Penetrating traumatic brain injury (pTBI) remains one of the most devastating and lethal forms of trauma. Prognosis is generally poor and, for those who survive long enough to make it to the hospital, the management of penetrating brain injury presents complex challenges to medical and surgical providers in the civilian sector. Recent experiences in Operation Iraqi Freedom and Operation Enduring Freedom have provided opportunities to study and refine the surgical and medical management of pTBIs that may impact civilian evaluation and management of similar traumas. These experiences demonstrated that aggressive pre-hospital and emergency department resuscitation, followed by immediate surgical management and post-operative intensive care to monitor for and intervene on surgical and medical complications could significantly improve patient outcomes. We begin with a brief case vignette that will introduce a comprehensive discussion on the epidemiology, pathophysiology, evolution of current surgical and medical therapies, complications, and prognostic indicators that may improve outcomes in these challenging cases.
Penetrating traumatic brain injury (pTBI) is the most lethal form of traumatic head injury. Approximately 70-90% of these victims die before arriving at the hospital, and 50% of those who survive to reach the hospital die during resuscitation attempts. Approximately 32,000-35,000 civilian deaths are attributed to penetrating brain injury each year, with firearms-related injuries being the leading cause of mortality. Less than 20% of civilians who reach a trauma center will undergo a neurosurgical procedure.
Mechanism of Injury
Traumatic brain injury is the result of energy being transferred from an object to the human skull and underlying brain. The penetrating object has kinetic energy that is proportional to the projectile equal to the mass times the square of its velocity (Ek=1/2mv2). Most non-bullet penetrating objects, such as nails or knives, impart less damage to the skull and brain because they have less kinetic energy to transfer on impact. Bullets tend to have less mass, but travel at higher velocities, though bullet velocities can vary based on a number of factors, such as the muzzle velocity, travel through the air, and travel through the impacted target. Modern firearm projectile velocities can range from 200m/s in handguns to more than 1000 m/s in some rifles. High velocity bullets fired from rifles have the potential to do more damage than bullets fired from handguns, though some large caliber handgun rounds are of sufficient mass to make up for their lower velocities with regard to kinetic energy. Other factors to consider include the distance from which the round was fired, the yaw, or tumbling that occurs when the bullet impacts soft tissue, and whether the bullet design causes it to deform or fragment on impact. Bullets fired from closer ranges often cause more damage than when the same bullet is fired from a longer distance. Non-deforming projectiles have a tendency to yaw inside tissue, which increases penetration and results in a moderate wound cavity size, while deforming rounds have more superficial penetrations, but form larger wound cavities.
Pre Hospital Care
Pre-hospital management has developed an increasingly important role in the care of pTBI patients and has the potential to significantly impact outcomes. Pre-hospital care is focused on minimizing secondary injury and delivering the patient to a trauma center alive. This is achieved through effective airway maintenance and optimizing oxygenation, ventilation, and cerebral perfusion. General measures to achieve this include elevating the patient’s head to 30 degrees and maintaining the head in a midline position. Systolic blood pressures 90mmHg should be targeted and maintained. Additionally, oxygen saturation >90%, a PCO2 between 35-40 mmHg (if capnography is available) are common pre-hospital and resuscitation goals.
Emergency Departmental Care
Aggressive resuscitation following pTBI has been associated with improved survival. Furthermore, it is recommended that aggressive therapy be continued through the resuscitation phase, even in patients with initially low GCS scores, as patients who may benefit from hyperosmolar therapy and surgery may be overlooked based on the initial poor neurological exam upon presentation. Treatment in the emergency department should include correction of hypotension and hypoxia, airway maintenance to include placement of a surgical airway if there is co-existing oromaxillofacial trauma, control of any associated hemorrhaging (i.e. packing facial wounds), hyperosmolar therapy with mannitol or hypertonic saline, correction of traumatic coagulopathy, placement of a cervical immobilization device, an urgent CT scan of the head and neck, and tetanus and antibiotic prophylaxis. Plain films are not necessary if a CT is obtained. Seizure prophylaxis is typically started in the emergency room. Excessive crystalloid should be avoided, and colloid is contraindicated given the association with elevated ICPs. Steroids, including recent trials evaluating the use of progesterone in severe TBI, have either shown no benefit or increased risk of death and should also be avoided. Blood products should be available for transfusion, as well as cryoprecipitate, prothrombin complex concentrates and, in rare cases, recombinant Factor VIIa to help control bleeding.
The surgical treatment of penetrating brain injury has evolved significantly over the past century. Prior to 1889, pTBI patients did not typically undergo surgery due to ineffective hemostasis and poor post-operative infection control. Dr. Harvey Cushing was the first to develop a formal approach to the management of pTBI.
A challenging aspect to the surgical management of pTBI is the selection of appropriate surgical candidates. There is extensive literature that has attempted to identify which patients may benefit from surgery. Poor prognostic indicators have previously been identified as old age, low admission GCS, abnormal pupil reactivity, bi-hemispheric involvement, path of the projectile, and loss of the basal cisterns on imaging. A GCS of 3-5 and/or a projectile path crossing the midline at the level of the corpus callosum, through the bilateral thalami, basal ganglia posterior fossa/brainstem or through an area 4cm above the dorsum sellae containing the vessels of the Circle of Willis known as the “zona fatalis” has historically resulted in the withholding of surgical care.
Post-Operative Medical Management
Post-operative management of pTBI patients is critical to improving survivability and functional outcomes and requires a multidisciplinary approach. For approximately two weeks following the onset of injury, close monitoring of intracranial dynamics allows secondary injury to be identified and for prompt intervention when this occurs. Intracranial hypertension is common, and may be associated with, decreased cerebral perfusion pressures (CPP), cerebral ischemia, seizures, vasospasm, arteriovenous fistula formation, or traumatic aneurysm rupture as a direct result of pTBI. Maintaining ICP 60mmHg using general measures (head mid-line, head of bed elevated to 30 degrees, control of pain and temperature) hyperosmotic therapy, sedation, neuromuscular blockade, and induced hypothermia may improve outcomes by limiting secondary injury. TCD can help monitor cerebral blood flow as well as assess for evidence of developing cerebral vasospasm in the setting of traumatic subarachnoid hemorrhage.
Patients who have sustained pTBI are at higher risk for the development of non-neurologic complications as well. For example, pTBI patients are at high risk for Acute Respiratory Distress Syndrome (ARDS). This condition is also associated with the use of fluids and vasopressors used to maintain an adequate CPP. When this occurs, patients may require extracorporeal membrane oxygenation or high frequency oscillations since hypercapnea and prone positioning can worsen secondary brain injury. Patients also require observation of their cardiovascular status (to include cardiac rate, rhythm, and blood pressure), monitoring for the development of diffuse intravascular coagulopathy, infection, kidney injury, and skin breakdown.
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