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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 efforts, these injuries unfortunately

continue to be commonplace in large trauma centers as well as

in metropolitan and large community emergency departments.

Great efforts 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 thataggressive 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

(Neurosurg Q 2009;19:249–254)

After significant multidisciplinary collaboration, theevidence-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 themanagement of patients specifically injured by penetrat-ing objects including gun shot wounds and stabbinginjuries. In 1998 the International Brain Injury Associa-tion, the Brain Injury Association of the United Statesof America, members of the American Association of Neurological Surgeons and the Congress of NeurologicalSurgeons began to work on this effort.

In August 2001 the Journal of Trauma introducedthe Guidelines for the Management of Penetrating BrainInjury (PBI),3 which has standardized both the medicaland surgical management of these unique and challenging

injuries. These guidelines are principally founded upon

published literature that mainly includes retrospectivecivilian and military analysis. Herein this article, wereview the principles of the Guidelines of PenetratingBrain Injury3 as well as perform a current literaturesearch with emphasis on medical and surgical manage-ment of these challenging patients. In addition, we discusssome of our adaptations in our fairly extensive cohort of penetrating injuries.

LITERATURE SEARCH

The Guidelines for the Management of PenetratingBrain Injury3 was reviewed in its entirety. Additionally,PubMed and MEDLINE search engines were used toperform a current literature search using the following keywords in all practical combinations: ‘‘abscess,’’ ‘‘angio-gram,’’ ‘‘antibiotic,’’ ‘‘arteriogram,’’ ‘‘ballistics,’’ ‘‘braininjury,’’ ‘‘cerebral injury,’’ ‘‘cerebrospinal fluid (CSF)leak,’’ ‘‘computed tomography,’’ ‘‘craniocerebral injury,’’‘‘craniotomy,’’ ‘‘epilepsy,’’ ‘‘gunshot wounds,’’ ‘‘intracranialpressure,’’ ‘‘magnetic resonance,’’ ‘‘meningitis,’’ ‘‘neuro-surgery,’’ ‘‘penetrating,’’ ‘‘posttraumatic seizures.’’

BALLISTIC PRINCIPLES INVOLVED IN PBIThe ability to penetrate the skull is determined

primarily by the energy and the shape of the object alongwith the angle of the trajectory of the projectile.4,5 Inaddition to the shape of the projectile, understandingthe concept of kinetic energy is crucial to the under-standing of the primary injury involved in PBI. Pleaserecall that kinetic energy is characterized by the equation:E=1/2mv2. In other words, the kinetic energy of aprojectile represents one half of the mass of the projectilemultiplied by the velocity of the projectile to the secondpower. Hence the velocity of the projectile has a greaterinfluence than the mass of the projectile alone.

In addition, for understanding the total energy of the projectile, it is paramount to understand thepathophysiology6,7 involved in PBI. As the projectiletravels through the brain parenchyma, it is preceded by atransient sonic wave that has a minimal influence of surrounding tissue. Soon after the projectile travels in thebrain, it is followed by a temporary cavitation of the brainparenchyma, which can be several times the diameter of the projectile. This temporary cavity then collapses uponitself only to reexpand in progressively smaller undulatingwave-like patterns. Every cycle of temporary expansionand collapse creates significant surrounding tissue injuryto the brain. This can result in shear-like injury of theCopyright r 2009 by Lippincott Williams & Wilkins

From the Department of Neurosurgery, University of MississippiMedical Center, Jackson, Mississippi.

Financial Disclosure: Neither of the authors has any financial orcommercial interests in association with products or informationmentioned in this manuscript.

Proprietary Statement: Neither of the authors has any proprietaryinterests in association with products or information mentioned inthis manuscript. No internal or external grants were received for thismanuscript.

Reprints: James B. Walker, MD, Department of Neurosurgery,University of Mississippi Medical Center, 2500 North State Street,Jackson, MS 39216 (e-mail: [email protected]).

ORIGINAL ARTICLE

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neurons or can result in epidural hematomas, subduralhematomas, or parenchymal contusions.5

Another important principle to recognize is theprinciple of air resistance’s influence upon the ballistics of a projectile. A projectile loses its kinetic energy rapidly asit travels through air because of its resistance.4,5 There-

fore, a PBI is likely to be much more severe if theprojectile source is close to the patient head. Once againthis is due the notion that a large percentage of the initialkinetic energy is being transferred to the surroundingbrain parenchyma.

NEUROIMAGING IN THE MANAGEMENT OF PBI

Computer tomography (CT) scanning of the head isstrongly recommended in all PBI3 when it is available.This is largely due to the fact that CT scanning provides aimproved identification of embedded bone fragments andthe missile trajectory.8–10 It is also superior to the plain

films in determining the extent of the brain injury andthe detection of hematomas causing mass effect.11,12

Although plain films may give some indication for theprojectile path,13,14 it can sometimes be misleading in thecase of ricochet injuries. A ricochet injury occurs whenthe bullet ricochets against the contralateral skull surfaceand then travels in another direction through the brainparenchyma.

