrating brain injury includes all traumatic brain

injury that is not the result of a blunt mechanism. Concerning
these injuries, gunshot wounds are by far the most prevalent.
Despite law enforcement eorts, these injuries unfortunately
continue to be commonplace in large trauma centers as well as
in metropolitan and large community emergency departments.
Great eorts have been undertaken to standardize the medical
and surgical management of these patients. The authors review
the Guidelines of Penetrating Brain Injury published in 2001
and performed an updated literature search concerning this
topic. There is evidence to suggest based upon current data that
aggressive antibiotic prophylaxis and avoidance of aggressive
debridement of deep-seated bone and bullet fragments has
improved morbidity and mortality over the last 35 years.
Key Words: debridement, penetrating brain injury, surgical
management
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fter signicant multidisciplinary collaboration, the

evidence-based Guidelines for the Management of
Severe Head Injury1 was introduced to the trauma
community in 1995 followed in 20072 by the third edition.
Both of these previous guidelines did not address the
management of patients specically injured by penetrating objects including gun shot wounds and stabbing
injuries. In 1998 the International Brain Injury Association, the Brain Injury Association of the United States
of America, members of the American Association of
Neurological Surgeons and the Congress of Neurological
Surgeons began to work on this eort.
In August 2001 the Journal of Trauma introduced
the Guidelines for the Management of Penetrating Brain
Injury (PBI),3 which has standardized both the medical
and surgical management of these unique and challenging
injuries. These guidelines are principally founded upon
From the Department of Neurosurgery, University of Mississippi
Medical Center, Jackson, Mississippi.
Financial Disclosure: Neither of the authors has any nancial or
commercial interests in association with products or information
mentioned in this manuscript.
Proprietary Statement: Neither of the authors has any proprietary
interests in association with products or information mentioned in
this manuscript. No internal or external grants were received for this
manuscript.
Reprints: James B. Walker, MD, Department of Neurosurgery,
University of Mississippi Medical Center, 2500 North State Street,
Jackson, MS 39216 (e-mail: jbwalker@neurosurgery.umsmed.edu).
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published literature that mainly includes retrospective

civilian and military analysis. Herein this article, we
review the principles of the Guidelines of Penetrating
Brain Injury3 as well as perform a current literature
search with emphasis on medical and surgical management of these challenging patients. In addition, we discuss
some of our adaptations in our fairly extensive cohort of
penetrating injuries.

LITERATURE SEARCH
The Guidelines for the Management of Penetrating
Brain Injury3 was reviewed in its entirety. Additionally,
PubMed and MEDLINE search engines were used to
perform a current literature search using the following key
words in all practical combinations: abscess, angiogram, antibiotic, arteriogram, ballistics, brain
injury, cerebral injury, cerebrospinal uid (CSF)
leak, computed tomography, craniocerebral injury,
craniotomy, epilepsy, gunshot wounds, intracranial
pressure, magnetic resonance, meningitis, neurosurgery, penetrating, posttraumatic seizures.

BALLISTIC PRINCIPLES INVOLVED IN PBI

The ability to penetrate the skull is determined
primarily by the energy and the shape of the object along
with the angle of the trajectory of the projectile.4,5 In
addition to the shape of the projectile, understanding
the concept of kinetic energy is crucial to the understanding of the primary injury involved in PBI. Please
recall that kinetic energy is characterized by the equation:
E = 1/2mv2. In other words, the kinetic energy of a
projectile represents one half of the mass of the projectile
multiplied by the velocity of the projectile to the second
power. Hence the velocity of the projectile has a greater
inuence than the mass of the projectile alone.
In addition, for understanding the total energy of
the projectile, it is paramount to understand the
pathophysiology6,7 involved in PBI. As the projectile
travels through the brain parenchyma, it is preceded by a
transient sonic wave that has a minimal inuence of
surrounding tissue. Soon after the projectile travels in the
brain, it is followed by a temporary cavitation of the brain
parenchyma, which can be several times the diameter of
the projectile. This temporary cavity then collapses upon
itself only to reexpand in progressively smaller undulating
wave-like patterns. Every cycle of temporary expansion
and collapse creates signicant surrounding tissue injury
to the brain. This can result in shear-like injury of the
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Esposito and Walker

