Management of Penetrating and Blast Injuries of the Nervous System


Historical Overview

The various conflicts of the 20th century have given rise to the principles used in the management of penetrating brain injuries (PBIs). Injuries resulting from projectiles (e.g., gunshot wounds, knives) or blast injuries that cause bone fragments to breach the cranium and enter the cerebral parenchyma are defined as PBIs. The treatment of these injuries has evolved from the early use of Lister’s aseptic techniques in the Second Boer war. In World War I, Harvey Cushing implemented techniques of en bloc bone resection, suction debridement, magnet removal of metallic fragments, and two-layered closure of penetrating head injuries to effectively decrease mortality from 54% to 28%. He also brought Wilhelm Roentgen’s (Röntgen’s) novel x-ray technology to the operating room for localization of foreign bodies. His techniques have remained the standard of care for over 50 years. Early medical imaging with x-rays and angiography enabled visualization of penetrating bone and metallic fragments, which were thought to be associated with increased rates of infection and seizures. Hugh Cairns introduced mobile neurosurgical units, reducing length of stays to 6 days and, along with the introduction of antibiotics, doubled survival in World War II.

Most advances in the management of PBIs have occurred in or near the battlefield. Infection rates during World War II were significantly reduced using antibiotics, followed by the Korean War’s emphasis on early evacuation of these patients. The Vietnam conflict provided additional experience and data in dealing with these severe injuries. Military medical doctrine advocated the pursuit of all retained bone fragments, even when this entailed multiple operation;, however, follow-up studies of Vietnam veterans with retained fragments have failed to find increased rates of either infectious complications or epilepsy.

Advances in imaging, such as the routine use of diagnostic computed tomography (CT) scanning, coincided with the Arab-Israeli conflict in Lebanon. Long-term analysis of Israeli survivors found 48% had retained in-driven intracranial bone, further questioning the need to aggressively remove all penetrating fragments. The Iran-Iraq war also led to a wealth of published data, including reports on the causes of infections and the vascular complications of penetrating head injuries. The conflicts in Lebanon, and more recently in Iraq, provide data from management of closed head injury secondary to bomb blasts, emphasizing the challenges of managing a head injury with a penetrating as well as a blast component. , ,

Civilian gun violence now accounts for 25 times more deaths in the United States when compared to the causes of homicide in other high-income countries, with almost 96 Americans being killed with guns on a daily basis, according to the Center for Disease Control and Prevention. The overall firearm death rate is 11.4 times higher in the United States than in other high-GDP countries. In fact, the most common cause for traumatic brain injury (TBI)–related deaths is civilian gunshot wounds to the head (34.9%). This is more than that attributed to motor vehicle accidents (31.4%) for the year 2007. Overall, more than half of the approximately 50,000 GSW PBIs that occur yearly in the United States are from small firearms. The mortality rates remain high, with over 70% of victims dying at the scene and with the survival of hospitalized patients ranging from 7.69% to 69.70% in various studies. Kaufman and colleagues reported that 71% of civilian gunshot wounds result in death at the time of event occurrence, a 14% mortality within 5 hours and a 13% mortality between 5 and 48 hours after the shooting, with less than 2% surviving longer than 48 hours. Civilian gunshot wounds, however, can widely differ in regard to ammunition and weapons used, injury type, treatment, complications, and prognosis. Although many of the principles in the management of these patients remains the same, current practice continues to develop in the battlefield. To this end, the following chapter will address the most up-to-date knowledge of the pathophysiology, evaluation, and management of these PBIs.

