Ballistics, Wounding Energy, and Pathogenesis

There are three components to ballistics: (1) interior, (2) exterior, and (3) terminal. Interior ballistics is defined as the science of motion of a projectile through a gun barrel as a result of combustion and expansion of a powder charge, a science extensively studied in the early 18th century by the British scientist Benjamin Robins and the Anglo-American researcher Benjamin Thompson.^44,45 Exterior ballistics is the projectile’s behavior in a medium such as air and is dependent on the projectile’s shape, caliber, weight, initial velocity, and ballistic coefficient. Niccolo Tartaglia and Galileo defined the parabolic trajectory of a bullet in space until it loses all of its kinetic energy.^44–50 The behavior of a projectile on impacting its target is termed terminal ballistics. Factors important in terminal ballistics include penetration, tissue density, fragmentation, detonation, shape of the charge, blast overpressure, combustion, and incendiary effect.^{44–46,48,50} The science of ballistics has evolved considerably since 1411 when the first matchlocks appeared in Europe. The introduction of rifling in 1520, elongated bullets by Delvigne in 1841, minié bullets in 1847, and breech loading and coated bullets in the 1850s resulted in projectiles with velocities greater than 2000 ft/sec (615 m/sec).^{44,45,50–52} The wounding energy (E) of a projectile depends mainly on its weight and velocity; hence, E = M(VI² − VR²), where M is the projectile’s weight, VI is the impact velocity, and VR is the residual velocity if the projectile has a perforating mode.^45,53 The small-firearm injuries encountered in civilian GSWHs follow conventional ballistic rules of wounding energy; however, when the velocity of a projectile crosses 700 m/sec, the wounding energy depends on the power (P) of the projectile and is expressed as P = MV³. Many of the victims in the vicinity of a cased explosive or an improvised explosive device (IED) will incur injuries by fragments with a velocity of greater than 700 m/sec and low ballistic coefficient. Translation of kinetic energy into tissue damage is brought about by the tremendous amount of crushing pressure exerted on the brain parenchyma. Juxtamissile pressure affects the brain tissue immediately in the path of a projectile and may be in the thousands of atmospheres. Longitudinal strong shock waves (Fig. 336-1) start immediately after impact of the projectile with brain tissue and travel in spheres ahead of the projectile with velocities in excess of 1460 m/sec.⁵⁴ Shock waves last up to 10 µsec and measure up to 80 atm. Ordinary pressure waves measuring up to 20 to 30 atm are generated as the projectile transfers its kinetic energy to the surrounding brain tissue and produces a temporary cavity.⁵⁴ The negative pressure generated by the temporary cavity can suck contaminated material into the cavity, which must be débrided during surgical management of the permanent cavity.^45,54,55 Experiments with 20% gelatin have indicated that as the projectile is dissecting its way through a gelatin cube, it produces a head cone and a tail splash (Fig. 336-2).^55,56 Tissue density is critical in defining parenchymal damage. Solid organs such as the brain have tissue densities up to 800 times that of air, thus giving high-velocity bullets explosive power.⁵² The sectional area defines the impact surface of a projectile and is determined by the shape and flight characteristics of a projectile, including yaw (Fig. 336-3), spin, precession, tumbling, nutation, and drag, all of which determine the ballistic coefficient.^{44–51,54,56–58} GSWHs, being contact or near-contact injuries, not only plow through the brain but also deposit a tremendous amount of energy that disrupts brain tissue and major blood vessels, displaces the brainstem, arrests cardiorespiratory function, and results in instantaneous death in more than 70% of victims (Fig. 336-4).^31–3354

FIGURE 336-1 Schematic representation of longitudinal shock waves.

FIGURE 336-2 Schematic representation of the temporary cavity produced by a fragment generating ordinary pressure waves as it enters a cube of gelatin. For details see text.

FIGURE 336-3 Schematic representation of yaw as a bullet is traveling along its longitudinal axis in a medium such as air or brain.

FIGURE 336-4 Non–contrast-enhanced computed tomographic view of a typical perforating civilian gunshot wound to the head crossing the sagittal plane, involving at least two lobes, and complicated by intracerebral and subdural hematomas and intraventricular hemorrhage. The permanent cavity is indicated by white lines. BF, bullet fragment; EN, entrance; EX, exit; ICH, intracerebral hematoma; IVH, intraventricular hemorrhage; RB, retained bone; SDH, subdural hematoma.

