Wars tend to be associated with their own 'signature' injury: shell shock in WWI and Agent Orange exposure in Vietnam, for example. Traumatic brain injury may well be the signature injury of the war in Iraq. The percentage of soldiers suffering traumatic brain injury (TBI) is significantly greater in this war than in prior conflicts. This increased incidence is predominately due to the fact that victims are far more likely to survive their battlefield injuries than in any other war in American history. The war in Iraq is also characterized by a different type of weaponry i.e., explosive munitions. Unlike previous conflicts, where gunshot injuries caused the majority of casualties, the vast majority of trauma in this war is caused by whole body blast trauma due to improvised explosive devices (IED).
Since the war began on March 19, 2003, more than 1.75 million U.S. troops have served in Iraq and approximately 160,000 are currently deployed. According to the Department of Defense, as of August 1, 2007, there have been approximately 30,000 non-fatal casualties and 3,641 deaths (PDF of official casualty figures). Of the 30,000 troops wounded in action, more than half returned to duty within 72 hours, thus potentially setting themselves up for 'second-impact syndrome'. Preliminary information suggests that the occurrence of TBI may be as high as 50 per cent of soldiers surviving combat blast injuries. This casualty toll does not include the 22,000 private U.S. civilian contractors working in Iraq.
My one-month volunteer 'tour of duty' at Landstuhl Regional Medical Center (LRMC) in Southern Germany taught me a tremendous amount about how combat trauma differs from civilian trauma, and about the system in place to care for our wounded warriors. LRMC is the largest NATO controlled air base on the European continent. It is the first stop for all American casualties leaving Iraq and Afghanistan. This article summarizes ten lessons that I learned from that experience. I hope that these lessons will be helpful in understanding the sequelae of future terrorist attacks, as well as natural disasters that can overwhelm local medical facilities.
Lesson #1: In comparison to prior wars, far more troops survive their injuries.
The war in Iraq has an extraordinarily high ratio of wounded to deaths, on the order of 16:1. In contrast, the Vietnam War had an injury-to-death ratio of 2.5:1. In World War II, one in three casualties died. In Iraq, however, 96 per cent of the wounded have survived. This remarkably high survival rate can be attributed partly to a more 'urban' battlefield than in prior conflicts, thus allowing more immediate access to medical treatment.
Far more important however, is the military's radical improvements to its systems of soldier protection, injury management, and patient evacuation. Significant advances in combat medic training, better designed tourniquet and hemostat bandages, and rapid access to fresh whole blood and Recombinant Activated Factor VII, all give frontline physicians powerful new means of controlling hemorrhage that prevents severely wounded patients from bleeding to death. Improved understanding of how to care for victims of polytrauma (see Lesson #3); advances in body armor and helmet technology (see Lesson #4); and more expeditious transportation (see Lesson #2) also contribute. The Air Force's use of specially configured aircraft to move thousands of casualties from war zones is a crucial innovation. The time that it now takes for a patient to be transported from the battlefield to the U.S. has decreased from three months (in WWII) to 30 days (in Vietnam), to 30 hours (in Iraq).
Lesson #2: Combat trauma, unlike civilian trauma, is characterized by a carefully choreographed staged continuum of care.
Civilian trauma management typically involves emergency surgery with definitive/reconstructive surgery at a single site and at a single point in time. In contrast, because of the more remote location of battlefield trauma, five stages of patient care are in place to care for the wounded soldier:
- Level 1: the field combat medic stabilizes the soldier at the time of injury. The patient is placed on a 'litter', which literally represents the backbone of battlefield patient transport from the time of the initial injury until the patient arrives back in the U.S.
Figure 1. 21-year-old soldier status post-IED blast. Non-contrast axial CT demonstrates a disproportionate amount of left temporal lobe edema relative to the extent of intrparenchymal hemorrhage.
- Level 2: the mobile forward surgical team, with two operating tables, provides emergency damage control surgery, in close proximity to the frontline infantry.
