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Review

Impact & Blast Traumatic Brain Injury: Implications for Therapy

by
Satoshi Yamamoto
*,†,
Douglas S. DeWitt
† and
Donald S. Prough
†
Department of Anesthesiology, University of Texas Medical Branch, Galveston, TX 77555, USA
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Molecules 2018, 23(2), 245; https://doi.org/10.3390/molecules23020245
Submission received: 26 December 2017 / Revised: 22 January 2018 / Accepted: 24 January 2018 / Published: 26 January 2018
(This article belongs to the Special Issue Neuroprotective Agents)
Versions Notes

Abstract

:
Traumatic brain injury (TBI) is one of the most frequent causes of combat casualties in Operations Iraqi Freedom (OIF), Enduring Freedom (OEF), and New Dawn (OND). Although less common than combat-related blast exposure, there have been significant numbers of blast injuries in civilian populations in the United States. Current United States Department of Defense (DoD) ICD-9 derived diagnoses of TBI in the DoD Health Care System show that, for 2016, severe and moderate TBIs accounted for just 0.7% and 12.9%, respectively, of the total of 13,634 brain injuries, while mild TBIs (mTBIs) accounted for 86% of the total. Although there is a report that there are differences in the frequency of long-term complications in mTBI between blast and non-blast TBIs, clinical presentation is classified by severity score rather than mechanism because severity scoring is associated with prognosis in clinical practice. Blast TBI (bTBI) is unique in its pathology and mechanism, but there is no treatment specific for bTBIs—these patients are treated similarly to TBIs in general and therapy is tailored on an individual basis. Currently there is no neuroprotective drug recommended by the clinical guidelines based on evidence.

1. Introduction

Traumatic brain injury (TBI) is one of the most frequent causes of combat casualties in Operations Iraqi Freedom (OIF), Enduring Freedom (OEF), and New Dawn (OND) [1,2,3,4]. As many as 23% of warfighters returning from the conflicts in Iraq and Afghanistan sustained a TBI [5,6] and at least 60% of these TBIs are due to blast exposure [7,8]. According to Department of Defense statistics from 2015, blast exposure is the main cause of combat casualties with 73% of combat injuries in U.S. forces due to blasts [9,10]. Although less common than combat-related blast exposure, there have been significant numbers of blast injuries in civilian populations in the U.S. [11]. Kapur et al., reported 5931 injuries and 699 deaths due to blasts in the U.S. from 1983 to 2002 [12].
In this article, we review the current understanding of blast TBIs (bTBIs), contrasting with traditional TBIs, and feature common approaches to clinical management to highlight the guidelines for TBIs in general.

2. Epidemiology

2.1. Blast TBI

According to reports from OIF and OEF (Operations Iraqi and Enduring Freedom), the patterns of combat-related injuries have shifted from penetration injuries to blastrelated injuries. Since 4 November 2006, blasts have been the most common cause of injury among American soldiers [13]. Through to March of 2004, 97% of the casualties suffered by the First Light Armored Reconnaissance Battalion of the First Marine Division were related to blast [14]. Of the approximately one million veterans screened for TBI between 2007–2015, 8.4% were characterized as having sustained a TBI; most were mild and the majority due to blast exposure. Since an additional 45,000 had a previous diagnosis of mTBI, a total of 137,841 (13.8%) of those screened had sustained a combat-related TBI [15]. One striking feature of the mTBI cases seen in veterans of the wars in Iraq and Afghanistan is the high association between mTBI and posttraumatic stress disorder [2]. Approximately 75% of non-combat TBIs (e.g., motor vehicle accidents, sports-related TBI, etc.) sustained by U.S. military personnel annually are classified as mild [16]. Between 2000 and 2016, 82.3% of TBIs among military personnel were mild [17,18] and approximately 80% of mTBIs were due to blast [19].

2.2. TBI in General

Approximately 1.74 million people sustain a TBI in the United States each year [20]. As injuries to the brain are been classified as “head and neck” injuries [21], it might be difficult to know the precise ratio of TBIs that occur. Current United States Department of Defense (DoD) ICD-9 derived diagnoses of TBI in the DoD Health Care System show that, for 2016, severe and moderate TBI accounted for just 0.7% and 12.9%, respectively, of the total of 13,634 brain injuries, while mTBI brain injury accounted for 86% of the total [18].
The prognosis for an appropriately managed mTBI patient is good, generally resulting in complete recovery [22,23]. Those who have experienced mTBI usually fully recover within a year. Nevertheless, there can be a variety of short- and long-term sequelae of mTBIs in some patients [24,25,26,27,28]. Potential chronic effects of mTBI include post-concussion syndrome [23,29], post-traumatic headaches [30,31,32], post-traumatic epilepsy [33], post-traumatic vertigo [34,35], and chronic traumatic encephalopathy [29,36,37,38].
Moderate and severe TBIs are associated with lingering neurological deficits and functional impairments [28], and only one fourth of survivors of severe TBIs are able to achieve long-term functional independence [39,40,41]. The prevalence of long-term disability related to severe TBIs is reported to be approximately 1–2% of the population in the United States [42,43].
While a myriad of outcome prediction models designed to guide clinical decision-making have been developed, the complexity of severe head injury makes it difficult to apply many of these models to clinical decision-making in individual TBI patients [44,45,46].