Pathophysiology

The biomechanical effects of a missile strike on tissue were originally described in 1945 by E. Newton Harvey and more recently simulated in cold gel blocks by Martin Fackler and colleagues. Carey utilized a cat model to study the wounding effects of a projectile through an intact skull. The model was created by causing a direct crush injury resulting in a permanent cylindrical cavity. The pressure wave resulting from kinetic energy (KE) transfer, termed “ordinary pressure waves,” is propelled radially from the missile path, creating a temporary cavity lasting approximately 20 ms, as the walls of the permanent cavity first expand, then contract. The ordinary pressure waves sometimes result in stretch injury to adjacent tissues even at distances far removed from the projectile tract. Collapse of the temporary cavity is followed by extravasation of blood from around the missile track, which may expand to occupy a much larger space than the initial cavity. In perforating injuries, the exit wound is inevitably larger than the entrance wound. They also demonstrated that a marked rise in mean arterial blood pressure (MABP) in the first minute after injury actually results in a short-lived rise in cerebral perfusion pressure (CPP); however, the rise in intracranial pressure (ICP) is more sustained over time, and larger in magnitude relative to baseline values, than the rise in MABP and leads to a reduction in CPP. Carey and colleagues noted that severe respiratory changes occur after projectile injury, even when the missile is of low energy and the tract is distant from the brain stem. Carey hypothesized that the location of the medullary respiratory center (directly below the fluid-filled fourth ventricle) may make those neurons more susceptible to the ordinary pressure waves generated by a missile. Above a certain level of energy, a missile often produces an apnea that is fatal unless the animal is supported by mechanical ventilation. The probable correlate in human injuries may be a significant factor responsible for mortality in PBI. Carey’s experiments suggest that only a narrow window exists between the level of energy required for a missile to penetrate the skull and the level that causes fatal apnea.

Animal models have been utilized to study the effects of a missile strike to the brain on the physiologic parameters of ICP, MABP, and CPP. In a monkey model, Crockard and colleagues showed that a rapid rise in ICP immediately follows penetrating injury, peaking 2 to 5 minutes after injury and declining gradually thereafter. Levett and colleagues, using Crockard’s model, showed that CPP values fell within 1 minute of injury to 41 mm Hg from a baseline of 90 mm Hg. In this model, cerebral blood flow was also reduced to a level more than 50% below control values following penetrating injury. These pathophysiologic changes following PBI likely contribute to further neuronal damage and lend the theoretical justification for the monitoring of ICP and CPP after PBI.

Primary Injury

The principal pathologic effect of PBI results from brain swelling, intracranial hemorrhage, and piercing the cranial vault with bone, metal, and other fragments.

The injury sustained by the brain upon impact with a projectile depends upon four factors:

  • 1.

    The nature of the projectile (blunt or sharp)

  • 2.

    The approach of the projectile through the cranium

  • 3.

    The kinetic and thermal energy transferred by the projectile

  • 4.

    The susceptibility factors of the victim.

The skull has been shown to withstand impacts exceeding 5000 N/cm over the frontal bone and more than 2000 N/cm over the temporal bone. The cranium is often penetrated due to the sharpness and/or the KE of the foreign body. Bone fragments can act as additional projectiles, causing their own tracts of injury. The formula for calculating KE of a projectile is discussed in the next section on ballistics.

At impact, the skull absorbs most of the energy of the projectile, but the brain parenchyma must absorb the remainder. A penetrating bullet usually causes a narrow, carrot-shaped tract. Higher-velocity projectiles transfer additional energy to the parenchyma in the form of expansile–contractile cavitation waves, leaving wide, turnip-shaped tracts. Biophysicists have used high-speed digital video and pressure transducers in brain parenchyma simulant to demonstrate that a 9-mm round (379 m/s) transfers six times the energy and 1.5 times the cavitation volume of a 25-caliber round (238 m/s). The parenchymal damage mediated by direct laceration and indirect pressure waves, or primary injury, is instantaneous and irreversible.

Ballistics

There are several ballistic aspects that need to be considered when evaluating a PBI from a projectile. These include the type of weapon, proximity from the weapon, caliber of the projectile, and velocity. The KE released by a missile fragment is related to its mass (M) and velocity (V) and may be estimated by the formula :


KE = 1 2 M ( V entry V exit ) 2

The KE imparted by the missile to the brain determines the volume of injured brain and the size of cavitation. Brain injury extent from a missile also depends on size, shape, spin, and yaw of the missile and whether it fragments. A missile’s energy is greatest when it is launched, and decays with time and distance. Weapons and ammunition are designed to create friction-free flight in air but to enhance resistance to passage in tissue. The equation for KE highlights the importance of missile velocity relative to mass. Most modern high-velocity rifles can fire projectiles that surpass 2500 ft/s (762 m/s), whereas most handguns can fire 800 to 1400 ft/s (244 to 427 m/s). Shrapnel typically has a velocity of 600/s (183 m/s). Bone fragments driven into neural elements may act as secondary missiles. Thus, even a tangential missile strike can achieve a release of energy leading to significant injury to the central nervous system (CNS). Thus, the missile fragment largely determines the wounding potential of the missile or penetrating object. Expansion, tumbling, yaw, and fragmentation all enhance energy delivery to the tissue.