- Level 3: combat surgical hospitals (CSH, pronounced 'cash') are located in Balad and Baghdad. The CSH continues the 'full court press' approach to patient care and performs " 21year M s p IED intracranial contusion, BLE AK stumps, large segments devitalized necrotic tissue dirt shrapnel, pulmonary edema, ?open abdomen?, 25 per cent burns, LUE fasciotomy escharotomy, hypovolemic blast with and of P shock.?<>
The unique aspects of burn physiology and wound care that frequently accompany blast trauma complicate patient care and can adversely impact the injured brain. In addition, 'blast lung injury' interferes with normal oxygenation. Bowel contusions, perforations, mesenteric tears, and renal failure secondary to myoglobinuria caused by crush injuries, can all be potentially harmful to the injured brain. Deducing the presence and extent of the brain injury in the acute setting can be hard for several reasons. First, patients often arrive at LRMC under sedation, so it is difficult to assess their neurological status. Second, the patient - and physician - can both be distracted by other injuries. Third, TBI is not always diagnosable using current imaging technology, particularly when computed tomography (CT) is the mainstay of diagnosis.
Lesson #4: The primary mechanism of injury in the war in Iraq is a blast injury.
As in previous wars, the weapons deployed in the Iraq War, by all of the combatants, relate directly to the injuries sustained. They include IEDs (improvised explosive devices) and the subsets of vehicle-borne IEDs and house-borne IEDs; grenades; mortars (explosive ordinance or XO; UXOs are unexploded ordinance); booby-traps and land mines; RPG (rocket propelled grenades); AK-47s; and EFP (explosively formed projectiles).
Rare in civilian society, blast injuries occur daily on the battlefield and in war-torn urban areas. The most common are the result of explosive munitions. Nearly one-third of all combat forces are exposed to a blast force and the vast majority of these blast injuries are secondary to IED explosions.
Figure 2. 23-year-old soldier status post-IED blast and near drowning in Tigris River. Note complete effacement of the cerebral sulci and cisterns with loss of the gray-white differentiation and symmetric low attenuation of the basal ganglia, consistent with severe anoxic injury.
If TBI is the signature injury of the war in Iraq, the IED is its signature weapon. Troops are also susceptible to the same types of crush injuries and the rapid acceleration/deceleration injuries and blunt trauma found in civilian TBI, such as diffuse axonal injury and coupcontrecoup hemorrhage.
There are four types of blast injury, and most are a complex mix of all four:
- Primary: the result of direct blast wave-induced changes in atmospheric pressure (i.e., barotrauma). It primarily affects air-filled organs such as the lung, colon, and middle ear (tympanic membrane), but it may also cause cardiac contusions, bowel perforation, mesenteric shear injury, and brain injury. Primary blast injuries are characterized by tissue edema. Extremity fasciotomies may be necessary to relieve the distal decrease in perfusion and to avoid the development of a compartment syndrome.
Pulmonary edema (so-called blast lung) and intestinal edema (open abdomen) are characteristic. The brain injuries associated with blast trauma also tend to be characterized by a disproportionate amount of cerebral edema relative to parenchymal hemorrhage (Figure 1). The edematous response of the tissue to a blast injury may be exacerbated by the massive fluid resuscitation that occurs in the field, superimposed on the primary blast force.
- Secondary: basically, numerous penetrating injuries that result from multiple objects put in motion by the blast force. The patient's skin surface appears 'peppered' with innumerable wounds.
- Tertiary: resulting from the victim being thrown or crushed by the collapse of a structure. These injuries resemble blunt traumatic injuries found in the majority of civilian trauma such as a motor vehicle accidents, falls, and crush injuries.
- Quaternary: usually a thermal injury resulting in varying degrees of burn severity. The inhalation of toxic fumes and asphyxia are also examples of quaternary blast injury. In particular, phosgene-like combustion by-products from the Teflon-coated interiors of armored vehicles may cause severe pulmonary compromise. Burns associated with IED explosions seem to behave differently from typical domestic burns; this may result from a combination of the thermal injury superimposed on the primary and secondary blast injury.
