Traumatic brain
injury (TBI) is the fourth leading cause of death in the United States and is
the leading cause of death in persons aged 1-44 years. Approximately 2 million
traumatic brain injuries occur each year, and an approximate $25 billion per
year is spent in social and medical management of people with such injuries.
Analysis of the trauma literature has shown that 50% of all trauma deaths are
secondary to TBI, and gunshot wounds to the head caused 35% of these (see Picture 1). The
current increase in firearm-related violence and subsequent increase in
penetrating head injury remains of concern to neurosurgeons in particular and to
the community as a whole.
The definition of a penetrating head trauma is a wound in which a projectile
breaches the cranium but does not exit it. Despite the prevalence of these
injuries, the morbidity and mortality of penetrating head injury remains high.
Improvements in the understanding of the mechanisms of injury and aggressive
medical and surgical management of patients with these injuries may lead to
improved outcomes.
This chapter focuses on the pathophysiology of both primary and secondary
mechanisms of injury, describes the treatment of patients from presentation to
discharge, and concludes with a discussion of possible complications and patient
outcome.
History of the Procedure: The earliest reported series about
head injuries and their management appears in the Edwin Smith papyrus around
1700 BC, reporting 4 depressed skull fractures treated by the Egyptians by
leaving the wound unbandaged, providing free drainage of the intracranial
cavity, and anointing the scalp wound with grease. Hippocrates (460-357 BC)
performed trephination for contusions, fissure fractures, and skull
indentations. Galen's experience in 130-210 AD treating wounded gladiators led
to recognition of a correlation between the side of injury and the side of motor
loss.
During the Dark Ages, little progress was made in the surgical management of
head wounds and medicine continued to hold a pessimistic view of head wounds
with torn dura mater. In the 17th century, Richard Wiseman provided a better
understanding of surgical management of penetrating brain injuries; he
recommended the evacuation of subdural hematomas and the extraction of bone
fragments. In his experience, deep wounds had a much worse prognosis than
superficial ones.
Major advances in the management of penetrating craniocerebral injuries in
the mid-19th century were related to the work of Louis Pasteur (1867), Robert
Koch in bacteriology (1876), and Joseph Lister in asepsis (1867). Such advances
dramatically reduced the incidence of local and systemic infections, as well as
mortality.
Problem: In the past 20 years, a dramatic increase in the
incidence of penetrating injuries to the brain has occurred. Gunshot wounds to
the head have become the leading or second leading cause of head injury in many
cities in the United States. These injuries are devastating to the patient,
family, and society.
Siccardi et al (1991) prospectively studied a series of 314 patients with
craniocerebral missile wounds and found that 73% of the victims died at the
scene, 12% died within 3 hours of injury, and 7% died later, yielding a total
mortality of 92% in his series. In another study, gunshot wounds were
responsible for at least 14% of the head injury–related deaths from 1979-1986.
Age-adjusted death rates for injury by firearms have increased nearly every
year since 1985. A study using multiple logistic regressions found that injury
from firearms greatly increases the probability of death and that the victim of
a gunshot wound to the head is approximately 35 times more likely to die than is
a patient with a comparable nonpenetrating brain injury.
Frequency: A National Institutes of Health survey estimates
that in the United States, 1.9 million persons annually experience a skull
fracture or intracranial injury, and, of these cases, one-half have a suboptimal
outcome. In 1992, firearms accounted for the largest proportion of deaths from
traumatic brain injury in the United States, and gunshot wounds were the most
common cause of mortality in African Americans.
Etiology: Penetrating head injuries can be the result of
numerous intentional or unintentional events, including missile wounds, stab
wounds, and motor vehicle or occupational accidents (nails, screwdrivers).
Stab wounds to the cranium typically are caused by a weapon with a small
impact area and wielded at low velocity. The most common wound is a knife
injury, although bizarre craniocerebral-perforating injuries have been reported
that were caused by nails, metal poles, ice picks, keys, pencils, chopsticks,
and power drills.
Pathophysiology: The pathological consequences of
penetrating head wounds depend on the circumstances of the injury, including the
properties of the weapon or missile, the energy of the impact, and the location
and characteristics of the intracranial trajectory. Following the primary injury
or impact, secondary injuries may develop. Secondary injury mechanisms are
defined as pathological processes that occur after the time of the injury and
adversely affect the ability of the brain to recover from the primary insult. A
biochemical cascade begins when a mechanical force disrupts the normal cell
integrity, producing the release of numerous enzymes, phospholipids, excitatory
neurotransmitters (glutamate), Ca, and free oxygen radicals that propagate
further cell damage.