Nonmissile penetrating injuries to the skull and brain can occur from a variety of objects such as knives, nails, crowbars, scissors, and screwdrivers ( Fig 127.1A and B ; Fig. 127.2 ). Penetrating skull injuries require a force of at least 49 N to pierce the skin, with forces upward of that ranging from 255 N to penetrate the temporal bone to 540 N for the parietal bone. With the frontal bone being a common location, variation of energy to puncture depends on the location of bone and thickness. Each specific type of projectile creates a unique type of entry wound and parenchymal injuries.

FIGURE 127.1, (A and B) 26-year-old male patient presented to the ER with multiple stab wounds in the thorax and a clasp knife lodged in his skull. The knife was lodged in the left frontal region above the orbit. On exam he had no focal deficits but required interventions with a chest tube for his hemo-pneumothorax and intubation for surgical removal of the foreign body. (C) Lateral X-ray revealing the depth of the blade at 113 mm. Rotating the handle around the fulcrum (yellow marker) results in larger angulation at the tip as the blade acts like a class I lever (handle is the short lever arm) and the blade within the skull (the longer lever arm, displaced more). (D) Computed tomography (CT) scan. Axial and sagittal views on a CT angiogram revealing the tip being adjacent to the anterior cerebral artery. Wedging or attempting to wiggle the blade outside the operating room could result in injury of the deeper vasculature, resulting in life-threatening hemorrhage. (E) Craniotomy should be made around the penetrating object (purple arc) , and the entire object along with the craniotomy bone needs to be pulled along its axis (black arrow) .

FIGURE 127.2, (A) An 82-year-old disabled male patient attempted suicide by using a pen to penetrate his skull. (B) Computed tomography scans, sagittal and axial, revealing the tip of the pen penetrating the sphenoid sinus and adjacent to the basilar artery. This was removed uneventfully via an endoscopic approach to close the defect once the foreign body was removed.

Secondary Injury

The events that follow primary injury are a cascade of reactions secondary to ischemia, neuroinflammation, excitotoxicity, and oxidative stress that together create a self-perpetuating cycle of blood-brain barrier (BBB) breakdown, cerebral edema, ICP, and ultimately decreased CPP. This subsequent chain of reactions is referred to as secondary injury. Most of these reactions occur within the first 12 to 24 hours postinjury, but have been observed to persist for days, and even weeks. Multiple experimental models using intracarotid xenon 133 have revealed decreases in CPP by 50% within the first minute following injury. When the pressure waves created by a missile rise sufficiently high, they may pass through the fourth ventricle, affecting the medullary respiratory center and causing apnea. Extracranial pathology secondary to PBI, especially myocardial dysfunction, coagulopathy, and acute lung injury, also contributes to hypoxemia and brain ischemia. The primary aim in management is to halt or slow the cycle of secondary brain injury to preserve the neurovascular unit (neuronal circuit, microvasculature, and astrocyte), with the goal of preserving cerebral function. Therefore, the clinical management of PBI requires a comprehensive approach, as discussed in the next section.

Initial Management: Basic Advanced Trauma Life Support Guidelines

Advanced Trauma Life Support principles guide initial assessment and resuscitation of the patient with penetrating neurologic injuries.