Several factors determine the severity of a blast injury: helmet and body armor; peak blast pressure; distance from the explosion; whether the blast occurs outdoors or in an enclosed space; the mass, velocity, and shape of the secondary blast fragments; and the type of tissue injured. It should be noted that the peripheral nervous system is not immune to combat injury. Plantar fasciitis, tarsal tunnel syndrome (boot trauma), entrapment neuropathy (from constantly holding a weapon), penetrating peripheral nerve trauma, and demyelination from a blast injury are all encountered on the battlefield.
Lesson #5: Battlefield TBI patients are particularly vulnerable to secondary TBI.
The initial, primary head injury sets in motion a series of deleterious biochemical processes (secondary TBI) that worsen patient outcome.
Figure 3. ED blast with lumbar burst fracture that was surgically repaired. Abnormal mental status post-surgery due to fat emboli. Axial CT (above) and FLAIR imaging (below) reveal multiple T2 hyperintense foci involving predominately the supratentorial white matter, but also the cortex and cerebellum.
Secondary TBI occurs most often in the first 24 hours after the injury and is potentially preventable. The battlefield patient is particularly vulnerable to secondary TBI for many reasons. First, the management of the polytrauma combat victim is complex and therefore at risk for complications. Because amputations are an inevitable consequence of improved body armor, controlling the victim's blood pressure in the setting of extreme blood loss is challenging. The massive fluid resuscitation that occurs in the field can have both positive and negative effects on the injured brain. Specifically, because the injured 'young' brain is particularly prone to cerebral dysautoregulation, excess fluid can exacerbate intracranial hypertension, whereas hypotension can result in cerebral ischemia, so tailored cerebral blood volume is crucial.
The staged continuum of care described in Lesson #2 is, by its very design, associated with multiple patient transfers. Each transfer sets up the potential risk for hypotension. Impaired cerebral perfusion can have a dramatic effect on the injured brain - a single episode can nearly double patient mortality. Impaired cerebral oxygenation can also result from concomitant pulmonary trauma. The lungs may be affected by primary blast injury (edema/contusion/burns), pulmonary embolism, and aspiration pneumonia, all of which can result in hypoxemia, hypocapnia, and metabolic acidosis.
Hyperthermia also makes soldiers wounded on the battlefield vulnerable to secondary TBI. The weather in Iraq can be very hot, the troops are heavily garbed, and they undertake intense physical activity, thus predisposing them to the harmful effects of hyperthermia. On a microscopic level, the massive release of catecholamines, hyperglycemia, excitotoxic injury due to glutamate excess, and cytokines exacerbate the injury. Lactic acidosis caused by mitochondrial dysfunction, free radical oxidative stress with lipid peroxidation, and ruptured erythrocytes release Hgb - all of which amplify the oxidative injury. The secondary insults to the brain may be peri-lesional, widespread, or cause focal ischemic hippocampal injury.
Injuries caused by supersonic shock waves tend to evolve over time. Unlike blunt and penetrating injuries, the edematous response is not initially obvious. It sometimes takes 24 hours for the primary blast injury to declare itself. It may be that the presence of a blast/burn injury, coupled with the complexity of combat TBI evolves over time, more so than civilian TBI.
Lesson #6: Stroke is more common in combat TBI than in civilian TBI.
Ischemic infarction affects our young troops for several reasons, including:
- The increased incidence of penetrating injuries results in a combination of vascular occlusion, dissection, and pseudoaneurysm formation.
- Hypotension due to massive blood loss from amputation(s) and/or coagulopathy. Hypoxemia in the setting of an inhalational burn (both chemical e.g., chlorine and thermal) or drowning. (Figure 2)
- Embolic infarction secondary to a patent foramen ovale combined with the increased incidence of pulmonary emboli. Risk factors in our troops for deep vein thrombosis include dehydration, sepsis, and prolonged air-evacuation with constraining straps.
- Traumatic vasospasm.
- Hyperthermia (heat stroke).
- Post-herniation infarction.
- Cardiovascular derangement (triad: apnea, bradycardia, hypotension).
- Meningitis resulting from implanted clothing and debris in penetrating injuries.
- Air embolism secondary to disrupted pulmonary alveoli.
- Fat embolism from long bone disruption or blast injury. This can result in cerebral infarction directly or indirectly via ARDS. (Figure 3)
Lesson #7: 'Comminution, contamination, mutilation, and amputation' is a frequent theme.
