Penetrating Head Trauma
- Author: Federico C Vinas, MD; Chief Editor: Brian H Kopell, MD more...
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.
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 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, 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. 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.
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.
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.
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.
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.
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.
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. 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 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, 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.
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.
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.
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.
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 (Open Table in a new window)
|Points||Eye Opening||Best Verbal||Best Motor|
|4||Spontaneous||Inappropriate||Withdraws to pain|
|3||In response to voice||Moaning||Flexion (decorticate)|
|2||In response to pain||Incomprehensible||Extension (decerebrate)|
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.
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.
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|Points||Eye Opening||Best Verbal||Best Motor|
|4||Spontaneous||Inappropriate||Withdraws to pain|
|3||In response to voice||Moaning||Flexion (decorticate)|
|2||In response to pain||Incomprehensible||Extension (decerebrate)|