neurons or can result in epidural hematomas, subdural

hematomas, or parenchymal contusions.5
Another important principle to recognize is the
principle of air resistances inuence upon the ballistics of
a projectile. A projectile loses its kinetic energy rapidly as
it travels through air because of its resistance.4,5 Therefore, a PBI is likely to be much more severe if the
projectile source is close to the patient head. Once again
this is due the notion that a large percentage of the initial
kinetic energy is being transferred to the surrounding
brain parenchyma.

NEUROIMAGING IN THE MANAGEMENT OF PBI

Computer tomography (CT) scanning of the head is
strongly recommended in all PBI3 when it is available.
This is largely due to the fact that CT scanning provides a
improved identication of embedded bone fragments and
the missile trajectory.810 It is also superior to the plain
lms in determining the extent of the brain injury and
the detection of hematomas causing mass eect.11,12
Although plain lms may give some indication for the
projectile path,13,14 it can sometimes be misleading in the
case of ricochet injuries. A ricochet injury occurs when
the bullet ricochets against the contralateral skull surface
and then travels in another direction through the brain
parenchyma.
Magnetic residence imaging (MRI) is seldom
indicated in the setting of PBI.15,16 Moreover, MRI
should also be highly discouraged when the substance of
the projectile is unknown. Even in instances when the
projectile is of an MRI compatible substance, CT
scanning provides much more useful and prognostic
information when compared with MRI.
At our institution, CT angiography is often
obtained once the CT scan of the head is reviewed and
suggests a wound tract that travels near major vascular
structures. Projectile trajectories that create concern for
vascular injuries include areas that cross the sylvian
ssure (location of middle cerebral artery), the subfalcine
areas (location of anterior cerebral artery), and around
the carotid canal (location of the internal carotid artery).
If CT angiography is suggestive of a vascular injury or
the patients ndings on neurologic examination suggest
a vascular injury, a formal cerebral angiogram is then
obtained.
Vascular complications most commonly involved in
PBI patients are the development of traumatic aneurysms
or arteriovenous stulas.1719 Once identied, surgical or
endovascular repair may be warranted. Occasionally a
vascular injury will develop in a delayed fashion.18,19 This
often presents as a delayed hematoma formation seen on
a repeat CT scan.
The incidence of subarachnoid hemorrhage after
PBI ranges from 31% to 78% which has been calculated
from various retrospective CT scanning data.3,20,21 The
presence of subarachnoid hemorrhage after PBI has been
shown to correlate signicantly with mortality.20 Moreover, subarachnoid hemorrhage is of greatest concern

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when identied around large vascular territories and in

association with intraventricular hemorrhage.12
A common yet potentially life threatening complication of subarachnoid hemorrhage is the development of
vasospasm.22 Vasospasm results from a reactive phenomenon of smooth muscle contraction within the walls of the
vasculature. This leads to a decrease diameter of the
vasculature with resulting decrease cerebral blood ow
to the brain tissue. When severe, vasospasm can lead to
ischemia and ultimately cerebral infarction. Interestingly,
there was no dierence in outcome based on a 3 month
Glasgow Outcome Scale (GOS) when PBI patients with
or without vasospasm were compared.23 When vasospasm is detected (often diagnosed by increased transcranial Doppler ultrasound velocities), therapeutic measures
should be immediately used.
Treatments of vasospasm include intravascular
expansion and endovascular angioplasty. Medical management of vasospasm includes conventional HHH
Therapy where the HHH stands for hypertension,
hypervolemia, and hemodilution. Here, measures are
taken to increase the patients blood pressure, to hydrate
the patient with intravenous uids, as well as dilute the
patients blood volume to decrease the hematocrit. All of
these measures have been shown to increase the cerebral
blood ow.24 When HHH therapy fails, the patient
should be considered for selective transluminal balloon
angioplasty of the spasmodic vessels when available.
Balloon angioplasty involves the insertion of an inatable
compliant balloon that stretches the vascular wall to
increase the cerebral blood ow.