3. Blast Physics

Blast processes involve the energy propagation of an explosive source into the surrounding environment, followed by interaction, loading, and damage of materials, structures, and systems. In biological systems, the extreme shifts of blast wave over (positive) pressure and under (negative) pressure of explosions brings substantial cellular disruption due to the stresses imparted by those rapidly changing positive and negative pressures [28].
In blast TBI, the blast wave encountering the head reflects and diffracts, resulting in highly transient and spatially non-uniform loading over the skull. High reflected pressures appear on the surface facing the incident wave. The combination of head size, skull thickness, and skull elasticity may exaggerate biomechanical responses to blast-wave loading [47].

4. Mechanism and Pathophysiology

4.1. Blast TBI

In most respects, blast TBI has clinical aspects of closed head injury. Primary blast injuries are defined as injuries that are a direct result of blast wave-induced over and under pressures. Secondary blast injury is due to impact from objects (e.g., shrapnel) put in motion by the blast. Tertiary blast injury is due to the acceleration of the body by the blast wind, and quaternary blast injury is any other type of injury (e.g., burns, lung damage from toxic gases, etc.) [48,49].
Although the exact mechanisms through which primary blast exposure causes tissue injury are uncertain, the most commonly stated are spallation, implosion, inertial effects [50,51,52], and cavitation [53,54]. Spallation occurs when the shock wave passes from a dense to a less dense material, causing the more dense material to fragment into the less dense material [52]. A relatively simple example is an explosion under water, causing the more dense water to spall (spray) into the less dense air [52]. Spallation may contribute to primary blast-induced lung injury [55]. Cavitation and implosion are related phenomena that occur as the negative pressure phase causes dissolved gases to form bubbles in fluids [54,56]. These bubbles are compressed (imploded) by the negative pressure and then expand explosively as the negative pressure phase passes [53,54]. Cavitation and implosion also have been implicated in the pathophysiology of pulmonary primary blast injury [55]. Inertial forces occur at the boundaries of tissues with different densities when the blast pressure accelerates materials of different densities at different rates, thereby creating shearing forces [52]. To date, there is no direct experimental evidence implicating any of these mechanisms in the pathophysiology of bTBI. However, studies using computerized and physical models suggest that cavitation may contribute to tissue injury secondary to blast exposure [54]. Furthermore, finite element modeling studies indicate that cerebrospinal fluid (CSF) cavitation could occur at the pressures and durations encountered in real-world blast events [57,58]. Generally, these effects occur primarily at the junction between tissues of different densities, which is consistent with observations of prominent astroglial scarring at grey–white matter junctions and in structures lining the ventricles [59]. Although primary blast overpressure may be a factor that contributes to brain injury and cognitive dysfunction, especially if amplified by the proximity of vehicles, buildings, and other solid structures, the threshold for bTBI remains to be known [28].
Some blast-exposed patients have evidence of TBI in the absence of trauma. These indirect blast effects may be precipitated by the transmission of blast energies through thoracic and abdominal blood vessels, as well as vagally-mediated bradycardia, arterial hypotension, and perhaps the resulting cerebral hypoperfusion [28]. There are two types of theoretical proposals for this mechanism. One is blast wave propagation directly through the skull or sinus openings [60]. Another is thoracoabdominal compression that transmits blast pressures to cerebral vascular and cerebrospinal fluid systems [61]. The integrity of the blood–brain barrier is impaired by increased cerebral vascular pressure, leading to the damage of small cerebral vessels [62]. As noted above, blast-induced damage to air-filled organs, such as the lungs, can create air emboli through the process of spallation [63]. The emboli may travel to the cerebral vasculature, leading to cerebral ischemia and infarction [49]. Also, exposure to blast pressures leads to arterial remodeling that may be associated with blast-induced vasospasm [64].