The science of ballistics and quantification of the wounding energy in cased ammunitions and complex explosives, such as car bombs and IEDs, is much more unpredictable in that it is a combination of primary blast overpressure, PBI, and closed head injury.^{4,10,11,13,16} Although injuries during the American Civil War were primarily due to bullets, injuries in subsequent international and regional conflicts have been caused to a major extent by shell fragments.^55,59–64 In a recent presentation at the annual meeting of the conference on Advanced Technology Applications for Combat Casualty Care (ATACCC) in Florida, Bell and coauthors reported that 228 of 408 patients who sustained TBI in OIF suffered PBI and 139 had closed head injury.⁶⁵ In 229 patients the predominant mechanism was exposure to complex explosive devices, which resulted in significant blast overpressure on the brain parenchyma in addition to PBI and closed TBI (Fig. 336-5). Additional mechanisms behind TBI in modern warfare and terror attacks include thermal and ischemic injuries and energy sources not appreciated in a typical measurement spectrum, such as electromagnetic energy.^4,10,11 Fragments tend to most commonly be low-velocity spall (see Fig. 336-7).^{4,10,11,60,63,66–70} This spall can emanate from the casing of the explosive device and from packed supplemental bolts, nails, ball bearings, or the metal from a vehicle-borne explosive (i.e., a car bomb). In some cases this spall can also contain body parts of the suicide bomber, window frames, glass, gravel, or in-driven bone fragments acting as secondary impacting fragments. When such explosives impact a patient, the results vary. Factors such as proximity to the explosion, protection by both personal and vehicular armor, and the effect of the environment are all important.⁴ Open field explosions are less likely to have the effect of reverberating pressure waves, building collapse, or fragmenting glass, as is commonly seen when victims are located within a closed structure.⁴ Explosions occurring within a closed space are particularly lethal because of the proximity to the explosion, the incendiary nature of the blast, and the reverberation of the blast force.^4,10,16 This lethality is commonly witnessed in bombs detonated in buses, trains, planes, and enclosed buildings.^69,70 The number of survivors is typically inversely proportional to the size of the enclosure, with bus bombs having the highest lethality.⁶⁹

FIGURE 336-5 Computed tomographic scans from a 21-year-old soldier victim of a suicide bomber. Patient had an initial Glasgow Coma Scale score of 6 that rapidly dropped to 4, indicative of severe swelling of the brain, obliteration of the basal cisterns, subarachnoid and intraventricular hemorrhage, and widespread ischemia. The patient expired despite urgent decompressive craniectomy.

Pathology

Low-velocity sharp objects, which lack any definable ballistics, penetrate the scalp, skull, and dura and lacerate the brain parenchyma, including the cortex, subcortical white matter, basal ganglia, and diencephalon or brainstem and any blood vessels in their path (Fig. 336-6).^71,72 Similarly, low-velocity projectiles from artillery shells, IEDs, and spent bullets cut into the brain just like sharp objects do (Fig. 336-7). The focal motor, cognitive, and behavioral consequences of these injuries depend on the neuronal circuitry that is interrupted and the completeness of injury to blood vessels, hence producing subarachnoid hemorrhage, intracranial hematomas or traumatic intracranial aneurysms (TICAs), and arteriovenous fistulas (AVFs).^71–83

FIGURE 336-6 Composite picture of a cranial stab wound. Plain skull film indicating the extent of penetration of the left supraorbital region (A), three-dimensional and transaxial computed tomography of the head depicting the site of penetration into the left frontal lobe (B and C), and a left carotid cerebral angiogram showing no evidence of any vascular lesion. ICA, internal carotid artery, K, knife.

FIGURE 336-7 Computed tomographic scan of the head of a 28-year-old soldier with a small left frontal injury from a shell fragment and a schematic representation showing it penetrating the brain without forming a major permanent cavity.

