Primary Blast Injury Research Articles

Cerebellar White Matter Abnormalities following Primary Blast Injury in US Military Personnel

Little is known about the effects of blast exposure on the human brain in the absence of head impact. Clinical reports, experimental animal studies, and computational modeling of blast exposure have suggested effects on the cerebellum and brainstem. In US military personnel with isolated, primary blast-related ‘mild’ traumatic brain injury and no other known insult, we found diffusion tensor MRI abnormalities consistent with cerebellar white matter injury in 3 of 4 subjects. No abnormalities in other brain regions were detected. These findings add to the evidence supporting the hypothesis that primary blast exposure contributes to brain injury in the absence of head impact and that the cerebellum may be particularly vulnerable. However, the clinical effects of these abnormalities cannot be determined with certainty; none of the subjects had ataxia or other detected evidence of cerebellar dysfunction. The details of the blast events themselves cannot be disclosed at this time, thus additional animal and computational modeling will be required to dissect the mechanisms underlying primary blast-related traumatic brain injury. Furthermore, the effects of possible subconcussive impacts and other military-related exposures cannot be determined from the data presented. Thus many aspects of topic will require further investigation.

Electrophysiological white matter dysfunction and association with neurobehavioral deficits following low-level primary blast trauma

There is strong evidence that primary blast injuries can cause neuropathological alterations in the brain. Clinical findings from war veterans indicating evidence of diffuse axonal injury have been corroborated by numerous primary blast models in animals. However, the effect of a subclinical blast (blast with no obvious sign of external trauma or lung injury) as a contributing factor to the neurological symptoms and neuropathology is less clear. Our group recently developed a model of low-level primary blast and characterized aberrant expression of white matter cytoskeletal proteins in the cortex and hippocampus following a subclinical wave shock exposure. Here we examined the susceptibility of the corpus callosum following subclinical blast. We also demonstrate that white matter dysfunction is associated with neurobehavioral deficits associated with anxiety and stress in rats. Anesthetized male Sprague–Dawley rats (~300g) were exposed to a primary blast (approx. 28kPa), below the threshold required to induce pulmonary trauma. Rats were evaluated on three behavioral outcome measures; the rotarod, the light/dark box and open field anxiety test. We used Western blotting to examine expression and degradation of axonally expressed αII-spectrin, NF200 and voltage-gated sodium channels (VGSC) in the corpus callosum. Acute slice preparations were used for electrophysiological analysis of evoked compound action potentials (CAPs) in the corpus callosum. There was evidence of αII-spectrin degradation in the corpus callosum at 48h post-injury detectable up to 14days post-injury, as well as increased heavy neurofilament expression. A reduction in VGSC expression was observed at 48h post-blast as well as a reduction in the interaction between ankyrin G and intact αII-spectrin. Blast exposed rats had significantly lower rotarod latency times relative to sham rats (p=0.002). Increased anxiety-related and stress-related behavior were observed in blast rats relative to sham animals as indicated by the increased frequency of fecal droppings (p=0.029) and reduced exploratory activity (p=0.036) in the open-field test. Blast rats had fewer transitions and time spent in lit sections of the light/dark box. Electrophysiological recordings from the corpus callosum indicated greater deficits in unmyelinated fibers of the corpus callosum relative to myelinated fibers characterized by reduced CAP amplitude response at 14days post-injury. Analysis of the relationship between stimulation distance to evoked response indicated an underlying abnormality in N1 myelinated fibers at close stimulation distances. Collectively, our results indicate that subclinical blast exposure can result in persistent neurological changes in cerebral white matter occurring in parallel with detectable neurobehavioral deficits.

Primary Blast Injury to the Eye and Orbit: Finite Element Modeling

Primary blast injury (PBI) mostly affects air-filled organs, although it is sporadically reported in fluid-filled organs, including the eye. The purpose of the present paper is to explain orbit blast injury mechanisms through finite element modeling (FEM). FEM meshes of the eye, orbit, and skull were generated. Pressure, strain, and strain rates were calculated at the cornea, vitreous base, equator, macula, and orbit apex for pressures known to cause tympanic rupture, lung damage, and 50% chance of mortality. Pressures within the orbit ranged between +0.25 and -1.4 MegaPascal (MPa) for tympanic rupture, +3 and -1 MPa for lung damage, and +20 and -6 MPa for 50% mortality. Higher trinitrotoluene (TNT) quantity and closer explosion caused significantly higher pressures, and the impact angle significantly influenced pressure at all locations. Pressure waves reflected and amplified to create steady waves resonating within the orbit. Strain reached 20% along multiple axes, and strain rates exceeded 30,000 s(-1) at all locations even for the smallest amount of TNT. The orbit's pyramidlike shape with bony walls and the mechanical impedance mismatch between fluidlike content and anterior air-tissue interface determine pressure wave reflection and amplification. The resulting steady wave resonates within the orbit and can explain both macular holes and optic nerve damage after ocular PBI.