Magnetic residence imaging (MRI) is seldomindicated in the setting of PBI.15,16 Moreover, MRIshould also be highly discouraged when the substance of the projectile is unknown. Even in instances when theprojectile is of an MRI compatible substance, CTscanning 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 andsuggests a wound tract that travels near major vascularstructures. Projectile trajectories that create concern forvascular injuries include areas that cross the sylvianfissure (location of middle cerebral artery), the subfalcineareas (location of anterior cerebral artery), and aroundthe carotid canal (location of the internal carotid artery).If CT angiography is suggestive of a vascular injury orthe patient’s findings on neurologic examination suggesta vascular injury, a formal cerebral angiogram is thenobtained.

Vascular complications most commonly involved inPBI patients are the development of traumatic aneurysmsor arteriovenous fistulas.17–19 Once identified, surgical orendovascular repair may be warranted. Occasionally avascular injury will develop in a delayed fashion.18,19 Thisoften presents as a delayed hematoma formation seen ona repeat CT scan.

The incidence of subarachnoid hemorrhage afterPBI ranges from 31% to 78% which has been calculatedfrom various retrospective CT scanning data.3,20,21 Thepresence of subarachnoid hemorrhage after PBI has beenshown to correlate significantly with mortality.20 More-over, subarachnoid hemorrhage is of greatest concern

when identified around large vascular territories and inassociation with intraventricular hemorrhage.12

A common yet potentially life threatening compli-cation of subarachnoid hemorrhage is the development of vasospasm.22 Vasospasm results from a reactive phenom-enon of smooth muscle contraction within the walls of the

vasculature. This leads to a decrease diameter of thevasculature with resulting decrease cerebral blood flowto the brain tissue. When severe, vasospasm can lead toischemia and ultimately cerebral infarction. Interestingly,there was no difference in outcome based on a 3 monthGlasgow Outcome Scale (GOS) when PBI patients withor without vasospasm were compared.23 When vasos-pasm is detected (often diagnosed by increased transcra-nial Doppler ultrasound velocities), therapeutic measuresshould be immediately used.

Treatments of vasospasm include intravascularexpansion and endovascular angioplasty. Medical man-agement of vasospasm includes conventional ‘‘HHH

Therapy’’ where the HHH stands for hypertension,hypervolemia, and hemodilution. Here, measures aretaken to increase the patient’s blood pressure, to hydratethe patient with intravenous fluids, as well as dilute thepatient’s blood volume to decrease the hematocrit. All of these measures have been shown to increase the cerebralblood flow.24 When HHH therapy fails, the patientshould be considered for selective transluminal balloonangioplasty of the spasmodic vessels when available.Balloon angioplasty involves the insertion of an inflatablecompliant balloon that stretches the vascular wall toincrease the cerebral blood flow.

ICP MONITORINGOne of the greatest advancements in modern

management of traumatic brain injuries and PBI injuriesis the development of monitoring of intracranial pressure(ICP). ICP monitoring involves drilling a burr hole in theskull and the insertion of a monitoring device or a boltthat 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 theintracranial space is a fixed volume (once the fontanelleshave fused). Moreover, the rigidity of the skull accountsfor its noncompliance where small increases in volume

result in larger increases in pressure. Consequently, thereexists a limited area for the brain to swell as a result of cytotoxic edema or expanding hematomas. In addition,cerebral blood flow is also a common influence uponICP. As cerebral blood flow increases then there is moreblood volume within the intracranial space which raisesintracranial pressure in concordance with the Monro-Kellie doctrine (ICP is determined by the relative cranialcontents of brain tissue, CSF, and blood].25 Paradoxi-cally, cerebral blood flow can decrease to a point wherethe brain parenchyma is not adequately perfused leadingto ischemia and subsequent cytotoxic edema which raisesintracranial pressure.

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The indications for ICP monitoring and its applica-tions in PBI have been incompletely studied. This is moreprominent in regards to civilian data when compared withmilitary data. However from the available data, elevatedICP seems to be frequent after PBI11,26–28 and whenpresent is predictive of worse outcomes.12,29 In one

particular earlier series, 92% of patients who underwentICP monitoring demonstrated intracranial hypertension(ICP> 20 mm Hg).27 Unfortunately when compared withthe Guidelines for the Management of Traumatic BrainInjury, there is little data to reveal how successfulmanagement of intracranial pressure improves outcomesin PBI patients.3 Although because of these short comings,general aspects of ICP management discussed in theliterature of nonpenetrating traumatic brain injury hasbeen generalized to the PBI population. At our institu-tion, threshold to begin treatment for elevated ICP is setat 20 mm Hg. This value is slightly above normal ICPmeasurements in normal individuals. Medical manage-

ment of intracranial hypertension includes sedation withbenzodiazepines and narcotics, nondepolarizing paralytics,mannitol, and gentle hypothermic induction (35.51C).Long-term hyperventilation and steroid administrationshould be strictly avoided and has been conclusively shownto increase morbidity and mortality in all traumatic braininjury.1,2