Missile wounds
Missiles range from low-velocity bullets used in handguns or shotguns to
high-velocity metal-jacket bullets fired from military weapons (see Picture 6).
Low-velocity civilian missile wounds occur from air rifle projectiles, nail guns
used in construction devices, stun guns used for animal slaughter, and shrapnel
produced during explosions. Bullets can cause damage to brain parenchyma through
3 mechanisms—(1) laceration and crushing, (2) cavitation, and (3) shock waves.
The injury may range from a depressed fracture of the skull resulting in a focal
hemorrhage to devastating diffuse damage to the brain.
As stated previously, a wound in which the projectile breaches the cranium
but does not exit is described technically as penetrating, and an injury in
which the projectile passes entirely though the head, leaving both entrance and
exit wounds, is described as perforating. This distinction has some prognostic
implications. In a series of missile-related head injuries during the Iran-Iraq
war, a poor postsurgical outcome occurred in 50% of patients treated for
perforating wounds, as compared to only 20% of those with penetrating wounds.
In missile wounds, the amount of damage to the brain depends on numerous
factors including (1) the kinetic energy imparted, (2) the trajectory of the
missile and bone fragments through the brain, (3) intracranial pressure (ICP)
changes at the moment of impact, and (4) secondary mechanisms of injury. The
kinetic energy is calculated employing the formula 1/2mv2, where m is
the bullet mass and v is the impact velocity.
At the time of impact, injury is related to (1) the direct crush injury
produced by the missile, (2) the cavitation produced by the centrifugal effects
of the missile on the parenchyma, and (3) the shock waves that cause a stretch
injury. As a projectile passes through the head, tissue is destroyed and is
either ejected out of the entrance or exit wounds or compressed into the walls
of the missile tract. This creates both a permanent cavity that is 3-4 times
larger than the missile diameter and a pulsating temporary cavity that expands
outward. The temporary cavity can be as much as 30 times larger than the missile
diameter and causes injury to structures a considerable distance from the actual
missile tract.
Stab wounds
This group of wounds represents a smaller fraction of penetrating head
injuries. The causes may be from knives, nails, spikes, forks, scissors, and
other assorted objects (see Picture 2 and Picture 3).
Penetrations most commonly occur in the thin bones of the skull, especially in
the orbital surfaces and the squamous portion of the temporal bone. The
mechanisms of neuronal and vascular injury caused by cranial stab wounds may
differ from those caused by other types of head trauma. Unlike missile injuries,
no concentric zone of coagulative necrosis caused by dissipated energy is
present. Unlike motor vehicle accidents, no diffuse shearing injury to the brain
occurs.
Unless an associated hematoma or infarct is present, cerebral damage caused
by stabbing is largely restricted to the wound tract. A narrow elongated defect,
or so-called slot fracture, sometimes is produced by a stab wound and is
diagnostic when identified. However, in some cases in which skull penetration is
proven, no radiological abnormality can be identified. In a series of stab
wounds, de Villiers (1975) reported a mortality of 17%, mostly related to
vascular injury and massive intracerebral hematomas.
Stab wounds to the temporal fossa are more likely to result in major
neurological deficits because of the thinness of the temporal squama and the
shorter distance to the deep brain stem and vascular structures. Patients in
whom the penetrating object is left in place have a significantly lower
mortality than those in whom the objects are inserted and then removed (26%
versus 11% respectively).
Skull perforations and fractures
The local variations in thickness and strength of the skull and the angle of
the impact determine the severity of the fracture and injury to the brain (see
Picture 4 and
Picture 5).
Impacts striking the skull at nearly perpendicular angles may cause bone
fragments to travel along the same trajectory as the penetrating object, to
shatter the skull in an irregular pattern, or to produce linear fractures that
radiate away from the entry defect. Grazing or tangential impacts produce
complex single defects with both internal and external beveling of the skull,
with varied degrees of brain damage.
Clinical: The clinical condition of the patient depends
mainly on the mechanism (velocity, kinetic energy), anatomical location of the
lesions, and associated injuries.