A model for predicting primary blast lung injury

This article presents a model-based method for predicting primary blast injury. On the basis of the normalized work injury mechanism from previous work, this method presents a new model that accounts for the effects of blast orientation and species difference. The analysis used test data from a series of extensive experimental studies sponsored by the US Army Medical Research and Materiel Command. In these studies, more than 1200 sheep were exposed to air blast in free-field and confined enclosures, and lung injuries were quantified as the percentage of surface area contused. Blast overpressure data were collected using blast test devices placed at matching locations to represent loadings to the thorax. Adopting the modified Lobdell model with further modifications specifically for blast and scaling, the thorax deformation histories for the left, chest, and right sides of the thorax were calculated for all sheep subjects. Using the calculated thorax velocities, effective normalized work was computed for each test subject representing the irreversible work performed on the lung tissues normalized by lung volume and ambient pressure. Dose-response curves for four categories of injuries (trace, slight, moderate, and severe) were developed by performing log-logistic correlations of the computed normalized work with the injury outcomes, including the effect of multiple shots. A blast lethality correlation was also established. Validated by sheep data, the present work revalidates the previous understanding and findings of the blast lung injury mechanism and provides an anthropomorphic model for primary blast injury prediction that can be used for occupational and survivability analysis. Economic and decision analysis, level III.

Pattern and mechanism of traumatic limb amputations after explosive blast

Traumatic amputation of limbs caused by bomb blast carries a high mortality; we present our experience of 07/07 London terrorist bombing that resulted in a large number of survivors with amputated limbs. We think that the unique underground bombing, the shape of the carriages, and the enclosure by the underground tunnel caused amputation of the limb by the channeling of the blast wave as a result of the device being floor based, which resulted in lower-limb amputation without other fatal primary blast injuries. We present our results of the traumatic amputation in the fatalities and survivors as well as the possible mechanism and protective measure that could save lives. Data for traumatic amputations were collected from several sources and made anonymous. Traumatic amputations were specifically classified in both the survivors and the fatalities. Our results have shown that 24.5% of those with traumatic amputations will survive. Most of the lower-limb amputations occurred in the shaft of the long bones. Only one person with an upper limb amputation survived the injuries. This study does not support the previously held belief that traumatic amputations from a bomb blast results from simple avulsions by the blast winds. However, it reinforces the belief that the principal mechanism of primary traumatic amputation of the limbs in such circumstances occurs primarily [corrected] from the direct coupling of blast waves, resulting in a fracture of the long bone rather than at a joint. This study is unique because it looks at the effects of blast at a very close range (<2 m) at the four London bombing scenes. Epidemiological study, level V.

Attenuation of blast pressure behind ballistic protective vests

BackgroundClinical studies increasingly report brain injury and not pulmonary injury following blast exposures, despite the increased frequency of exposure to explosive devices. The goal of this study was to determine...

A mouse model of ocular blast injury that induces closed globe anterior and posterior pole damage

We developed and characterized a mouse model of primary ocular blast injury. The device consists of: a pressurized air tank attached to a regulated paintball gun with a machined barrel; a chamber that protects the mouse from direct injury and recoil, while exposing the eye; and a secure platform that enables fine, controlled movement of the chamber in relation to the barrel. Expected pressures were calculated and the optimal pressure transducer, based on the predicted pressures, was positioned to measure output pressures at the location where the mouse eye would be placed. Mice were exposed to one of three blast pressures (23.6, 26.4, or 30.4 psi). Gross pathology, intraocular pressure, optical coherence tomography, and visual acuity were assessed 0, 3, 7, 14, and 28 days after exposure. Contralateral eyes and non-blast exposed mice were used as controls. We detected increased damage with increased pressures and a shift in the damage profile over time. Gross pathology included corneal edema, corneal abrasions, and optic nerve avulsion. Retinal damage was detected by optical coherence tomography and a deficit in visual acuity was detected by optokinetics. Our findings are comparable to those identified in Veterans of the recent wars with closed eye injuries as a result of blast exposure. In summary, this is a relatively simple system that creates injuries with features similar to those seen in patients with ocular blast trauma. This is an important new model for testing the short-term and long-term spectrum of closed globe blast injuries and potential therapeutic interventions.