4.2. TBI in General

TBI itself is divided into two separate, but related categories: primary brain injury and secondary brain injury.
Primary brain injury occurs at the time of trauma, i.e., damage resulting directly from external mechanical forces transferred to intracranial contents. These include a combination of focal contusions and hematomas, as well as shearing of white matter tracts (diffuse axonal injury) along with cerebral edema and swelling [65,66]. Shearing mechanisms lead to diffuse axonal injury (DAI), which is visualized pathologically and on neuroimaging studies as multiple small lesions seen within white matter tracts.
Focal cerebral contusions are the most frequently encountered lesions. Contusions are commonly seen in the basal frontal and temporal areas, which are particularly susceptible due to direct impact on basal skull surfaces in the setting of acceleration/deceleration injuries.
Extra-axial hematomas are, in general, encountered when forces are distributed to the cranial vault and the most superficial cerebral layers. These are seen as epidural, subdural, and subarachnoid hemorrhage.
Secondary brain injury results from a cascade of molecular mechanisms that are initiated at the time of the first contact and sustained for hours or days. These mechanisms include neurotransmitter-mediated excitotoxicity from glutamate release, free-radical injury to cell membranes, electrolyte imbalances, mitochondrial dysfunction, inflammatory responses, apoptosis, secondary ischemia from vasospasm, focal microvascular occlusion, and vascular injury [41,59,67,68,69,70,71,72]. The mechanisms involved in cell death and tissue loss after TBI include complex, multifaceted interactions between acute and delayed biochemical, molecular, physiological, and anatomical events. In the affected brain region with high oxidative stress, free iron released from hemoglobin contributes to the production of free radicals [73]. Nitrosylation of proteins, another indicator of oxidative/nitrative stress, is also markedly increased [28]. The specific combination and magnitude of secondary mechanisms may vary with the actual biomechanics of the initial injury process.

5. Clinical Presentation and Classification

Although there is a report of differences in the frequency of long-term complications in mTBIs between blast and non-blast TBIs [74], the preponderance of evidence indicates that the neurological, psychological, and behavioral consequences of blast and non-blast TBIs are similar [17,75,76,77].
Regardless of the biomechanical causes of injury, it is important to make a careful, accurate initial diagnosis, especially with mTBI patients who may be unable to recall what happened at the at the time of injury due to alterations in consciousness. Immediately after TBI, patients often exhibit loss of consciousness, memory loss, headache, confusion, nausea, and focal neurologic deficits. In the long term, patients with TBI report cognitive impairment and neuropsychological symptoms (behavior and personality changes, depression, and suicidality), Parkinsonism, and other speech and gait abnormalities [29,36,78,79].
TBI has traditionally been classified using injury severity scores, the most common of which is the Glasgow Coma Scale (GCS) [80] (Table 1). The GCS is universally accepted as a tool for TBI classification due to its simplicity, reproducibility, and predictive value for overall prognosis. A GCS score of 13 to 15 is considered mild injury, 9 to 12 is considered moderate injury, and 8 or less as severe traumatic brain injury. However, for practical clinical use, the severity of initial impairment after TBI is subdivided into two major categories: mild TBI and moderate/severe TBI. The Marshall scale (Table 2) and the Rotterdam scale (Table 3) are two currently used CT-based grading scales [65,81].
Mild TBI is defined by loss or alteration of consciousness for up to 30 min after injury, a confused or disoriented state lasting less than 24 h, normal structural brain imaging on computerized tomographic (CT) scanning, and a Glasgow Coma Scale score of 13–15.
Moderate/severe TBI is defined by a traumatically-induced physiological disruption of brain function as manifested by either loss of consciousness for greater than 30 min, an initial GCS of 12 or less after 30 min, or post-traumatic amnesia for greater than 24 h.

6. Management

As there is no treatment specific for bTBI, these patients are treated similarly to TBI in general and therapy is tailored on an individual basis. For mild TBI, the mainstay of treatment is rest and targeted treatment of clinical symptoms. Observation is recommended for at least 24 h after a mild TBI [82,83]. Hospital admission is recommended for patients at risk for such immediate complications from head injury as GCS < 15, abnormal CT findings, seizures, and comorbid coagulopathy [84,85,86,87]. Attention has been focused on mTBI recently because of the putative relationship between repeated mTBI and the early onset of dementias such as Alzheimer’s in retired athletes, especially professional football players [88]. The numbers of sports-related concussions has been estimated to be as high 300,000 annually in the United States [89]. Based on the assumption that the 300,000 mTBIs involving loss of consciousness represented only 8% [90] and 19.2% [91] of sports-related TBIs, Langlois et al. estimated that the actual number of TBIs in contact sports may range from 1.6 to 3.8 million [92]. The considerable range of the estimates of the number of sport-related TBIs (i.e., 50,000 to 3.8 million) emphasizes the importance of accurate definitions of and/or criteria for mTBI.
Surgical treatment is indicated based on neurological status and head CT result criteria for moderate/severe TBI. The initial treatment of moderate/severe TBI should follow Adult Trauma Life Support (ATLS) guidelines [93] as to take into consideration systemic stabilization. Anesthesiologists play a critical role in securing airways, as well as obtaining large bore intravenous or central lines for cardiopulmonary resuscitation, in addition to placing arterial lines to closely monitor hemodynamics. Since patients with moderate/severe TBI often wear neck collars for cervical spine stabilization, fiberoptic intubation may be required. Moreover, in cases requiring placement of a central line in the internal jugular vein, stabilization of the neck with assistance is vital. Although hypotension and hypoxia should be avoided, hyperoxia with a PaO2 > 300 mmHg in patients with severe TBI is associated with higher in-hospital fatalities [94].
For moderate/severe TBIs without surgical indications, the goal of treatment is to limit the likelihood of secondary posttraumatic hypotension and hypoxia, both of which markedly increase mortality and morbidity [95,96], by maintaining BP (systolic > 90 mmHg) and oxygenation (PaO2 > 60 mmHg) for TBI patients in the ICU. In general, patients with TBI should be monitored closely to maintain euvolemia. Electrolyte disturbances are commonly seen in patients with TBI and should be assessed on a regular basis with other labs.
Although there has been some debate about the specifics of treatment and monitoring for patients with TBI, the Brain Trauma Foundation recently published revised 4th edition guidelines for severe TBI, which is endorsed by neurosurgical professional organizations [97]. The guidelines have been reviewed by high quality studies [95].
Currently, there are no evidence-based recommendations for the use of neuroprotective agents in TBI patients. However, there have been some clinical studies that show the effectiveness of neuroprotective agents in TBI [98,99,100,101,102], but none of these studies is of sufficiently high quality to warrant the use of neuroprotective agents.