The pathology with contact or near-contact injuries by civilian GSWHs is much more devastating.^{23,27,40,41,84} In a detailed necropsy study of 254 patients who died of firearm injuries, Freytag noticed single-track injury (permanent cavity) from ricochets in 82% of cases and multiple tracks in the remaining cases. In her study an ischemic ring was seen surrounding the permanent cavity and was topped by a layer of small hemorrhages from disruption of blood vessels.²³ A robust class III literature indicates that in victims of civilian GSWHs who survived the initial injury to reach a trauma center, the path of penetration and the extent of brain injury defined the mortality. The mortality was 48% after lobar injuries,^{22,31,41,42,85,86} 72% after unilateral multilobar injuries,^22,31,35,43 77% if the midsagittal plane was crossed,^{22,30,31,40–43,87} 84% if the midcoronal plane was crossed,^86,87 and 96% if both the midsagittal and midcoronal planes were crossed.^86,87 In 2000, 45 patients survived long enough to reach one of the eight trauma centers in the state of Maryland. Of the 24 patients admitted to the shock trauma center, 10 survived: 2 of 12 patients with perforating, 5 of 9 patients with penetrating, and 3 of 3 patients with tangential injuries. The relationship of the injury mode to mortality was also reflected in 816 soldiers from the Iran-Iraq War.⁸⁸ In this study the proportion of patients who survived a median of 41 hours to reach an academic center were as follows: 54.8% with penetrating, 22.4% with tangential, and 7.5% with perforating injuries. The incidence of intracranial hematomas differs between reports: acute subdural hematoma, 3% to 56%^27,42; intracerebral hematomas, 4% to 37%^24,42; intraventricular hematoma, 1% to 56%^24,27; and subarachnoid hemorrhage, 9% to 78%.^21,35

In soldiers with varying amounts of body armor, the pattern is quite different. What had previously been fatal PBIs now become treatable brain injuries as a consequence of secondary damping of energy by the helmet.^4,11,15 The energy absorbed by the helmet results in mechanical deformation of the inner and outer protective covering of the shield. The outer deformity tends to be smaller and focal and rarely completely penetrates, whereas the inner deformity tends to have a broader base with less depth and also rarely penetrates. The deformation of the inner aspect of the helmet may impact on the underlying scalp, transfer energy to the skull, and deform the calvaria and intracranial compartments. A piston-like deformity of this inner table can lead to a stellate scalp laceration with a severe abrasion or burn, and the resulting impact on the skull leads first to a fracture and loss of anatomic continuity of the skull. In extreme cases, commonly seen after an IED impact, the dura is violated and the local cerebral tissue will be contused by both blunt trauma and secondary impacting fragments of bone or body armor (or both). These fragments of bone typically course in a radial direction from the point of impact. Traveling perpendicular to the cortical vasculature underlying the sulci and gyri, they disrupt the vessels in their path (Fig. 336-8).

FIGURE 336-8 A, Computed tomographic scan of the head of a soldier with a secondary blast injury to the neck at the level of C2 and subarachnoid hemorrhage at the level of left cerebellopontine angle (arrows). B, Lateral vertebral angiogram showing a barely visible traumatic aneurysm (arrow) at the takeoff of the posterior inferior cerebellar artery. C, Lateral vertebral angiogram 5 days after evacuation showing a traumatic intracranial aneurysm (arrow) that was coiled. D, Angiogram indicating complete obliteration of the aneurysm.

Military personnel incurring complex injuries from explosive devices sustain blast overpressure and penetrating or closed head injuries.^4,11,13,16 Reporting on 234 American soldiers who were evacuated a mean of 7.4 ± 8.6 days after their war injuries, Bell and coauthors noted severe head injury (Glasgow Coma Scale [GCS] score <9) in 61 (26%).⁶⁵ It was projected that a significant proportion of wounded OIF soldiers suffered from high-frequency low-amplitude or low-frequency high-amplitude shock waves, which rendered these injuries much more complex to comprehend.^4,10,16 Low-intensity blast waves are not necessarily accompanied by pulmonary or gastrointestinal injuries. Because disruptive energy is transmitted to the brain with complex and high-energy blasts and may even occur through major blood vessels, TBI is not prevented by a protective helmet.¹⁰ High- and low-frequency blast waves disrupt the blood-brain barrier and produce massive brain swelling in a very short time,^89–92 thereby necessitating urgent decompressive craniectomy, and when low in energy, such blast waves may result in cytoskeletal and diffuse axonal injury that leads to neurodegeneration.^{4,10,11,20,93}

Clinical Findings

Level of Consciousness

When sharp objects,^{71,72,76,79,83} low-velocity spall,^{59,60,63,64,66,100} and spent bullets penetrate the brain, they may cause focal deficits; however, if they do not disrupt the neuronal circuitry in the brainstem tegmentum or ascending reticular activating system, they may not cause a depressed level of consciousness or coma.^{18,27,71,72,76,79,83,101–108}