Primary Blast Injuries—An Updated Concise Review

Blast injuries have been increasing in the civilian setting and clinicians need to understand the spectrum of injury and management strategies. Multisystem trauma associated with combined blunt and penetrating injuries is the rule. Explosions in closed spaces increase the likelihood of primary blast injury. Rupture of tympanic membranes is an inaccurate marker for severe primary blast injury. Blast lung injury manifests early and should be managed with lung-protective ventilation. Blast brain injury is more common than previously appreciated.

Diagnosis and management of evacuated casualties with cervical vascular injuries resulting from combat-related explosive blasts

Explosive blasts are common in the modern military environment. These blasts incorporate a concussive component (primary blast injury) and a penetrating component (secondary blast injury). Penetrating injuries are the leading cause of death and injury in these attacks. This review characterizes the vascular injuries associated with penetrating blast injuries to the neck and provides recommendations on the early management of these casualties for the surgeon unfamiliar with these injuries. The Landstuhl Regional Medical Center Trauma Registry was queried for admissions from January 1, 2006, to June 30, 2010, coded for a penetrating injury to the neck caused by a blast mechanism. Medical records were abstracted from the patient's initial presentation and care through the deployed military medical system. We recorded the vascular injuries, diagnostic studies, operative events, and early postinjury course for all identified patients. Query of the Landstuhl Regional Medical Center Trauma Registry initially identified 252 patients, of which 53 were excluded because their injuries arose from other mechanisms or were only superficial. Among the remaining 199 patients, 38 (19.1%) sustained 44 vascular injuries requiring treatment. Compelling physical examination findings ("hard signs") were present in 15 (7.5%), who underwent immediate neck exploration. Another 12 patients also underwent neck exploration without any prior imaging studies. Computed tomography (CT) or CT angiography (CTA) examinations were done in 172 patients without hard-sign physical examination findings. Of these, the result of the imaging study was negative in 106 patients, and no further investigation or treatment for cervical vascular trauma was initiated. Of 66 patients who underwent CT/CTA before operative neck exploration, CT/CTA identified a vascular injury in 26 that was later confirmed on neck exploration. The combination of physical examination and CT/CTA resulted in a sensitivity of 96.3% and a specificity of 97.2% in diagnosing cervical vascular injury. Penetrating cervical wounds from war-related blast trauma are associated with potentially life-threatening vascular injuries. The presenting physical examination, availability of CT/CTA, local surgical expertise, and tactical combat situation all contribute to surgical decision making in these patients. In patients without hard signs of vascular trauma and a normal CT/CTA of the neck, there is no evidence to support mandatory surgical neck explorations or further immediate diagnostic studies to exclude cervical vascular injury.

Primary blast survival and injury risk assessment for repeated blast exposures

The widespread use of explosives by modern insurgents and terrorists has increased the potential frequency of blast exposure in soldiers and civilians. This growing threat highlights the importance of understanding and evaluating blast injury risk and the increase of injury risk from exposure to repeated blast effects. Data from more than 3,250 large animal experiments were collected from studies focusing on the effects of blast exposure. The current study uses 2,349 experiments from the data collection for analysis of the primary blast injury and survival risk for both long- and short-duration blasts, including the effects from repeated exposures. A piecewise linear logistic regression was performed on the data to develop survival and injury risk assessment curves. New injury risk assessment curves uniting long- and short-duration blasts were developed for incident and reflected pressure measures and were used to evaluate the risk of injury based on blast over pressure, positive-phase duration, and the number of repeated exposures. The risk assessments were derived for three levels of injury severity: nonauditory, pulmonary, and fatality. The analysis showed a marked initial decrease in injury tolerance with each subsequent blast exposure. This effect decreases with increasing number of blast exposures. The new injury risk functions showed good agreement with the existing experimental data and provided a simplified model for primary blast injury risk. This model can be used to predict blast injury or fatality risk for single exposure and repeated exposure cases and has application in modern combat scenarios or in setting occupational health limits.