Because the predominant mechanism of injury in battlefield trauma is a blast injury from an IED, the tissue literally explodes. It is lacerated, shredded, or crushed, but not cleanly cut. The resultant mangled soft tissue defects and embedded foreign bodies require multiple wound 'washouts', serial debriding, and a heightened vigilance for sepsis. Unlike small arms fire and the AK-47 wound, most secondary blast injuries are contaminated. The superimposed burn injuries also contribute to the horrific physical appearance and the heightened risk for infection. The soldier's body armor helps protect the torso, but leaves the extremities vulnerable, hence the high number of single, double, and triple amputees returning from combat.(Figure 4)
Lesson #8: Diagnostic imaging plays a crucial role in the initial assessment and follow-up of combatrelated TBI.
The imaging approach in the acute setting is no different from civilian trauma in that CT remains the initial exam of choice. However, there are numerous differences between civilian and combat imaging.
- Total-body scans are routine on the battlefield due to the extreme polytrauma nature of combat injuries.
- Plain radiographs are obtained more often because of the large number of troops with extremity injuries. In addition, there is a greater incidence of foreign bodies in battlefield trauma and these are also well visualized on plain radiographs.
- The evolving nature of combat lesions tends to warrant more follow-up imaging examinations.
- The combination of total-body scans with multiple follow-up studies increases the radiation exposure to this young patient population.
- Magnetic resonance imaging (MRI) is not available in Iraq. When the soldier arrives at LRMC, MRI must be performed judiciously because of the frequent contamination of the wounds by ferromagnetic foreign bodies. When the soldier returns to the U.S., various functional imaging techniques may provide evidence of metabolic derangement not evident on macroscopic anatomic imaging. There are wounds that we currently cannot see with routine CT and MRI.
Figure 4. 21-year-old status post-IED blast injury. As noted in Lesson 7, this plain radiograph of the right UE reveals extensively comminuted fractures of the radius, ulna, carpal, and metacarpal bones. Numerous radiopaque metallic foreign bodies are lodged within severely macerated soft tissue. A subsequent upper extremity amputation was performed on this soldier.
Lesson # 9: The combat patient population is more homogenous than the civilian population.
Our troops are characteristically young, extremely healthy, and male. Their youth and preinjury excellent health confers improved prognosis. The data from this relatively homogeneous population may not, therefore, necessarily translate into the mass casualty experience of future terrorist attacks. However, over a quarter of U.S. troops are in the National Guard and Reserve, and are older than active duty soldiers and therefore more likely to have heart problems or back trouble. Privately hired contractors are also a more heterogeneous group that resembles typical civilian trauma patients.
Lesson # 10: We must apply the learning from combat TBI to treating civilian TBI.
TBI is the leading cause of death in individuals under age 45. The number of people diagnosed annually with TBI exceeds HIV/AIDS, multiple sclerosis, spinal cord injury, Alzheimer's, and breast cancer combined. The cost of TBI in the U.S. is estimated at anywhere from $50 to $150 billion, but quantifying the cost of the pain and suffering of the victims and their families is difficult. These staggering statistics are surprisingly unknown to the American public. It is no wonder that the CDC describes TBI as a 'silent' epidemic.
As is the case with civilian TBI, no one really knows the true incidence of combat TBI. We do know that victims of both tend to be young men in the prime of life. We also know that post-traumatic stress syndrome plays a greater role in combat trauma than in civilian trauma, but the neuropsychological symptoms of the two overlap. As described above, combat injuries are somewhat different from civilian injuries, and the U.S. health care system will have to learn to care for this 'new' type of patient. In addition, future terrorist attacks on the home front will further introduce these types of injuries into our society.
In conclusion, the nation's health care system for veterans (and civilians) is already overburdened. This is an opportunity to refocus on domestic TBI and to give it the attention and quality of care equivalent to our troops in the war zone. We need to speak up about the true scope of this silent epidemic.
Alisa D. Gean, MD is a professor of radiology, neurology, and neurosurgery at UCSF, and chief of neuroradiology at San Francisco General Hospital.