Traumatic intracranial hematomas
These can occur alone or in combination and constitute a common and treatable
source of morbidity and mortality resulting from brain shift, brain swelling,
cerebral ischemia, and elevated ICP. Patients present with the signs and
symptoms of an expanding intracranial mass, and the clinical course varies
according to the location and rate of accumulation of the hematoma. The classic
clinical picture of epidural hematomas is described as involving a lucid
interval following the injury; the patient is stunned by the blow, recovers
consciousness, and lapses into unconsciousness as the clot expands.
Epidural hematomas
Most traumatic epidural hematomas become rapidly symptomatic with progression
to coma. Acute subdural hematoma occurs in association with high rates of
acceleration and deceleration of the head that takes place at the time of
trauma. This remains one of the most lethal of all head injuries because the
impact causing acute subdural hematoma commonly results in associated severe
parenchymal brain injuries.
Intracerebral hematomas
These result from direct rupture of small vessels within the parenchyma at
the moment of impact. Patients typically present with a focal neurological
deficit related to the location of the hematoma or with signs of mass effect and
increased ICP. The occurrence of delayed traumatic intracerebral hematomas is
well documented in the literature.
Delayed intracerebral hematomas
The time interval for the development of delayed intracerebral hematomas
ranges from hours to days. Although these lesions may develop in areas of
previously demonstrated contusion, they frequently occur in the presence of
completely normal results on the initial computed tomography (CT) scan. Patients
with this diagnosis typically meet the following criteria: (1) a definite
history of trauma, (2) an asymptomatic interval, and (3) an apoplectic event
with sudden clinical deterioration.
Contusions
These consist of areas of perivascular hemorrhage about small blood vessels
and necrotic brain. Typically, they assume a wedgelike shape, extending through
the cortex to the white matter. When the pia-arachnoid layer is torn, the injury
is termed a cerebral laceration. Clinically, cerebral contusions serve as
niduses for delayed hemorrhage and brain swelling, which can cause clinical
deterioration and secondary brain injury.
Traumatic subarachnoid hemorrhage
This type of hemorrhage usually is a result of various forces that produce
stress sufficient to damage superficial vascular structures running in the
subarachnoid space. Traumatic subarachnoid hemorrhage may predispose to cerebral
vasospasm and diminished cerebral blood flow, thereby increasing morbidity and
mortality as a result of secondary ischemic damage.
Diffuse axonal injury or shearing injury
This has become recognized as one of the most important forms of primary
injury to the brain. In the most extreme form, patients present with immediate
prolonged unconsciousness from the moment of injury and subsequently remain
vegetative or severely impaired.
 |
INDICATIONS |
Section 3 of 11    |
A critical factor
in early treatment decisions and in long-term outcome after penetrating head
injuries is the patient's initial level of consciousness. Although many methods
of defining level of consciousness exist, the most widely used measure is the
Glasgow Coma Score (GCS) introduced by Teasdale and Jennett in 1974.
Table 1. Glasgow Coma Scale Score
| Points |
Eye Opening |
Best Verbal |
Best Motor |
| 6 |
… |
… |
Follows commands |
| 5 |
… |
Appropriate |
Localizes pain |
| 4 |
Spontaneous |
Inappropriate |
Withdraws to pain |
| 3 |
In response to voice |
Moaning |
Flexion (decorticate) |
| 2 |
In response to pain |
Incomprehensible |
Extension (decerebrate) |
| 1 |
None |
None |
None |
The level of consciousness can be lowered independent of head injury for
numerous reasons, including shock, hypoxia, hypothermia, alcohol intoxication,
postictal state, and administration of sedatives or narcotics. Therefore, a more
reliable assessment of severity and, thus a more meaningful predictor of
outcome, is provided by the postresuscitation GCS, which generally refers to the
best level obtained within the first 6-8 hours of injury following nonsurgical
resuscitation. This allows patients to be categorized into 3 levels, as follows:
- Minor or mild injury includes those patients with an initial level of
13-15.
- Moderate injury includes patients with a score of 9-12.
- Severe injury refers to a postresuscitation level of 3-8 or a subsequent
deterioration to 8 or less.