7. Conclusions

Although blast TBIs appear to be unique in terms of pathology and biomechanical injury mechanisms, bTBI patients are indistinguishable from non-bTBI patients [17,48,75,76,77]. Although standards of care for TBI patients have been developed and refined over the last 20 years with several revisions of national and international guidelines, solid evidence is scarce. Clinical decisions should be made case-by-case based on current standard of care guidelines.

Conflicts of Interest

The authors declare no conflict of interest.

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Table
Table 1. Glasgow Coma Scale (GCS). A GCS score of 13 to 15 is considered mild injury, 9 to 12 is considered moderate injury, and 8 or less as severe traumatic brain injury.
Table 1. Glasgow Coma Scale (GCS). A GCS score of 13 to 15 is considered mild injury, 9 to 12 is considered moderate injury, and 8 or less as severe traumatic brain injury.
ResponseScore
Eye opening
Spontaneous4
Response to verbal command3
Response to pain2
No eye opening1
Best verbal response
Oriented5
Confused4
Inappropriate words3
Incomprehensible sounds2
No verbal response1
Best motor response
Obeys commands6
Localizing response to pain5
Withdrawal response to pain4
Flexion to pain3
Extension to pain2
No motor response1
Table
Table 2. Marshall CT score of traumatic brain injury.
Table 2. Marshall CT score of traumatic brain injury.
CategoryDefinition
Diffuse injury I (no visible pathology)No visible intracranial pathology seen on CT scan
Diffuse injury IICisterns are present with midline shift of 0–5 mm and/or lesions densities present; no high or mixed density lesion >25 cm3 may include bone fragments and foreign bodies
Diffuse injury III (swelling)Cisterns compressed or absent with midline shift 0–5 mm; no high or mixed density lesion >25 cm3
Diffuse injury IV (shift)Midline shift >5 mm; no high or mixed density lesion >25 cm3
Evacuated mass lesion VAny lesion surgically evacuated
Non-evacuated mass lesion VIHigh or mixed density lesion >25 cm3; not surgically evacuated
Table
Table 3. Rotterdam CT score. In adults, mortality at six months increases with the score; score 1: 0%, score 2: 7%, score 3: 16%, score 4: 26%, score 5: 53%, score 6: 61%.
Table 3. Rotterdam CT score. In adults, mortality at six months increases with the score; score 1: 0%, score 2: 7%, score 3: 16%, score 4: 26%, score 5: 53%, score 6: 61%.
Predictor ValueScore
Basal cisterns
Normal0
Compressed1
Absent2
Midline shift
No shift or shift ≤ 5 mm0
Shift > 5 mm1
Epidural mass lesion
Present0
Absent1
Intraventricular blood or subarachnoid hemorrhage
Absent0
Present1

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Yamamoto, S.; DeWitt, D.S.; Prough, D.S. Impact & Blast Traumatic Brain Injury: Implications for Therapy. Molecules 2018, 23, 245. https://doi.org/10.3390/molecules23020245

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Yamamoto S, DeWitt DS, Prough DS. Impact & Blast Traumatic Brain Injury: Implications for Therapy. Molecules. 2018; 23(2):245. https://doi.org/10.3390/molecules23020245

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Yamamoto, Satoshi, Douglas S. DeWitt, and Donald S. Prough. 2018. "Impact & Blast Traumatic Brain Injury: Implications for Therapy" Molecules 23, no. 2: 245. https://doi.org/10.3390/molecules23020245

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