In civilian PBI an altered level of consciousness is the rule.* In a prospective study of 100 civilian GSWHs by the Barrow Neurological Institute, Grahm and associates reported postresuscitation GCS scores to be 3 to 5 in 58 patients, 6 to 8 in 8 patients, 9 to 12 in 12 patients, and 13 to 15 in 22 patients.⁴¹ Unpublished data from the University of Maryland Trauma Registry in Baltimore showed 333 patients with GSWHs in the period 2000 to 2005.⁹⁹ Of these 333 patients, 187 (56%) had a GCS score of 3 to 5, 31 (9%) a GCS score of 6 to 8, 20 (6%) a GCS score of 9 to 12, and 95 (29%) a GCS score of 13 to 15. Similarly, Liebenberg and coauthors reported a GCS score of 3 to 8 in 70.4% of their patients evaluated from West Sussex England (Fig. 336-9).²⁸

FIGURE 336-9 Stratified admission Glasgow Coma Scale (GCS) scores of victims of penetrating brain injury from the frontlines of the Iran-Iraq War, the Israeli involvement in Lebanon, and civilian gunshot wounds to the head (see references 41, 60, 66, 99).

Military experience in recent years has recorded varied levels of consciousness at the time of arrival at a medical facility. In 1990, Aarabi reported the functional outcomes of 435 patients from the Iran-Iraq War.⁶⁶ In that study, 274 (63%) patients were admitted to a tertiary hospital with a GCS score of 13 to 15, 57 (13%) with a GCS score of 9 to 12, 58 (13%) with a GCS score of 6 to 8, and 46 (11%) with a GCS score of 3 to 5. In 1991, Brandvold and coworkers, reporting on 113 war casualties from the Israeli involvement in Lebanon, recorded 41% with a GCS score of 13 to 15, 16.5% with a GCS score of 9 to 12, 9.5% with a GCS score of 6 to 8, and 33% with a GCS score of 3 to 5.⁶⁰ Natural selection by prolongation of time at the scene may explain some of the differences. In the Iran-Iraq War, time after injury to admission to the tertiary academic facility was 49 hours, whereas in Israel the average time at the scene was 2 hours.^60,110 Bell and colleagues recorded the following GCS scores in 234 patients from OIF who were treated by neurosurgeons within 0.5 to 1.5 hours of their injury and evacuated to the continental United States (CONUS) within 7 days of their injury, with the last 38 patients arriving in CONUS within 4 days of their injury: GCS scores of 12 to 15 in 103, 9 to 11 in 70, 6 to 8 in 37, and 3 to 5 in 24 subjects.⁶⁵ In a report presented by Ling, almost 20% of the military personnel deployed in OIF were subject to TBI; however, only a minority suffered secondary blast injuries and had a very low GCS score.⁴

Management

Surgical Management

Débridement and Repair of the Scalp

Scalp lacerations from missile head wounds are usually contaminated, have devitalized edges, and may be hard to repair. Several studies have indicated that wound contaminants originate from organisms on the skin of the soldier or civilian subject. Staphylococci with or without gram-negative organisms (coliform bacteria, Aerobacter aerogenes, Klebsiella species, and Acinetobacter species) were the most frequently encountered skin contaminants during WWII and the Vietnam and Iran-Iraq wars.^{67,134,146,147} Preliminary unpublished data indicate that Acinetobacter species is one of the contending organisms encountered in OIF, and it was also cultured from the skin of soldiers during the Iran-Iraq War.^134,148 When scalp is penetrated by a projectile, it is shredded, torn, or burned with devitalized edges of up to a few millimeters. If feasible, it is strongly recommended that a plastic surgeon be consulted for primary closure of the skin over a torn dura, especially if the dural tear is at the base in the vicinity of the basal cisterns, near the air sinuses or mastoid air cells, to prevent CSF fistulas.^88,132 In addition, patients with ventricular penetration are subject to CSF leakage from the skin incision.⁸⁸ Tripod incisions are not favored because of the possibility of delayed healing at their center. The skin edges are débrided and approximated in two layers. We prefer a continuous monofilament skin closure. Sutures are not to be removed for up to 2 weeks.