Patients with severe head injury typically fulfill the criteria for coma,
have the highest incidence of intracranial mass lesions, and require intensive
medical and, often, surgical intervention.
| |
RELEVANT ANATOMY AND CONTRAINDICATIONS
|
Section 4 of 11 |
Relevant
Anatomy: Penetrating objects to the cranium must traverse through the
scalp, through the skull bones, and through the dura mater before reaching the
brain.
The scalp consist of 5 different anatomical layers that include the skin (S);
the subcutaneous tissue (C); the galea aponeurotica (A), which is continuous
with the musculoaponeurotic system of the frontalis, occipitalis, and
superficial temporal fascia; underlying loose areolar tissue (L); and the skull
periosteum (P).
The subcutaneous layer possesses a rich vascular supply that contains an
abundant communication of vessels that can result in a significant blood loss
when the scalp is lacerated. The relatively poor fixation of the galea to the
underlying periosteum of the skull provides little resistance to shear injuries
that can result in large scalp flaps or so-called scalping injuries. This layer
also provides little resistance to hematomas or abscess formation, and extensive
fluid collections related to the scalp tend to accumulate in the subgaleal
plane.
The bones of the calvarium have 3 distinct layers in the adult—the hard
internal and external tables and the cancellous middle layer, or diploë.
Although the average thickness is approximately 5 mm, the thickest area is
usually the occipital bone and the thinnest is the temporal bone. The calvarium
is covered by periosteum on both the outer and inner surfaces. On the inner
surface, it fuses with the dura to become the outer layer of the dura.
Aesthetically, the frontal bone is the most important because only a small
portion of the frontal bone is covered by hair. In addition, it forms the roof
and portions of the medial and lateral walls of the orbit. Displaced frontal
fractures therefore may cause significant deformities, exophthalmus, or
enophthalmos. The frontal bone also contains the frontal sinuses, which are
paired cavities located between the inner and outer lamellae of the frontal
bone. The lesser thickness of the anterior wall of the frontal sinus makes this
area more susceptible to fracture than the adjacent tempora-orbital areas.
The dura mater or pachymeninx is the thickest and most superficial meninx. It
consists of 2 layers—a superficial layer that fuses with the periosteum and a
deeper layer. In the same region between both layers, large venous compartments
or sinuses are present. A laceration through these structures can produce
significant blood loss or be responsible for producing epidural or subdural
hematomas.
Lab Studies:
- The assessment of patients with penetrating brain injuries should include
routine laboratory tests, electrolytes, and coagulation profile.
- Many patients have lost a significant amount of blood before reaching the
emergency department or might present with disseminated intravascular
coagulation (DIC); consequently, determining the hemoglobin concentration and
platelet count is important.
- Type and cross match should always be obtained with the initial
orders.
- Obtaining a toxicology screen, including alcohol levels, also is
appropriate.
Imaging Studies:
- The radiological methods of evaluation depend on the patient's
condition.
- In general, a lateral cervical spine and chest x-rays are obtained in
the resuscitation room.
- A CT scan of the head should be obtained as soon as the patient's
cardiopulmonary condition has been stabilized to determine the extent of
intracranial damage and the presence of intracranial metallic fragments. The
study always should include bone windows to evaluate for fractures,
especially when the skull base or orbits are compromised.
- Some centers can perform computed tomographic angiography (CTA) for the
evaluation of intracranial and extracranial vessels.
- Cerebral angiography: If a vascular injury is suspected and the patient is
stable, cerebral angiography often is used to diagnose injuries such as
carotid and/or vertebral artery dissections, traumatic pseudoaneurysms, or
arteriovenous fistulas.
- Magnetic resonance imaging
- In patients with penetrating injuries and intracranial metallic
fragments, an MRI scan is contraindicated. If the presence of bullets or
intracranial metallic fragments has been ruled out, an MRI scan of the brain
provides valuable information on posterior fossa structures and the extent
of sharing injuries.
- A fluid-attenuated inversion recovery (FLAIR) sequence allows the
evaluation of contusions or hemorrhages.
- Diffusion or perfusion scan sequences are useful to evaluate areas of
stroke or cerebral ischemia.
- Magnetic resonance angiography (MRA) and magnetic resonance venogram
(MRV) are useful if vascular or sinus injuries are suspected.
| |
TREATMENT |
Section 6 of 11 |
Medical
therapy: Patients with severe penetrating injuries
should receive resuscitation according to the Advanced Trauma Life Support
guidelines. Specific indications for endotracheal intubation include inability
to maintain adequate ventilation, impending airway loss from neck or pharyngeal
injury, poor airway protection associated with depressed level of consciousness,
and/or the potential for neurological deterioration.