SURGICAL MANAGEMENT OF PBI

Immediately upon arrival of a PBI patient to anemergency facility, a thorough inspection of the super-ficial wound should be noted after routine resuscitationmaneuvers have been applied. An entrance wound should

be identified and its location recorded as well as any exitwounds when they exist. The superficial scalp should beobserved for powder burns, which would imply a closerange firearm injury. Any CSF, bleeding, or brain paren-chyma emerging from the wound should be documented.In addition, the size of the deficit should be documentedand when extensive complex skin flap closure may beneeded. After the wound has been inspected, a thoroughneurologic examination should be noted and a postre-suscitative GCS should be obtained. It is important todocument any cranial nerve or motor deficits. The eyesshould be carefully inspected and pupillary responses andsize recorded. When the patient has been adequately

resuscitated and stabilized for transfer, a CT scan shouldbe immediately obtained. When not available, plain skullfilms should obtained.

Treatment of small entrance wounds with localwound care and closure in patients whose scalp hasnot been devitalized and have no significant intracranialpathologic findings on CT scan (Fig. 1) is not only ade-quate but recommended according to the guidelines.3

However, in the presence of significant mass effect,debridement of necrotic brain tissue along with safelyaccessible bone fragments is recommended.30 It should benoted that any deeply seated bone fragments especiallythose in eloquent brain areas should not be retrieved

because this has been shown to correlate with worseoutcomes.9,31 This has marked a significant trend sinceVietnam era to proceed with a more conservative,minimally invasive approach toward cerebral debride-ment as this has been shown to improve outcomes andlower morbidity.27,30,32

Once a patient has been classified as a surgicalcandidate, attempts should be made to operate within 12hours of the injury to prevent infection and resultingabscesses.10,30,33 As with bone fragments, only acces-sible missile fragments in noneloquent brain should beretrieved although there has been some suggestion thatremoval of all missile fragments may decrease the risk of

seizures.34

When the trajectory of the bullet has been noted onCT scan to violate an open air sinus (Fig. 2), an operationis recommended for water-tight closure of the damageddura.3 It has been suggested that this may decrease therisk of abscess formation and CSF fistulas.33,35,36

In summary, the surgical management of PBI isbased largely on Class III data. There are no randomized-control studies that have examined the relative effect of various treatment of debridement to prevent infectionand minimize the development of seizure disorders. Thecurrent trend is to minimize the degree of debridementwhereas by obtaining a water-tight dura closure. In addition

FIGURE 1. This axial noncontrasted computed tomographyscan demonstrates a gunshot wound with a trajectoryconfined to the bifrontal convexity where the majority of thebullet fragments are confined to the left frontal white matter.Note there are minimal skull and tissue disruption and nosignificant hematoma formation. Such cases can be treatedwith local wound debridement and closure.

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at our institution, any patient with a salvageable examina-tion and midline shift that exceeds 5 mm where the midlineshift is greater than the width of the associated subduralor epidural hematoma is considered for a decompressivehemicraniectomy (Fig. 2).

MANAGEMENT OF CSF LEAK

A common finding among PBI patients is thedevelopment of a CSF leak, which has an incidence of 28% in one large series.33 This complication develops as aresult of the projectile’s violation of the dura along withfailure to adequately seal the defect through normal tissuehealing responses. CSF leaks can present through theentry or exit sites of the projectile as well as through theear or nose when the mastoid air cells and the open-airsinuses have been violated, respectively.

As stated in the guidelines, surgical correction iscurrently recommended for CSF leaks that do not stopspontaneously or are refractory to temporary CSF diver-sion through a ventricular catheter or lumbar drain.3

During surgery every effort should be made to close thedura.3 When the dura cannot be closed primarily withsuture approximation, a tissue graft can be used from thepatient’s pericranium, temporalis fascia, or fascia lata.Synthetic grafts can be used as well, however, they can actas a foreign body and thus increase the risk of infection,

especially in grossly contaminated wounds.37 Whenclosing the wound, a water tight closure of all layers isideal.