Experimental Animal Models for Studies on the Mechanisms of Blast-Induced Neurotrauma

A blast injury is a complex type of physical trauma resulting from the detonation of explosive compounds and has become an important issue due to the use of improvised explosive devices (IED) in current military conflicts. Blast-induced neurotrauma (BINT) is a major concern in contemporary military medicine and includes a variety of injuries that range from mild to lethal. Extreme forces and their complex propagation characterize BINT. Modern body protection and the development of armored military vehicles can be assumed to have changed the outcome of BINT. Primary blast injuries are caused by overpressure waves whereas secondary, tertiary, and quaternary blast injuries can have more varied origins such as the impact of fragments, abnormal movements, or heat. The characteristics of the blast wave can be assumed to be significantly different in open field detonations compared to explosions in a confined space, such an armored vehicle. Important parameters include peak pressure, duration, and shape of the pulse. Reflections from walls and armor can make the prediction of effects in individual cases very complex. Epidemiological data do not contain information of the comparative importance of the different blast mechanisms. It is therefore important to generate data in carefully designed animal models. Such models can be selective reproductions of a primary blast, penetrating injuries from fragments, acceleration movements, or combinations of such mechanisms. It is of crucial importance that the physical parameters of the employed models are well characterized so that the experiments can be reproduced in different laboratory settings. Ideally, pressure recordings should be calibrated by using the same equipment in several laboratories. With carefully designed models and thoroughly evaluated animal data it should be possible to achieve a translation of data between animal and clinical data. Imaging and computer simulation represent a possible link between experiments and studies of human cases. However, in order for mathematical simulations to be completely useful, the predictions will most likely have to be validated by detailed data from animal experiments. Some aspects of BINT can conceivably be studied in vitro. However, factors such as systemic response, brain edema, inflammation, vasospasm, or changes in synaptic transmission and behavior must be evaluated in experimental animals. Against this background, it is necessary that such animal experiments are carefully developed imitations of actual components in the blast injury. This paper describes and discusses examples of different designs of experimental models relevant to BINT.

Abdominal trauma in primary blast injury

Abdominal trauma in primary blast injury

Seabird and Dolphin Mortality Associated with Underwater Detonation Exercises

AbstractWe report the details of two wildlife mortality events that were associated with underwater detonations. The detonations occurred as part of military training activities at Silver Strand Training Complex in San Diego, California. In March 2006, an underwater detonation resulted in 70 western grebes (Aechmophorus occidentalis) being killed by subsequent sequential detonations in the same training exercise. Ten of the 70 western grebes impacted were necropsied, verifying cause of death as primary blast injury. In March 2011, a time-delayed underwater detonation resulted in the death of three or possibly four long-beaked common dolphins (Delphinus capensis). While these blast events were unlikely to impact these species on a population level, underwater detonations do have the potential for population-level impacts on wildlife. Both events were accidental mortalities and the first ever documented from Navy underwater detonation training in Hawaii, Southern California, and along the U.S. East Coast. The Navy updated its underwater explosive mitigation measures after each of these mortality events to limit the potential of future mortalities by requiring sequential detonations to occur either less than 5 s or more than 30 min apart and by suspending time-delayed detonation training exercises until more robust precautionary measures can be developed.

Controlled Blast Exposure During Forced Explosive Entry Training and Mild Traumatic Brain Injury

There is a paucity of data regarding the pathophysiology and short- and long-term neurologic consequences of primary blast injury in humans. The purpose of this investigation was to test the feasibility of implementing a research protocol in the context of a forced explosive entry training course. Instructors (n = 4) and students (n = 10) completing the Police Explosives Technicians-Forced Entry Instructors course were recruited to participate in the study. Participants underwent a physical examination, tests of postural stability and vestibular ataxia, and a neurocognitive battery 1 day before and 10 days following practical forced explosive entry exercises. The instructors reported significantly more blast exposures in their careers than the students (p < 0.05). Seventy-five percent of the instructors and 50% of the students reported a history of trauma to the head. A minority of the participants had deficits on cranial nerve, vestibular ataxia, and neurocognitive tests which did not change significantly postexposure. All the instructors and most of the students (90%) demonstrated postural stability deficits at baseline which did not change significantly postexposure. Studying the effects of blast exposure on the human brain in a controlled experimental setting is not possible. Forced explosive entry training courses afford an opportunity to begin examining this issue in real time in a controlled setting. This study underscores the importance of baseline testing of troops, of the consideration of subclinical implications of blast exposure, and of continued studies of the effects of blast exposures, including repeated exposures on the human brain.