Virtually all individuals with an admission GCS of 8 or less meet these
criteria. A systolic blood pressure of at least 90 mm Hg should be maintained.
In a large series of patients with severe traumatic brain injury, a single
episode in which systolic blood pressure fell below 90 mm Hg was associated with
an 85% increase in morbidity. Isotonic saline (0.9% NaCl) is the most common
preparation for volume resuscitation. In general, the acute loss of as much as
20% of total blood volume can be replaced with crystalloid solution, while loss
of 30% or more requires replacement with blood.
The cervical spine is stabilized, and a careful examination for injuries to
the neck, chest, abdomen, pelvis, and extremities is performed. A Foley catheter
should be inserted, appropriate IV access secured, and volume replacement
started.
In patients with anterior skull base fractures, nasogastric tubes always
should be avoided because of the increased risk of intracranial tube insertions.
An orogastric tube can be placed carefully under direct vision. During and after
resuscitation, a history is taken, and physical and neurological examinations
are performed.
The GCS (Table
1) should be noted at the scene, upon arrival to the emergency department,
and after resuscitation. If pharmacologic paralytic agents were administered
during resuscitation, these agents should be reversed in order to complete the
neurological examination. Tetanus prophylaxis is administered. Routine
laboratory tests, including CBC, electrolytes, coagulation profile, type and
cross, alcohol levels, and drug screen, are obtained. A sterile dressing is
applied on the entrance/exit wounds, and, if hemodynamically stable, the patient
is sent for diagnostic evaluation.
Patients are triaged based on their clinical condition and findings on CT
scan/angiography. Patients without significant mass lesions on CT scan are
triaged to the intensive care unit (ICU) for further management. An ICP monitor
is placed in all patients with a GCS of 8 or less. Ventriculostomy is preferred
because it is useful both for ICP monitoring and cerebrospinal fluid (CSF)
drainage for control of ICP. Head elevation to 30 degrees appears to facilitate
venous drainage and reduce ICP.
Sedation may be useful in comatose patients for control of ICP. Reversible
agents always should be used to facilitate hourly neurological evaluations. The
authors prefer to use propofol, a lipophilic rapid-onset hypnotic with a short
half-life that can be titrated to control ICP. In addition to monitoring the
ICP, the authors are evaluating the usefulness of other invasive devices, such
as jugular venous catheters and cerebral oximeters, to identify treatable causes
of cerebral ischemia in patients with severe brain injury.
Mannitol administered as intravenous bolus as needed results in decreased
ICP; reduces the viscosity of blood, improving cerebral blood flow; and it might
serve as a free-radical scavenger. Serum osmolality should not be allowed to
rise above 320 mOsm/kg in order to avoid systemic acidosis and renal failure. If
the ICP cannot be controlled, barbiturate coma or a decompressive craniectomy
may be indicated. Barbiturate therapy reduces ICP, cerebral metabolic rate of
oxygen (CMRO2), and cerebral blood flow. Barbiturate coma or a
decompressive craniectomy should be used in conjunction with a Swan-Ganz
catheter to ensure ideal cardiac output. Barbiturates are contraindicated if the
patient is initially hypotensive.
Additional routine orders include seizure prophylaxis (phenytoin 15-18 mg/kg
IV bolus followed by 200 mg IV q12h) and antibiotics. If seizures are not
evident in the acute phase, anticonvulsants are discontinued in 1 week. The
duration of use of antiepileptics remains somewhat controversial, but long-term
use does not seem to be beneficial. Broad-spectrum antibiotics should be
administered for at least a few days postoperatively. The duration of antibiotic
therapy also remains controversial and often is based on the experience of the
surgeon.
Because head injury is an independent risk factor for stress ulcers and
gastritis, prophylaxis with histamine blockers and/or antacids should be
implemented. The stress of head injury, which often is treated in conjunction
with other traumatic injury, leads to increased energy consumption by the
injured patient's body; thus, nutritional support is implemented in the first
few days following admission. Enteral nutrition is employed if no
contraindications exist; whereas, parenteral nutrition is reserved for patients
with associated abdominal injuries at the authors’ institution.