ICP MONITORING
One of the greatest advancements in modern
management of traumatic brain injuries and PBI injuries
is the development of monitoring of intracranial pressure
(ICP). ICP monitoring involves drilling a burr hole in the
skull and the insertion of a monitoring device or a bolt
that couples to a water column (or monitoring device)
that can produce continuous pressure measurements.
It is crucial to understand that the principle of
intracranial pressure results from the fact that the
intracranial space is a xed volume (once the fontanelles
have fused). Moreover, the rigidity of the skull accounts
for its noncompliance where small increases in volume
result in larger increases in pressure. Consequently, there
exists a limited area for the brain to swell as a result of
cytotoxic edema or expanding hematomas. In addition,
cerebral blood ow is also a common inuence upon
ICP. As cerebral blood ow increases then there is more
blood volume within the intracranial space which raises
intracranial pressure in concordance with the MonroKellie doctrine (ICP is determined by the relative cranial
contents of brain tissue, CSF, and blood].25 Paradoxically, cerebral blood ow can decrease to a point where
the brain parenchyma is not adequately perfused leading
to ischemia and subsequent cytotoxic edema which raises
intracranial pressure.
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The indications for ICP monitoring and its applications in PBI have been incompletely studied. This is more
prominent in regards to civilian data when compared with
military data. However from the available data, elevated
ICP seems to be frequent after PBI11,2628 and when
present is predictive of worse outcomes.12,29 In one
particular earlier series, 92% of patients who underwent
ICP monitoring demonstrated intracranial hypertension
(ICP>20 mm Hg).27 Unfortunately when compared with
the Guidelines for the Management of Traumatic Brain
Injury, there is little data to reveal how successful
management of intracranial pressure improves outcomes
in PBI patients.3 Although because of these short comings,
general aspects of ICP management discussed in the
literature of nonpenetrating traumatic brain injury has
been generalized to the PBI population. At our institution, threshold to begin treatment for elevated ICP is set
at 20 mm Hg. This value is slightly above normal ICP
measurements in normal individuals. Medical management of intracranial hypertension includes sedation with
benzodiazepines and narcotics, nondepolarizing paralytics,
mannitol, and gentle hypothermic induction (35.51C).
Long-term hyperventilation and steroid administration
should be strictly avoided and has been conclusively shown
to increase morbidity and mortality in all traumatic brain
injury.1,2

SURGICAL MANAGEMENT OF PBI

Immediately upon arrival of a PBI patient to an
emergency facility, a thorough inspection of the supercial wound should be noted after routine resuscitation
maneuvers have been applied. An entrance wound should
be identied and its location recorded as well as any exit
wounds when they exist. The supercial scalp should be
observed for powder burns, which would imply a close
range rearm injury. Any CSF, bleeding, or brain parenchyma emerging from the wound should be documented.
In addition, the size of the decit should be documented
and when extensive complex skin ap closure may be
needed. After the wound has been inspected, a thorough
neurologic examination should be noted and a postresuscitative GCS should be obtained. It is important to
document any cranial nerve or motor decits. The eyes
should be carefully inspected and pupillary responses and
size recorded. When the patient has been adequately
resuscitated and stabilized for transfer, a CT scan should
be immediately obtained. When not available, plain skull
lms should obtained.
Treatment of small entrance wounds with local
wound care and closure in patients whose scalp has
not been devitalized and have no signicant intracranial
pathologic ndings on CT scan (Fig. 1) is not only adequate but recommended according to the guidelines.3
However, in the presence of signicant mass eect,
debridement of necrotic brain tissue along with safely
accessible bone fragments is recommended.30 It should be
noted that any deeply seated bone fragments especially
those in eloquent brain areas should not be retrieved
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Penetrating Brain Injury

FIGURE 1. This axial noncontrasted computed tomography

scan demonstrates a gunshot wound with a trajectory
confined to the bifrontal convexity where the majority of the
bullet fragments are confined to the left frontal white matter.
Note there are minimal skull and tissue disruption and no
significant hematoma formation. Such cases can be treated
with local wound debridement and closure.