When a CSF leak occurs remote from the projec-tile’s entrance, CSF diversion should be considered.37

The patient’s CT scan of the head should be carefullyinspected before the placement of the lumbar drainbecause mass effect from hematomas and midline shiftare relative contraindications for lumbar drainage com-pared to a ventriculostomy because of the risk of her-niation syndromes. It has been demonstrated in severalretrospective studies that CSF leaks that persist aftersurgery have a high likelihood of developing meningitis

or abscess.36,38–40

ANTIBIOTIC PROPHYLAXIS FOR PBI

One of the most dreaded complications of PBI isthe development of infectious complications. These maypresent as local wound infections, meningitis, ventriculi-tis, or cerebral abscess. Unfortunately, infectious compli-cations are not uncommon and occur in as many as 15%of all PBI cases based on one series.41 It is highlysuggested from multiple retrospective studies that thepresence of air sinus wounds and CSF fistulas may furtherincrease the risk of infection33,36,38 with an incidence as

high as 49.5%.38

The early administration of broad spectrum anti-biotics likely decreases these infectious complicationsbased upon preantibiotic military data where infectiouscomplications reached as high as 58.8% in all penetratinghead injuries.42 Although performed in 1946 under poorlycontrolled conditions, Munslow43 additionally noted adecrease in infectious complications from 21% to 5.6%after the advent of parenteral penicillin. In one of thelargest retrospective reviews which included civilianPBI data, Benzel et al18 demonstrated a rate of infectionof 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 evidenceand lack of randomized controlled trials, they are stillrecommended because there is data to suggest a widevariety of organisms are pathogenic in PBI settings whereGram negative organisms were most common based ona large military series.36 Considerable variation existsin antibiotic preference; however, cephalosporins havebecome the preferred agent nationally.44 At our institu-tion, we routinely use prophylactic parenteral broadspectrum antibiotics for all of our PBI patients. Wecommonly use intravenous cephtriaxone, metronidazole,

FIGURE 2. This axial noncontrasted computed tomographyscan demonstrates a penetrating brain injury with significantdisruption of the left frontal bone and violation of the frontalsinus marked by the associated pneumocephalus. Suchpatients should undergo surgical debridement and duralrepair to prevent subsequent cerebrospinal fluid leaks andinfectious complications. In addition, this patient demon-

strates inappropriate midline shift and should also beconsidered for a decompressive craniectomy.




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and vancomycin and continue them for a minimum of 6 weeks. As we have initiated this protocol, we haveyet to encounter our first infectious complication over40 consecutive patients although we did have 1 case of ventriculitis after a patient inadvertently stopped hisantibiotics after 1 week.

ANTISEIZURE PROPHYLAXIS FOR PBI

Not only is the development of posttraumaticseizures a potential cause of morbidity for PBI patient,it is often a cause fear and concern for family membersinvolved in their care. Furthermore, seizures during thefirst week after an initial injury can be a cause of morbidity and mortality because of the development of raised intracranial pressures and increased metabolicdemands. Thus antiseizure medications are recommendedin the first week after PBI. This has been suggested toprevent early posttraumatic seizures in these patients

based upon military data analysis.

45–48

Prophylactictreatment with anticonvulsants beyond the first weekafter PBI has not been shown to prevent the developmentof new seizures and is currently not recommended. In ourseries that includes 187 patients since 2002, an incidenceof approximately 50% of posttraumatic epilepsy hasbeen observed. This has prompted us to continue anti-seizure prophylaxis in all but the most minimally injuredpatients.

PROGNOSIS IN PBI

Before determining the appropriate medical orsurgical management of PBI patients, it is paramount to

determine the prognosis of the patient based on the headCT and neurologic examination findings. Great careshould be executed when obtaining an appropriate GCSscore because surgery should only be considered forneurologically salvageable patients. It is imperative toensure that the patient’s GCS score is not obscured owingto simultaneous seizure activity or medications that caninfluence cognition and motor activity. These can includesedative or hypnotic agents used for intubation orparalytics that have been recently administered to thepatient.

Several factors have been suggestive to contribute toa worse outcome3 and include:

increase in age suicide attempts associated coagulopathy GCS score of 3 with bilaterally fixed and dilated pupils high-initial ICP

Moreover several CT scan findings (Fig. 3) havebeen suggested to be correlative to a worse outcome3 andinclude: bihemispheric lesions multilobar injuries intraventricular hemorrhage uncal herniation subarachnoid hemorrhage.

CONCLUSIONS

Care of patients with PBI has changed dramaticallyas the advent of Guidelines for the Management of Penetrating Brain Injury. There has been a move over thelast 35 years to avoid aggressive debridement of deep-seated bone and bullet fragments as this appears toimprove functional outcome. In its place, aggressiveadministration of prophylactic parenteral antibiotics hasbeen used to prevent infectious complications. Althoughthere is a paucity of Class I and II data on this topic, thereis adequate data on its cousin counterpartynonpenetrat-ing traumatic brain injury. There has been a call toperform large multicentered randomized controlled trials,which could alter our care of these challenging patients inthe future.

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