Despite the effectiveness of hyperventilation in rapidly reducing ICP in some
patients, its use is not recommended because it can result in marked reductions
of cerebral blood flow and may worsen long-term neurological outcome
significantly. Also, note that the efficacy of hypothermia remains
controversial, although some studies have shown an improvement in outcome with
moderate hypothermia.
Surgical therapy: The following are significant reasons for
surgery: (1) to remove masses such as epidural, subdural, or intracerebral
hematomas; (2) to remove necrotic brain and prevent further swelling and
ischemia; (3) to control an active hemorrhage; and (4) to remove necrotic
tissue, metal, bone fragments, or other foreign bodies to prevent infections.
The approach to surgery varies; some surgeons are conservative, while others are
more aggressive.
A major reason to operate is the removal of hematomas; however, the minimum
size of hematoma that requires surgical evacuation depends of multiple factors,
including patient's age and clinical condition and the location of the hematoma.
Hematomas and contusions in the temporal region or posterior fossa should be
treated more aggressively because they tend to cause herniation more frequently
than similar lesions elsewhere and more often are associated with vascular
injury.
Bullets and fragments may contain metals that cause electrolysis, may
predispose to fibroglial scarring with secondary epilepsy, or may migrate within
the intracranial or intraspinal compartments. Because retained fragments have
not been associated strongly with infection, most authors have suggested that
they should be removed only if the fragments are accessible. Scalp tissue,
clothes, and hair frequently are carried with bone into the brain, with the
associated risk of infection. This is variable and depends on the velocity of
the bullet and the size of the penetration.
Preoperative details: The approach to surgery varies; some
surgeons are conservative, while others are more aggressive. The surgical
management of penetrating injuries, as with any other neurosurgical procedure,
requires a careful preoperative planning.
- In preparation for surgery, the patient's head is shaved and thoroughly
prepped with an antiseptic solution under routine sterile conditions.
- The patient's head is positioned at a higher level than the chest.
- The head draping should cover all of the available surface of the scalp to
allow extension of the surgical incision beyond the actual confines of the
wound or to allow possible scalp rotation procedures.
- The skin incision is planned so that the blood supply to the scalp is not
compromised.
- Fresh frozen plasma and platelets should be administered (1) when an
elevated prothrombin time (PT) or elevated activated partial thromboplastin
time (aPTT) suggests a coagulopathy in a patient who requires evacuation of an
intracranial hematoma or (2) if an intraoperative coagulopathy is
suspected.
Intraoperative details:
- Often a craniotomy or craniectomy with removal of accessible bone
fragments and foreign bodies is performed.
- Gentle debridement of devitalized brain is performed using a combination
of suction and irrigation.
- In gun shot wounds, the bullet is not removed unless it is easily
accessible because the risk of brain injury from the retrieval of the bullet
exceeds the benefit of its removal.
- In cases of stab wounds, the knife or penetrating object should not be
removed until the dura is opened in the operating room and the procedure can
be performed under direct vision.
- In all cases, the surgeon should be prepared to manage potential vascular
injuries that may be encountered. The importance of a watertight dural closure
cannot be overemphasized in order to prevent centripetal infection and CSF
fistula.
- If a dural defect is present, pericranium or temporalis fascia may be
needed for the dural repair. The use of artificial synthetic or biological
dural substitutes should be avoided.
- Patients with penetrating head injury often require cranioplasty secondary
to craniectomy and/or damage by the missile. Cranioplasty should be delayed
for approximately 1 year, when the patient is medically stable and risk of
infectious complications is low.
Postoperative details: The same principles discussed under
Medical therapy
apply to the postoperative care of patients with penetrating head trauma. An ICP
monitor or a ventricular drain usually is placed intraoperatively in patients
with a GCS of 8 or less. This is placed to monitor and maintain an adequate
cerebral perfusion pressure. If the patient is neurologically stable, a CT scan
is obtained 24-72 hours postoperatively.
Follow-up care: Patients' cases are followed up clinically
with standard neurological checks, and their vital signs are assessed every
hour. Routine laboratory tests are performed as needed.