because this has been shown to correlate with worse

outcomes.9,31 This has marked a signicant trend since
Vietnam era to proceed with a more conservative,
minimally invasive approach toward cerebral debridement as this has been shown to improve outcomes and
lower morbidity.27,30,32
Once a patient has been classied as a surgical
candidate, attempts should be made to operate within 12
hours of the injury to prevent infection and resulting
abscesses.10,30,33 As with bone fragments, only accessible missile fragments in noneloquent brain should be
retrieved although there has been some suggestion that
removal of all missile fragments may decrease the risk of
seizures.34
When the trajectory of the bullet has been noted on
CT scan to violate an open air sinus (Fig. 2), an operation
is recommended for water-tight closure of the damaged
dura.3 It has been suggested that this may decrease the
risk of abscess formation and CSF stulas.33,35,36
In summary, the surgical management of PBI is
based largely on Class III data. There are no randomizedcontrol studies that have examined the relative eect of
various treatment of debridement to prevent infection
and minimize the development of seizure disorders. The
current trend is to minimize the degree of debridement
whereas by obtaining a water-tight dura closure. In addition
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During surgery every eort should be made to close the

dura.3 When the dura cannot be closed primarily with
suture approximation, a tissue graft can be used from the
patients pericranium, temporalis fascia, or fascia lata.
Synthetic grafts can be used as well, however, they can act
as a foreign body and thus increase the risk of infection,
especially in grossly contaminated wounds.37 When
closing the wound, a water tight closure of all layers is
ideal.
When a CSF leak occurs remote from the projectiles entrance, CSF diversion should be considered.37
The patients CT scan of the head should be carefully
inspected before the placement of the lumbar drain
because mass eect from hematomas and midline shift
are relative contraindications for lumbar drainage compared to a ventriculostomy because of the risk of herniation syndromes. It has been demonstrated in several
retrospective studies that CSF leaks that persist after
surgery have a high likelihood of developing meningitis
or abscess.36,3840

ANTIBIOTIC PROPHYLAXIS FOR PBI

FIGURE 2. This axial noncontrasted computed tomography

scan demonstrates a penetrating brain injury with significant
disruption of the left frontal bone and violation of the frontal
sinus marked by the associated pneumocephalus. Such
patients should undergo surgical debridement and dural
repair to prevent subsequent cerebrospinal fluid leaks and
infectious complications. In addition, this patient demonstrates inappropriate midline shift and should also be
considered for a decompressive craniectomy.

at our institution, any patient with a salvageable examination and midline shift that exceeds 5 mm where the midline
shift is greater than the width of the associated subdural
or epidural hematoma is considered for a decompressive
hemicraniectomy (Fig. 2).

MANAGEMENT OF CSF LEAK

A common nding among PBI patients is the
development of a CSF leak, which has an incidence of
28% in one large series.33 This complication develops as a
result of the projectiles violation of the dura along with
failure to adequately seal the defect through normal tissue
healing responses. CSF leaks can present through the
entry or exit sites of the projectile as well as through the
ear or nose when the mastoid air cells and the open-air
sinuses have been violated, respectively.
As stated in the guidelines, surgical correction is
currently recommended for CSF leaks that do not stop
spontaneously or are refractory to temporary CSF diversion through a ventricular catheter or lumbar drain.3

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One of the most dreaded complications of PBI is