Craniectomy versus Craniotomy

Although craniectomies around the entrance site of a projectile have been the favored technique in previous military conflicts,^{60,63,67,88,100,149} the present recommendation is craniotomy and débridement of the skull with replacement of the bone to avoid the future need for cranioplasty. Contrary to civilian decompressive craniectomies, where the bone flap is stored in a tissue bank or the patient’s abdominal wall for future reimplantation, this policy was stopped in OIF because of the increased risk for contamination and infection at the implanted site.^89,148

Débridement and Watertight Closure of the Dura Mater

In complex orbitofaciocraniocerebral and temporal fossa injuries with exposed air sinuses and mastoid air cells and in patients with extensive injury to the scalp, dura, and brain, a multidisciplinary approach to repair the dura and scalp is necessary to prevent postoperative CSF fistulas and deep infections.^110,132

Débridement of Devitalized Brain

The degree of surgical débridement of devitalized brain tissue remains controversial.⁶¹ On the basis of class III historical and limited experimental evidence,^{129,137–140,150–154} traditional protocol-driven military practices have been aggressive débridement and an attempt to extract all retained bone fragments.^{61,67,110,155} Brandvold and colleagues,⁶⁰ Taha and associates,¹⁵⁶ and more recently Amirjamshidi and coworkers,¹³⁵ based on their experience in Israel, Lebanon, and Iran, respectively, have reported on minimal débridement of missile head wounds in special circumstances (Figs. 336-10 and 336-11). Although we agree that every effort should be made to preserve eloquent cortex, one needs to understand that civilian GSWHs and a significant number of military missile head wounds are much more devastating and must be managed in consultation with ear, nose, and throat, ophthalmologic, oromaxillofacial, and plastic surgeons to preserve the integrity of the basal dura in the region of the orbits, mastoid air cells, and air sinuses.^{61,88,132,133,141} Minimalism is only applicable to small fragments with small entrance wounds and no evidence of massively devitalized scalp and no penetration of the air sinuses, ventricular system, or mastoid air cells. In a recent analysis of the data reported by the aforementioned authors, Carey found increased risk for deep infections with minimally débrided missile head wounds.⁶¹

FIGURE 336-10 Computed tomographic scan and its schematic representation of a tangential civilian gunshot wound to the head involving the left temporoparietal region. Retained bone fragments and intracerebral hematoma are indicated.

FIGURE 336-11 Schematic representation of adequate débridement and watertight closure of the dura and scalp.

Débridement of Retained Fragments

Retained bone fragments after a missile head wound with or without previous débridement are always a source of worry. Reports from WWII and the Vietnam War indicate that retained bone fragments could be a source of abscess and deep infections.^{67,129,137–140,152,154,157} Retained bone fragments after satisfactory débridement may not cause significant infection over the long run, and there does not seem to be a reason for aggressive pursuit of the fragments.^88,136

Repair of the Skull Base

Recent wartime explosive injuries from a transfrontal or transtemporal direction may disrupt the anterior and lateral skull base. Such injuries are associated with significant risk for CSF leaks and loss of anatomic continuity between the anterior cranial fossa, orbits, maxilla, and infratemporal fossa. During the recent conflict this has led to an aggressive strategy of early skull base repair with titanium mesh, local pericranium, fat, temporalis fascia, and muscle. This step is followed by more extensive skull base reconstruction at level 5 medical centers consisting of rotational or myocutaneous free flaps in patients with persistent CSF leaks, progressive skull base deformity, and encephalocele.^{88,110,132,133,148}

Complications

Vascular Injuries with Gunshot Wounds to the Head

The true incidence of traumatic neurovascular injury in patients with blast overpressure, closed brain injury, and PBI remains largely speculative.^{19,27,101,102,106,131,158} The incidence of TICA after such injuries ranges from 3% to 40%, depending on the timing of imaging studies. The urgency to detect and intervene is related to the consequences (delayed traumatic intracerebral hematoma, new stroke, persistent coma, death) associated with rupture.^{80,101,102,108,131} Before the first reported series of endovascular management of TICAs in 1993,¹⁵⁹ treatment options available to the neurosurgeon were limited to balloon occlusion,^160–165 balloon trapping,¹⁶⁶ copper wire thrombosis,^167,168 surgical ligation, and clipping or occlusion of the parent artery with or without bypass.^{101,102,104,166,169}