Steps include the following:

  • 1

    Acute control of airway, breathing, and circulation (ABC)

  • 2

    Prevention of hypoxia

  • 3

    Prevention of hypotension

  • 4

    A brief initial neurologic evaluation, including the Glasgow Coma Scale (GCS) (60, 61) assessment of the pupils, and an evaluation for any focal deficit (D—disability)

  • 5

    Assessment of the cranium and face for external injuries, and exposure (E—exposure)

  • 6

    Adjunct to the primary survey including lines, x-rays, and other immediate interventions followed by secondary survey

  • 7

    Evaluation of the spine for deformities and/or open abnormalities

  • 8

    Concomitant head-to-toe evaluation for other life- or limb-threatening injuries

In many areas, initial care in the field is performed by highly trained prehospital personnel. Primary resuscitation is begun in the field at the site of injury. Emphasis on airway maintenance and control, control of external bleeding, prevention of shock, immobilization, and transport to the closest appropriate facility is performed. It also includes intubation in the comatose or symptomatic quadriplegic patient. Upon arrival to the emergency department, a team including a general surgeon, anesthesia provider, and neurosurgeon should be involved in the initial evaluation and management. Any available history regarding the mechanism of injury is valuable. Prehospital personnel often have details about the patient’s neurologic status at the scene. This information should be documented and compared to the arrival examination ( Table 127.1 ).

TABLE 127.1
Emergency Room Treatment of Craniocerebral GSW
  • 1.

    Early aggressive resuscitation (“damage control resuscitation”)

  • 2.

    Correct hypotension, hypoxia

  • 3.

    Maintain PaCO 2 in the normal range

  • 4.

    Hypertonic saline for brain swelling

  • 5.

    Urgent control of cervical vascular injury

  • 6.

    Avoid excessive crystalloid

  • 7.

    Early correction of traumatic coagulopathy with combinations of blood, blood products (fresh-frozen plasma, platelets), cryoprecipitate, or prothrombin complex concentrate

  • 10.

    Surgical airway if gross maxillofacial trauma or facial/respiratory tract burns are present

  • 12.

    Packing nasal cavity and facial wounds to control hemorrhage

  • 13.

    Urgent computed tomography scan

  • 14.

    Tetanus prophylaxis

  • 15.

    Antibiotic prophylaxis

After primary survey for life-threatening injuries, vital signs are monitored frequently, and isotonic intravenous fluids are administered as needed. Blood products should be immediately available to replace lost volume. Hypotension without tachycardia warrants consideration of spinal shock. Oxygenation should be monitored with continuous pulse oximetry. Blood is drawn for laboratory tests including arterial blood gas, blood count, electrolytes, coagulation profile, and blood type analysis. Chest x-ray should follow intubation of the trachea. Decompression of the stomach and bladder also allows monitoring of outputs. Most modern trauma centers have replaced routine cervical and pelvic x-rays with whole-body CT scans. Cervical and thoracolumbar spine precautions are maintained in multitrauma patients and those with unclear histories. Radiologic clearance of the cervical spine may not be necessary in patients with isolated PBIs.

In the military, this is of importance due to time, safety, and resource limitations in the field of combat. Initial stabilization of the PBI patient requires constant surveillance of the ABC, with simultaneous initial neurologic evaluation and assessment for other life- or limb-threatening injuries. Specifically, the GCS is useful for neurologic assessment, making decisions about intubation in the field, and predicting outcomes. Shaving of the scalp may be necessary to expose wounds concealed behind hair clotted with blood. Immediately upon arrival, pulse and blood pressure monitoring, as well as pulse oximetry, should be initiated. If not already done, large-bore intravenous access for colloid or crystalloid volume resuscitation should be established immediately. Simultaneously, arterial blood gases are taken, and venous blood is drawn and sent for complete blood count, electrolytes, glucose, coagulation profile, type, and cross match.