the development of infectious complications. These may
present as local wound infections, meningitis, ventriculitis, or cerebral abscess. Unfortunately, infectious complications are not uncommon and occur in as many as 15%
of all PBI cases based on one series.41 It is highly
suggested from multiple retrospective studies that the
presence of air sinus wounds and CSF stulas may further
increase the risk of infection33,36,38 with an incidence as
high as 49.5%.38
The early administration of broad spectrum antibiotics likely decreases these infectious complications
based upon preantibiotic military data where infectious
complications reached as high as 58.8% in all penetrating
head injuries.42 Although performed in 1946 under poorly
controlled conditions, Munslow43 additionally noted a
decrease in infectious complications from 21% to 5.6%
after the advent of parenteral penicillin. In one of the
largest retrospective reviews which included civilian
PBI data, Benzel et al18 demonstrated a rate of infection
of 1% to 5% overall and less than a 1% rate of
development of brain abscess with use of broad spectrum
antibiotics.
Although the use of broad spectrum antibiotics is
primarily speculative owing to a paucity of evidence
and lack of randomized controlled trials, they are still
recommended because there is data to suggest a wide
variety of organisms are pathogenic in PBI settings where
Gram negative organisms were most common based on
a large military series.36 Considerable variation exists
in antibiotic preference; however, cephalosporins have
become the preferred agent nationally.44 At our institution, we routinely use prophylactic parenteral broad
spectrum antibiotics for all of our PBI patients. We
commonly use intravenous cephtriaxone, metronidazole,
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Penetrating Brain Injury

and vancomycin and continue them for a minimum of

6 weeks. As we have initiated this protocol, we have
yet to encounter our rst infectious complication over
40 consecutive patients although we did have 1 case of
ventriculitis after a patient inadvertently stopped his
antibiotics after 1 week.

ANTISEIZURE PROPHYLAXIS FOR PBI

Not only is the development of posttraumatic
seizures a potential cause of morbidity for PBI patient,
it is often a cause fear and concern for family members
involved in their care. Furthermore, seizures during the
rst week after an initial injury can be a cause of
morbidity and mortality because of the development of
raised intracranial pressures and increased metabolic
demands. Thus antiseizure medications are recommended
in the rst week after PBI. This has been suggested to
prevent early posttraumatic seizures in these patients
based upon military data analysis.4548 Prophylactic
treatment with anticonvulsants beyond the rst week
after PBI has not been shown to prevent the development
of new seizures and is currently not recommended. In our
series that includes 187 patients since 2002, an incidence
of approximately 50% of posttraumatic epilepsy has
been observed. This has prompted us to continue antiseizure prophylaxis in all but the most minimally injured
patients.

PROGNOSIS IN PBI
Before determining the appropriate medical or
surgical management of PBI patients, it is paramount to
determine the prognosis of the patient based on the head
CT and neurologic examination ndings. Great care
should be executed when obtaining an appropriate GCS
score because surgery should only be considered for
neurologically salvageable patients. It is imperative to
ensure that the patients GCS score is not obscured owing
to simultaneous seizure activity or medications that can
inuence cognition and motor activity. These can include
sedative or hypnotic agents used for intubation or
paralytics that have been recently administered to the
patient.
Several factors have been suggestive to contribute to
a worse outcome3 and include:
 increase in age
 suicide attempts
 associated coagulopathy
 GCS score of 3 with bilaterally xed and dilated pupils
 high-initial ICP
Moreover several CT scan ndings (Fig. 3) have
been suggested to be correlative to a worse outcome3 and
include:
 bihemispheric lesions
 multilobar injuries
 intraventricular hemorrhage
 uncal herniation
 subarachnoid hemorrhage.
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FIGURE 3. This axial noncontrasted CT scan demonstrates a

bihemispheric gunshot wound with marked intraventricular
hemorrhage, subarachnoid hemorrhage, and early ischemic
changes. In concordance with a low GCS score, a conservative
approach is an appropriate means of management and
surgical intervention should be discouraged.

CONCLUSIONS
Care of patients with PBI has changed dramatically
as the advent of Guidelines for the Management of
Penetrating Brain Injury. There has been a move over the
last 35 years to avoid aggressive debridement of deepseated bone and bullet fragments as this appears to
improve functional outcome. In its place, aggressive
administration of prophylactic parenteral antibiotics has
been used to prevent infectious complications. Although
there is a paucity of Class I and II data on this topic, there
is adequate data on its cousin counterpartynonpenetrating traumatic brain injury. There has been a call to
perform large multicentered randomized controlled trials,
which could alter our care of these challenging patients in
the future.
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