The incidence and natural history of TICA in war casualties are unknown. Although first reported by Lunn during WWII,¹⁰⁷ only a few cases of TICA were reported in Vietnam War casualties.^103,105 In one report from the Iran-Iraq War, cerebral angiography an average of 17 days after missile head wounds in 255 patients disclosed 8 aneurysms (3%). Of significance was discovery of 6 of these aneurysms before and 2 after rupture.¹³¹ A subsequent study of the same conflict by Amirjamshidi and colleagues described a series of 1150 penetrating head injuries.¹⁰² One specific and uniform subpopulation within this study was the 470 patients who underwent digital subtraction angiography 2 to 35 (average, 16.2) days after their initial injury. Twenty-seven traumatic aneurysms/AVFs were discovered in this group (5.7%).¹⁰² Jinkins and coworkers performed cerebral angiography within 24 hours of GSWHs in 12 patients and found 3 internal carotid/vertebral and 1 combined aneurysm/AVF (33%).¹⁰⁶ In a recent study by Cohen and colleagues, angiography was performed in 34 patients at high risk of harboring a TICA.^{19,101,131,158} These investigators found 10 TICAs in 25 (40%) patients with PBIs involving the pterion or when the fragment crossed the midline.¹⁹ The timing of angiography after a missile head wound may be an in important factor in detecting aneurysms.^{19,101,102,106,131,158} Figure 336-12 shows a 70-year-old man after attempted suicide by GSWH in the glabella. Angiography within an hour of admission to the emergency department showed extravasation of dye in the interhemispheric space. The patient died soon after admission. An autopsy study of Lunn’s case by Dr. Dorothy Russell and cases reported during the Iran-Iraq War indicated that TICA caused by shell fragments is due to partial laceration of the arterial wall (Fig. 336-13).^107,131

FIGURE 336-12 Left lateral carotid angiogram from a 70-year-old man with a gunshot wound to the head 1 hour before transfer to an emergency department. The bullet penetrated the frontal bone in the midline and stopped at the inner table of the parietal bone (arrowhead). The angiogram shows extravasation of contrast material from the injured callosomarginal branch of the anterior cerebral artery (ACA) (arrow). ECA, external carotid artery.

(From Aarabi B, Kaufman HH, eds. Missile Wounds of the Head and Neck, vol II. Rolling Meadows, IL: American Association of Neurological Surgeons; 1999. Reproduced with permission from the American Association of Neurological Surgeons, Rolling Meadows, Illinois.)

FIGURE 336-13 Lateral view of a carotid angiogram from a 26-year-old soldier with a left pterional shell fragment injury. The fragment crossed the sagittal plane and cut into one of the branches of the anterior cerebral artery. The view indicates the sac of a traumatic intracranial aneurysm, and the corresponding pathologic specimen shows the arterial wall laceration and the false sac of the aneurysm.

(From Aarabi B, Kaufman HH, eds. Missile Wounds of the Head and Neck, vol II. Rolling Meadows, IL: American Association of Neurological Surgeons; 1999. Reproduced with permission from the American Association of Neurological Surgeons, Rolling Meadows, Illinois.)

The “Management and Prognosis of Penetrating Brain Injury” guidelines recommend angiography for patients with PBI who are at risk for TICA.¹⁴¹ Risk factors include orbitofaciocraniocerebral injuries, injuries near the pterion, and patients harboring intracranial hematomas.^19,101,141 It is recommended that any patient with these risk factors undergo either CT angiography or conventional angiography to rule out TICA (Fig. 336-14).

FIGURE 336-14 Source images of a computed tomographic angiogram of the head and the corresponding left carotid angiogram from a 17-year-old male with a shotgun injury to the left parietal region. A traumatic intracranial aneurysm from one of the peripheral branches of the middle cerebral artery is apparent. The aneurysm was resected surgically. ICA, internal carotid artery; S, shotgun pellet.