The follow-up radiological studies to be obtained depend on the patient's
neurological evolution but typically consist of serial CT examinations.
| |
COMPLICATIONS |
Section 7 of 11 |
Patients who
survive penetrating craniocerebral injuries are at risk of experiencing multiple
complications, including persistent neurological deficits, infections, epilepsy,
CSF leak, cranial nerve deficits, pseudoaneurysms, arteriovenous fistulas, and
hydrocephalus.
Intracranial infections
These infections can complicate as many as 11% of penetrating craniocerebral
injuries. Therefore, prevention and proper management of infectious
complications can lead to improved outcome in these patients. Patients can
develop meningitis, epidural abscess, subdural empyemas, or brain abscess.
- Posttraumatic meningitis usually is associated with skull fractures or CSF
leak.
- Cranial epidural abscess is an uncommon infection that most often occurs
secondary to osteomyelitis or because of foreign bodies. The purulent
collection remains well localized due to the tight adherence of the dura to
the overlying calvarium; however, cranial epidural abscess can cause
meningitis and subdural empyema associated with significant morbidity and
mortality.
- The most frequent source of subdural empyema is penetration through
adjacent facial infections, such as paranasal sinusitis or mastoiditis.
- Brain abscess can occur after a long period of silent infection. Hida et
al (1978) reported a case of delayed brain abscess following a penetrating
gunshot injury, found 38 years after the insult. The treatment of epidural
abscess, subdural empyema, and brain abscess consists of prompt surgical
intervention followed by prolonged antibiotic therapy.
Epilepsy
The incidence of posttraumatic epilepsy varies widely, depending on the type
and severity of the injury. In closed head injury, the incidence of
posttraumatic epilepsy varies from 2.9-17% for moderate and severe head injury.
In contrast, the incidence of epilepsy for military craniocerebral missile
wounds is twice as high; most series report a 5- to 10-year incidence of
seizures of 32-51%.
Cerebrospinal fluid leak
Head trauma is the most common cause of CSF leak. Meningitis occurs in
approximately 20% of acute (within 1 wk) posttraumatic leaks and 57% of delayed
posttraumatic leaks. The use of prophylactic antibiotics administration for CSF
leak has been demonstrated to lead to serious infections, including
drug-resistant meningitis.
Patients with posttraumatic CSF leak initially are treated conservatively
with bed rest in a position that results in decrease or cessation of the
fistulous drainage. If the drainage has not ceased within 24-48 hours, a lumbar
drain is inserted and drained at a rate of 10 cc of CSF per hour for 5-7 days. A
lumbar drain should not be inserted in patients with significant pneumocephalus.
During CSF drainage, progressive diminution of the level of consciousness should
alert the clinician to the possibility of pneumocephalus. If the CSF leak does
not stop with the lumbar drainage, a surgical intervention to repair the
fistulous tract may be indicated.
Vascular injuries may result from direct injury of the vessels by the
penetrating object, blast effect at the time of trauma, or by skull fractures or
bone fragments producing vascular occlusion. Direct vascular injuries sustained
at the time of head injury initially may be clinically silent and may remain so
for weeks, months, or years. In addition, delayed posttraumatic pseudoaneurysms
can appear weeks to months after the injury.
Cranial nerve deficits
Patients who experience an injury to the temporal area and/or have a fracture
of the temporal bone are especially at risk for carotid artery injury as well as
injury to the facial nerve. Hence, in patients who experience penetrating brain
injuries, maintaining a high index of suspicion and obtaining follow-up
radiological studies, usually via cerebral angiography, is important.
Pseudoaneurysm
Pseudoaneurysms may result in a perturbation of the normal blood flow and can
act as foci of thrombus formation, or they can rupture, causing a subarachnoid
or intracerebral hematoma. They usually require surgical or endovascular
treatment. The role of anticoagulation in the treatment of pseudoaneurysms
remains controversial, but it may be beneficial in minimizing thrombus
propagation and embolization.
Arteriovenous fistula
Arterial dissections occur when a laceration through the intima and sometimes
the media permits entry of blood and separation of these inner and outer
vascular layers, compromising the vessel lumen. They usually present with
transient ischemic attacks or symptoms of stroke. Nonsurgical management of
arterial dissections with chronic anticoagulation usually is effective.
Probably the best-recognized posttraumatic arteriovenous fistula is the
posttraumatic carotid-cavernous sinus fistula. In general, these fistulae are
associated with the blast injury rather than the intracranial penetration, they
usually are high-flow fistulas, and they are clinically characterized by a
clinical syndrome consisting of pulsating exophthalmos, chemosis, and a bruit.
