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.[1, 2]
Analysis of the trauma literature has shown that 50% of all trauma deaths are secondary to traumatic brain injury (TBI), and gunshot wounds to the head caused 35% of these. 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 CT scan below is of a patient after a gunshot wound to the brain.
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A young man arrived in the emergency department after experiencing a gunshot wound to the brain. The entrance was on the left occipital region. A CT s....
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.
For excellent patient education resources, visit eMedicineHealth's Brain and Nervous System Center. Also, see eMedicineHealth's patient education article Brain Infection.
The earliest reported series of 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.
A dramatic increase in the incidence of penetrating injuries to the brain has occurred,[3] with gunshot wounds to the head becoming the leading or second leading cause of head injury in many cities in the United States.[4, 5, 3] These injuries are devastating to the patient, family, and society.
Siccardi et al 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.[6] 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.[3] 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.[7]
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. Firearms account for the largest proportion of deaths from traumatic brain injury in the United States. Each year close to 20,000 persons in the United States are involved in gunshot wounds to the head.[8, 9]
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 are typically 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.[10, 11]
In a study of 14 children with intracranial injuries due to spring- or gas-powered BB or pellet guns, 10 of the children required surgery, and 6 were left with permanent neurologic injuries, including epilepsy, cognitive deficits, hydrocephalus, diplopia, visual field cut, and blindness. According to the study authors, advances in compressed-gas technology have led to a significant increase in the power and muzzle velocity of such guns, with the ability to penetrate a child's skull and brain.[12]
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.[13] 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, as shown in the image below, or shotguns to high-velocity metal-jacket bullets fired from military weapons.[14, 15] 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.
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A 65-year-old man experienced a gunshot wound to the right frontoparietal region. A CT scan shows that the bullet crossed the midline, lacerated the s....
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 with only 20% of those with penetrating wounds.[16]
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, example depicted below, represents a smaller fraction of penetrating head injuries. The causes may be from knives, nails, spikes, forks, scissors, and other assorted objects.[10] 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.
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A CT scan of a young female who presented to the emergency department with a stab wound to the head produced by a large knife shows the extent of intr....
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 reported a mortality of 17%, mostly related to vascular injury and massive intracerebral hematomas.[11]
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).[11]
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, as shown below. 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.
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Lateral skull x-ray film of a patient who presented with a severe intracranial injury produced by a golf club.
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The patient presented to the emergency department with a golf club in his head. The club was removed in the operating room.
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.
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 Scale (GCS) introduced by Teasdale and Jennett.
Table. Glasgow Coma Scale
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See Table
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 score (hereafter referred to as GCS), which generally refers to the best level obtained within the first 6-8 hours of injury following nonsurgical resuscitation.[7, 9] 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.
Lack of abnormal pupillary response to light and the visibility of basal cisterns may increase the need for urgent care. In those with injuries close to the Sylvian fissure and with a projectile fragment crossing 2 dural compartments, computed tomography angiography and, if needed, digital subtraction angiography may be needed to rule out traumatic intracranial aneurysms.[9]
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 calvaria 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 calvaria 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.
In a study of 786 patients with gunshot wounds to the head, 712 (91%) died. Admission GCS score, trajectory of the missile track, abnormal pupillary response (APR) to light, and patency of basal cisterns were significant determinants of patient outcome. Exclusion of GCS score from the regression models indicated missile trajectory and APR to light were significant in determining outcome.[17]
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, is also appropriate.
The radiological methods of evaluation depend on the patient's condition. In general, a lateral cervical spine and chest radiographs 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. Multidetector-row CTA has improved the detectability of both vascular and extravascular injuries in patients with penetrating injuries.[8, 18, 19]
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.
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.
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 score (see Indications section) 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 count, 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° appears to facilitate venous drainage and reduce ICP.
Sedation may be useful in comatose patients for control of ICP. Reversible agents should always 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.
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 are frequently 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. In most cases, removal of a deep-seated bullet is not necessary, however, some authors have advocated the used of computer-image guided procedures for the removal of missiles or bullet fragments.
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 the entire 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.
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 gunshot 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.
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.
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.
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.[20] 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 calvaria; 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.[21] The treatment of epidural abscess, subdural empyema, and brain abscess consists of prompt surgical intervention followed by prolonged antibiotic therapy.
Epilepsy
Posttraumatic epilepsy is linked to psychosocial disability and is probably a contributing factor to premature death after penetrating head injury.[15] 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%. Almost 50% of victims of penetrating head trauma enrolled in military series become epileptic.
The exact pathophysiology of posttraumatic epilepsy after closed or penetrating head injury is not known. Many confounding risk factors, such as retained metal fragments, the extent and site of injury, level of consciousness, residual focal deficit, and complications, have been studied to pinpoint the importance of each in efforts to clarify the pathophysiological mechanisms of posttraumatic epilepsy.
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 are initially 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 is usually 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 are usually high-flow fistulas, and they are clinically characterized by a clinical syndrome consisting of pulsating exophthalmos, chemosis, and bruit. Carotid-cavernous fistulae can be diagnosed by a cerebral angiography and are best treated by endovascular occlusion.
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 is often used, 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).[4] 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.[7] 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.
The results from one study found that insulin deficiency due to diabetes mellitus (DM) imparts an increased risk for mortality in patients with moderate-to-severe traumatic brain injury (TBI) compared with patients without DM (14.4% versus 8.2% ).[22]
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 found that considerable variability exists among neurosurgeons currently as to what constitutes appropriate treatment of penetrating head injury.[23] 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.[24] 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 has significantly reduced the mortality and morbidity associated with these injuries. 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 health care providers.