The current conflicts in the Middle East have helped us better understand the pathogenetic mechanisms of TICA and cerebral vasospasm secondary to blast injuries and PBIs and to provide better management by endovascular navigation.^18,19 Over a 5-year period at the National Naval Medical Center in Bethesda, Maryland, and the Walter Reed Army Medical Center, 279 angiographic studies were performed in 187 patients (25 with closed craniocervical injury, 162 with penetrating craniocervical injury) and resulted in the detection of 64 vascular injuries in 47 patients and 47 cases of posttraumatic vasospasm. The vascular injuries were characterized by TICAs (31 aneurysms), traumatic extracalvarial aneurysms (TECAs) (19 aneurysms), dissecting aneurysms,¹⁷⁰ and AVFs.⁶⁶ The average TICA size on admission was 4.7 mm, with an observed increase in aneurysm size in 11 patients. Within the TICA/TECA group, 24 aneurysms in 23 patients were treated endovascularly with either coiling or stent-assisted coiling, which resulted in preservation of the parent artery in 12 of 24 vessels (50%). Three patients in this group progressed despite endovascular treatment and required definitive clip exclusion. Thirteen additional aneurysms in 8 patients were treated surgically, and the parent artery was preserved in 4 cases (31%). Twelve of the 13 TICAs/TECAs resolved spontaneously without treatment, with 1 of the 13 rupturing and resulting in death. Six aneurysms ruptured during the study and resulted in 3 deaths. Five of 6 ruptures occurred in TICAs in which an interval increase in size was noted angiographically. Of the 11 dissections, 6 were treated with either a stent or stent-assisted coiling if a significant aneurysm was present. The remaining 5 dissections resolved spontaneously with just antiplatelet therapy. Stents were deployed in all cases in the setting of minimal intracranial hemorrhage or in a delayed fashion after the resolution of intracranial hemorrhage. This is an important point because all patients with a deployed stent required pretreatment with aspirin and clopidogrel (Plavix) and a minimum of 6 weeks of antiplatelet therapy after deployment. In addition, a decision to stent the carotid or vertebral artery was made if an infarct occurred while the patient was receiving antiplatelet therapy or if a significant flow-limiting intimal flap was present. The three AVFs were treated in the following fashion. The first AVF was a direct carotid-cavernous fistula (CCF) with flow-limiting carotid dissection on the same carotid artery in a patient without significant intracranial injury. It was necessary to first stent the carotid dissection to access the diseased cavernous segment. The direct CCF was then treated by deployment of a stent and transarterial coiling of the cavernous sinus. The second CCF was occluded with transarterial coiling using 200 cm of coil. The last, a vertebral artery AVF, was surgically occluded 16 days after the initial injury. In the series of Cohen and colleagues, 1 of 13 patients treated with a bare stent and coiling had a growing intracavernous pseudoaneurysm necessitating occlusion and bypass of the internal carotid artery.¹⁹ No recanalization occurred in 12 patients. In no patient in this series was renewed bleeding seen after a mean follow-up of 2.6 years.

Prognosis

Evacuation within the first hour after injury, damage control by hemostasis and asepsis, and definitive management in well-equipped centers in Iraq, the Landstuhl Regional Medical Center in Germany, or even back in the United States at the Walter Reed Army Medical Center within 36 hours of injury have significantly reduced the mortality rate of American troops in Iraq and Afghanistan.¹⁸⁹ The percentages of lethal war wounds among U.S. Soldiers in the American Civil War, WWI, WWII, and the Korean, Vietnam, and Persian Gulf wars were 33%, 21%, 30%, 25%, 24%, and 24%, respectively.^38,189,190 It has been shown that 35% to 40% of all combat deaths are due to brain wounds.³⁸ From 2001 to the present, 34,943 American soldiers have been wounded in Iraq and Afghanistan, 3541 of whom died of their war wounds (10%), thus putting mortality from warfare at its lowest level.¹⁸⁹ Late mortality ranges anywhere from 8% to 12% and is usually related to craniocerebral missile head wounds.^138,191

Contrary to lethality as a consequence of missile head wounds during war, the prognosis for civilian GSWHs remains abysmal.^21,41–43 In the report of Siccardi and associates, 85% of 314 victims of civilian GSWHs died within 3 hours (228 at the scene and 38 in 3 hours).³¹ Carey analyzed mortality in four typical clinical series of GSWHs^21,41–43 by stratifying admission GCS scores and long-term GOS scores in 349 patients.⁹⁴ In his analysis only 2 of 231 patients with a GCS score of 3 to 5, 14 of 44 patients with a GCS score of 6 to 8, and 57 of 74 patients with a GCS score of 9 to 15 made a good recovery (GOS scores of 4 and 5). Mortality rates in the same strata were 93%, 45%, and 10%, respectively. Overall, 21% of patients admitted alive to the emergency department made a good recovery (73 of 349 patients). In 2000 in the state of Maryland, 250 subjects sustained GSWHs (unpublished data), 222 (89%) of whom eventually died (177 at the scene and 45 in the emergency departments of eight trauma centers). Only 10 patients were seen at the trauma resuscitation unit of a shock trauma center alive, 8 of whom underwent surgery and 6 (2.4%) eventually made a favorable recovery.