Carotid-cavernous fistulae can be diagnosed by a cerebral angiography and are
best treated by endovascular occlusion.
| |
OUTCOME AND PROGNOSIS |
Section 8 of 11 |
Many
studies have attempted to associate various prognostic factors with outcome. The
most important prognostic factor currently recognized is the GCS after
cardiopulmonary resuscitation. Traditionally, the higher the GCS after
resuscitation, the better the patient outcome. However, concern has developed
that, because patients who present in coma are thought to have a dismal
prognosis, less aggressive management often is employed, contributing to the
poorer outcome.
Studies over the last decade have examined the outcome of patients with a
postresuscitation GCS of 3-5 who underwent aggressive medical and surgical
management. Grahm et al (1990) found that no patient in a study of 100 patients
with postresuscitation GCS of 3-5 had a satisfactory outcome (good/moderately
disabled). They also found that no patients with a GCS of 6-8 and bihemispheric
or multilobar dominant hemisphere injuries had a satisfactory outcome.
In a review of 190 patients, Levy et al (1994) found that only 2 patients
with a GCS of 3-5 achieved a moderately disabled outcome. Further analysis
showed that these patients had reactive pupils at admission and did not have
bihemispheric/multilobar dominant hemispheric injuries. They concluded that
surgical intervention is not beneficial in most patients with a GCS of 3-5 but
may be beneficial for the rare patient with reactive pupils but without ominous
findings on CT scan. Despite these studies, some controversy remains regarding
surgery performed on patients with a GCS of less than 9 and especially regarding
patients with a GCS of less than 5.
Other poor prognostic factors include age, suicide attempt, and
through-and-through injuries. Patients who present with high ICP and/or
hypotension also tend to have worse outcomes. CT scan findings associated with
poor outcome include (1) bihemispheric injury, (2) intraventricular and/or
subarachnoid hemorrhage, (3) mass effect and midline shift, (4) evidence of
herniation, and/or (5) hematomas greater than 15 mL on CT scan. Morbidity and
mortality rates associated with penetrating brain injury remain unacceptably
high. For patients presenting with a GCS of 3-5, mortality rates remain near
90%, and a satisfactory outcome as defined by the GCS only rarely occurs.
Patients presenting with a GCS of 6-8 have a more variable outcome that may be
related to differences in management and/or the smaller numbers of patients
presenting in this category. Patients with a GCS greater than 9 have much lower
mortality rates. Approximately one half of these patients make good recoveries,
and 90% have satisfactory outcomes.
| |
FUTURE AND CONTROVERSIES
|
Section 9 of 11 |
Many
penetrating head injuries are incompatible with life, and people with these
injuries often die almost immediately. Moderately injured patients more
frequently are resuscitated and receive treatment. Upon presentation, beginning
aggressive medical and surgical treatment is important in patients who may
benefit from these interventions. Aggressive treatment of secondary mechanisms
of injury must be initiated, and the patient must be monitored closely for
possible complications.
Kaufman et al (1991) found that considerable variability exists among
neurosurgeons currently as to what constitutes appropriate treatment of
penetrating head injury. In particular, wide variations exist in the amount of
surgical debridement performed, the use of ICP monitoring, and the use of
various medical therapies. Duration of antiepileptics and antibiotics remains
controversial, as does the use of hyperventilation, hypothermia, and steroids.
Use of jugular bulb catheters and transcranial Doppler is institution-dependent.
Considerable research continues in the area of neurotrauma. Once secondary
mechanisms of injury are better understood and treatment modalities are studied
in prospective randomized clinical trials, less variation in management of
penetrating head injury is likely to occur. The medical community as a whole
will become more successful in the treatment of these patients.
Aggressive intensive care management in combination with surgical
intervention, when appropriate, already have reduced the mortality and morbidity
associated with these injuries significantly. Primary prevention of these
injuries remains important. With the increasing numbers of firearms and
firearm-related violence in our society, discussing the issues of violence with
patients and offering appropriate intervention becomes the duty of all
physicians.
| |
PICTURES |
Section 10 of 11 |
| |
BIBLIOGRAPHY |
Section 11 of 11  |
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