Neurologic secondary survey includes serial GCS determinations, reassessments of pupillary size and reactivity, and documentation of lateralizing or functional paresis. Sedation or chemical paralysis should be noted upon arrival and during treatment. Reversing agents can be administered to allow more accurate assessment of neurologic function. Hypoxia and hypotension are causes of altered mental status that may influence patient outcomes. Physical examination should include an assessment of the skull, spine, thorax, and abdomen for external injuries. Entry wounds should be sought out for each exit wound. Any sign of head injury warrants clipping of all scalp hair in search of other hidden findings. Burn marks and gunpowder tattooing suggest close-range injuries such as suicide attempts or execution-style shootings. Open depressed fractures may be palpated, but care should be taken to avoid triggering uncontrollable bleeding in regions near major arterial or venous anatomy. The face, mouth, and all other orifices should be inspected for signs of injury. Orbital penetration is frequently associated with intracranial injuries ( Fig. 127.3A and B ). Skull base injuries are frequently associated with cerebrospinal fluid (CSF) rhinorrhea or otorrhea and should be considered when external signs such as raccoon eyes or Battle sign are evident. Tetanus toxin is administered to all PBI patients.

FIGURE 127.3, (A) A 32-year-old male patient attempted suicide with a handgun, presented to the ER with altered sensorium, a Glasgow Coma Scale of 14, and complete loss of vision in the left eye with blast injury to the skull base. Computed tomography axial section of the head revealed disruption of the anterior cranial fossa, the frontal and ethmoid sinus, large subgaleal hematoma with bilateral basal frontal contusions. 3D reconstructed image. (B) Large bicoronal bifrontal incision is necessary to harvest a wide vascularized pericranial flap, debridement of the fragment, cranialization of the frontal sinus, and reconstruction of the anterior skull base. (C) Bifrontal craniotomy, frontal sinus exenterated of mucosa and obliterated followed by sandwich reconstruction of the skull base using a layer of artificial dura extending far posterior across the shattered skull base, tacking it in place with 4-0 neurolon, and fibrin glue around the margins to seal them, the layer of pericranium tucked under the frontal lobes, followed by another layer of artificial dura to seal the defect and prevent delayed meningoencephalocele. (D) Once sinus cranialization and reconstruction of the skull base is completed, the anterior skull over the orbits is reconstructed using bone with titanium mesh. (E) Completed reconstruction with bifrontal craniotomy flap and closure with drain.

Classification Systems for Traumatic Brain Injury

There have been three main systems by which head injuries have been classified. They include:

  • 1

    Clinical indexes of severity used in clinical research to compare patient outcomes across different institutions: The neurological Injury Severity Score (ISS) has been utilized in several clinical research trials involving TBI. The GCS is the most frequently used neurological injury score because of its high interobserver reliability, reproducibility, and good prognostic ability. Patients with severe TBIs have a GCS of 8 or less, commonly enrolled into clinical trials of TBI, having a high morbidity and mortality, with the likelihood of treatment effects being demonstrated in this group. The Brussels coma grade, Grady coma grades, Innsbruck coma scale, and the FOUR score scale have also been described but have not been used frequently in clinical practice. Extracranial injuries and physiological instability influence outcomes, and scoring systems have been developed to take these factors into account. They include the Abbreviated Injury Scale and the ISS. Factors such as age of the patient, systemic injuries, and physiological instability have a direct impact on patient outcomes, and hence it may be important to look at a combination of scoring systems while designing clinical research.

  • 2

    Pathological anatomic subtype to describe acute TBIs: describes the anatomic location going from outside the skull down to the brain parenchyma, and the associated imaging pathology.

  • 3

    Physical mechanism of the injury, used by biomechanical and preventative studies: The mechanism of the TBI appears to correlate with the pathological-anatomical injury type. Head injuries can be classified when there is contact or “impact” loading, in which case the head is struck by an object or meets an object. The alternative is noncontact or inertial loading, when the injury is secondary to movement of the brain parenchyma within the skull.

Although there is some overlap between each of these systems, combining the data enables researchers and biostatisticians to develop prognostication criteria and outcomes data, which in turn help to design treatment algorithms for these patients.

Penetrating Brain Injury: Specific Medical Management

Initial Medical Management

Any clinical evidence of brain herniation (e.g., unequal pupils) should be treated with prompt bolus administration of mannitol if the patient is hemodynamically stable. Patients that are in shock, hypotensive and hypovolemic, or dehydrated are better managed with boluses of hypertonic saline (HS). Moderate hyperventilation to a pCO 2 of around 30 mm Hg should also be considered in the early stages of management.

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