Extensive studies have evaluated long-term survival and cognitive, behavioral, and functional outcome after PBI, especially in war injuries sustained in WWII and the Korean and Vietnam conflicts.^{120,121,192–197} For patients who survive a PBI, the size and location of the parenchymal injury may have a long-lasting effect on intelligence test scores. Corkin noticed a long-lasting effect on hidden figures test performance when a missile head wound involved the left hemisphere.¹⁹⁸ Grafman and colleagues noted isolated memory problems when the penetrating fragment cut into the fornix.¹⁹⁶ Preinjury intelligence determined performance in intelligence tests, although the size and location of the penetrating missile head wound have a decisive effect on postinjury intelligence.^175,194,195 The Wisconsin Card Sorting test indicated that victims of left dorsofrontal injuries had the most severe perseverative errors.¹⁹⁴ Weinstein and Teuber noticed a long-term decline in intelligence in WWII war veterans,¹⁹⁷ which was confirmed by Corkin and colleagues,¹⁹² who used the Army General Classification Test to evaluate vocabulary, arithmetic, block counting, and hidden figures between a group of 57 patients with missile head wounds and 27 veterans of WWII with peripheral nerve injuries. The authors reported significant drops in intelligence test scores over time in patients with missile head wounds. They postulated the decline in intelligence to be due to the primary effects of the missile head wound and the added effects of advancing age and stress on the remaining brain tissue caused by functioning for decades in a compromised state. In the studies by Corkin and associates, life expectancy and drop in intelligence were compared between 190 WWII veterans with PBI and 106 veterans with peripheral nerve injuries.¹⁹³ These investigators found a significant relationship between formal education and life expectancy; however, change between preinjury and postinjury intelligence test scores did not determine survival.

In recent years, neuroscientists have focused specifically on MTBI secondary to blast trauma, PTSD, and their long-lasting effect on the functionality of victims of closed brain injury and PBI and exposure to primary blast overpressure.^{2,3,5–8,199–201} With the fall in the death rate among war casualties in Operation Enduring Freedom/Operation Iraqi Freedom^189,190 and the fact that nearly 20% of all the deployed forces in Iraq and Afghanistan (nearly 320,000) may have suffered TBI, the fundamental question is what are the long-term cognitive, functional, and psychosocial outcomes of patients with MTBI. There is evidence that soldiers returning home from combat duties in Iraq and Afghanistan may suffer from poor general health and be more susceptible to cardiovascular complications, both of which can ultimately affect their job performance and productivity.^{1–3,5–7,202–204} The major link between MTBI and poor physical performance seems to center on PTSD, which is seen in 5% to 11% of all patients with MTBI.^1–35 In the survey of Hoge and colleagues, 124 of 2525 (4.9%) soldiers surveyed 3 to 4 months after their return from a year-long deployment to Iraq suffered from loss of consciousness and 260 (10.3%) from altered mental state, consistent with MTBI.³ Moreover, 43.9% of soldiers with loss of consciousness and 27.3% with altered mental state suffered from PTSD. The incidence of PTSD was 16.2% in 435 soldiers with other injuries and 9.1% in those with no injuries.³ Soldiers with MTBI were significantly more likely to report high combat intensity, a blast mechanism of injury, more than one exposure to an explosion, and hospitalization during deployment. In a logistic regression analysis, only loss of consciousness and combat intensity remained significantly associated with PTSD.³ In another study, Schneiderman and associates surveyed 2235 soldiers with combat experience and found the incidence of MTBI to be 12% and that of PTSD to be 11%.⁵ Smith and coworkers noted PTSD symptoms in 7.6% to 8.7% of military personnel who reported combat exposure and in 1.4% to 2.1% of those who did not report combat exposure.⁶ It is possible that MTBI under unusually stressful circumstances, such as blast injuries resulting from the explosive effects of IEDs, may affect the neuronal circuitry designed to monitor stressful conditions, such as the amygdala, lateral hypothalamus, and pituitary/adrenal axis. This effect may result in excessive amounts of stressful hormones and icosanoids and deposition of implicit memory of trauma that will result in PTSD. Other systemic effects include cell-mediated immunity, disordered sleep physiology, and symptoms of altered perception.^1,3,10,16 Cernak and colleagues showed statistically significant elevations in blood thromboxane A₂, prostacyclin, and sulfidopeptide leukotrienes in 65 patients exposed to blast injury^10,16 as opposed to 62 patients who suffered from non–blast-related injuries in the Balkan conflict.¹⁶ A multiphasic research project is currently ongoing to investigate pathogenesis and the best ways to manage MTBI and PTSD.⁴