Federico C Vinas, MD, Consulting Neurosurgeon, Department of Neurological Surgery, Halifax Medical Center
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Ryszard M Pluta, MD, PhD, Associate Professor, Neurosurgical Department Medical Research Center, Polish Academy of Sciences, Poland; Clinical Staff Scientist, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH); Fishbein Fellow, JAMA
Disclosure: Nothing to disclose.
Chief Editor
Brian H Kopell, MD, Associate Professor, Department of Neurosurgery, Icahn School of Medicine at Mount Sinai
Disclosure: Received consulting fee from Medtronic for consulting; Received consulting fee from Abbott Neuromodulation for consulting.
Additional Contributors
Michael G Nosko, MD, PhD, Associate Professor of Surgery, Chief, Division of Neurosurgery, Medical Director, Neuroscience Unit, Medical Director, Neurosurgical Intensive Care Unit, Director, Neurovascular Surgery, Rutgers Robert Wood Johnson Medical School
Disclosure: Nothing to disclose.
Acknowledgements
Julie Pilitsis, MD Staff Physician, Department of Surgery, Division of Neurosurgery, Wayne State University
Julie Pilitsis, MD is a member of the following medical societies: American Medical Association
De Villiers JC. Stab wounds of the brain and skull. Vinken PJ, Bruyn GW, eds. Handbook of clinical neurology. New York, NY: Elsevier Science Publishing; 1975. Vol 23: 407-503.
Aarabi B. History of the management of craniocerebral wounds. Aarabi B, Kaufman HH, Dagi TF, George ED, Levy ML, eds. Missile Wounds of the Head and Neck. Park Ridge, Ill: American Association of Neurological Surgeons; 1999. Vol 1: 281-292.
Chesnut RM, Marshall LF, Marshall SB. Medical management of intracranial pressure. Cooper PR, ed. Head Injury. 3rd ed. Baltimore, Md: Williams & Wilkins; 1993. 225-246.
Feldman Z, Narayan RK, Robertson CS. Secondary insults associated with severe closed head injury. Contemporary Neurosurgery. 1992. 14:1-8.
Giannotta SL, Gruen P. Vascular complications of head trauma. Barrow DL, ed. Complications and sequelae of head injury. Park Ridge, Ill: American Association of Neurological Surgeons; 1992. 31-49.
Harris ME, Barrow D. Traumatic carotid-cavernous fistulas. Barrow DL, ed. Complications and sequelae of head injury. Park Ridge, Ill: American Association of Neurological Surgeons; 1992. 13-30.
Rosenberg WS, Harsh GR. Penetraing wounds of the head. Wilkins RH, Rengachary SS, eds. Neurosurgery. New York, NY: McGraw Hill; 1996. Vol 2: 2813-2820.
Salazar AM, Aarabi B, Levi L. Postraumatic epilepsy following craniocerebral missile wounds in recent armed conflicts. Aarabi B, Kaufman HH, Dagi TF, George ED, Levy ML, eds. Missile Wounds of the Head and Neck. Park Ridge, Ill: American Association of Neurological Surgeons; 1999. Vol 2: 281-292.
A young man arrived in the emergency department after experiencing a gunshot wound to the brain. The entrance was on the left occipital region. A CT scan shows the skull fracture and a large underlying cerebral contusion. The patient was taken to the operating room for debridement of the wound and skull fracture, with repair of the dura mater. He was discharged in good neurological condition, with a significant visual field defect.
A 65-year-old man experienced a gunshot wound to the right frontoparietal region. A CT scan shows that the bullet crossed the midline, lacerated the superior longitudinal sinus, and produced a large midline subdural hematoma. The patient presented with a Glasgow Coma Scale (GCS) score of 4 and died.
A CT scan of a young female who presented to the emergency department with a stab wound to the head produced by a large knife shows the extent of intracranial damage, which affects midline structures.
Lateral skull x-ray film of a patient who presented with a severe intracranial injury produced by a golf club.
The patient presented to the emergency department with a golf club in his head. The club was removed in the operating room.
A young man arrived in the emergency department after experiencing a gunshot wound to the brain. The entrance was on the left occipital region. A CT scan shows the skull fracture and a large underlying cerebral contusion. The patient was taken to the operating room for debridement of the wound and skull fracture, with repair of the dura mater. He was discharged in good neurological condition, with a significant visual field defect.
Lateral skull radiograph of a young female who presented to the emergency department with a stab wound to the head produced by a large knife.
A CT scan of a young female who presented to the emergency department with a stab wound to the head produced by a large knife shows the extent of intracranial damage, which affects midline structures.
Lateral skull x-ray film of a patient who presented with a severe intracranial injury produced by a golf club.
The patient presented to the emergency department with a golf club in his head. The club was removed in the operating room.
A 65-year-old man experienced a gunshot wound to the right frontoparietal region. A CT scan shows that the bullet crossed the midline, lacerated the superior longitudinal sinus, and produced a large midline subdural hematoma. The patient presented with a Glasgow Coma Scale (GCS) score of 4 and died.
Intraoperative view of a middle-aged male with an open depressed skull fracture.
Intraoperative view the surgical reconstruction repair of a complex skull fracture.
A 57-year-old male who suffered a motorcycle accident. He was not wearing a helmet. He suffered a severe abrasion with tissue loss through skin, temporalis muscle, temporal bone, and dura. Note brain tissue exposed through his wound. He was taken urgently to surgery for debridement and reconstruction using a rotational flap.
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