Clinical relevance of blast-related traumatic brain injury

The global war against terrorism has created new challenges for neurosurgeons, craniofacial surgeons and maxillofacial surgeons; United States military operations in Iraq and Afghanistan have resulted in the greatest incidence of head trauma since the Vietnam conflict. The more frequent use of improvised explosive devices (IED), in conjunction with increased survival from improved body armor and battlefield medicine, has contributed to the increasing number of craniomaxillofacial injuries and consequent head trauma [28]. IEDs usually contain an explosive that, during detonation, is converted into a gas that rapidly expands and forms a high-pressure wave [4]. This blast overpressure wave travels at supersonic speeds and causes primary blast injury. The subsequent blast wind that follows the initial blast wave can propel objects, leading to further harm [7, 29]. The effect of a primary blast wave on the brain remains poorly understood despite the various models and computer simulations used to predict different mechanisms of injury [5, 27]. Because 59% of the service members in Operation Iraqi Freedom (OIF) and Operation Enduring Freedom (OEF) suffered from TBI [21], a better understanding of mechanisms underlying primary blast injury and the establishment of guidelines of care are warranted. Persistent and debilitating symptoms are often associated with mild traumatic brain injury [24], underscoring the need for improved diagnostic and therapeutic modalities. Diffuse axonal injury (DAI) is widely hypothesized to be a principle mechanism of damage and the cause of persistent cognitive defects after traumatic brain injury (TBI). Angular forces can cause shearing or stretching of axons, leading to impaired axonal transport and swelling [9]. However, further elucidation of the pathological mechanism behind blast injury and determining the ideal diagnostic method to identify this condition may help lead to greater protection for military personnel and treatments for those already suffering from this disease. The majority (85%) of reported TBI cases are undetectable with imaging (computed tomography (CT) and magnetic resonance imaging (MRI) are usually insensitive to its characteristic small lesions [1, 13]) and are classified as mild [2, 25] based on the Department of Defense (DoD) screening criteria. The DoD defines mild TBI as loss of consciousness, amnesia, mental status alteration at time of injury, and/or focal neurological deficit or peri-injury confusion/disorientation in a patient with a Glasgow Coma Scale (GCS) score of 13–15 [18]. Once diagnosed, mild TBI is a treatable disease typically associated with a very favorable prognosis [15]. As a result, the recently published results by Mac Donald and colleagues have created a sense of cautious optimism regarding the use of diffusion tensor imaging (DTI) in detecting structural brain damage in blast-exposed patients suffering from mild TBI. In their study, Mac Donald et al. enrolled 63 patients, ages 19–58, from a screened population of 122 service members. The primary goal was to establish whether or not traumatic axonal injury is a primary feature of human blastG. Appelboom : J. Han : S. Bruce : E. S. Connolly Jr. Department of Neurological Surgery, The Neurological Institute, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA

Traumatisme crânien léger et syndrome post-commotionnel : un questionnement ré-émergent

Traumatisme crânien léger et syndrome post-commotionnel : un questionnement ré-émergent

Tympanic Membrane Rupture in the Survivors of the July 7, 2005, London Bombings

The goal of this study was to analyze the prevalence of tympanic membrane rupture in the survivors of the London bombings of July 2005 and to assess whether tympanic membrane rupture provides a useful biomarker for underlying primary blast injuries. Cross-sectional study. Survivors of the 4 blasts of London bombings on July 7, 2005. Data were gathered from medical records and the London's Metropolitan Police evidence documenting the injuries sustained by 143 survivors of the blasts. All patients with tympanic membrane rupture or primary blast injury were identified. Analysis was made of distance against prevalence of tympanic membrane rupture. Correlation between tympanic membrane rupture and other forms of primary blast injury was then assessed. Results from the 143 survivors showed a 48% prevalence of tympanic membrane rupture across all 4 sites. Fifty-one patients had isolated tympanic membrane rupture with no other primary blast injuries. Eleven patients had tympanic membrane rupture and other primary blast injuries, but only one of these was an initially concealed injury (blast lung). Tympanic membrane rupture in survivors of the London bombings on July 7, 2005, had a high prevalence affecting half of patients across a range of distances from the blasts. Tympanic membrane did not act as an effective biomarker of underlying blast lung. In a mass casualty event, patients with isolated tympanic membrane rupture with normal observations and chest radiography can be monitored for a short period and safely discharged with arrangement for ear, nose, and throat follow-up.

Detection of blast-related traumatic brain injury in U.S. military personnel.

Blast-related traumatic brain injuries have been common in the Iraq and Afghanistan wars, but fundamental questions about the nature of these injuries remain unanswered. We tested the hypothesis that blast-related traumatic brain injury causes traumatic axonal injury, using diffusion tensor imaging (DTI), an advanced form of magnetic resonance imaging that is sensitive to axonal injury. The subjects were 63 U.S. military personnel who had a clinical diagnosis of mild, uncomplicated traumatic brain injury. They were evacuated from the field to the Landstuhl Regional Medical Center in Landstuhl, Germany, where they underwent DTI scanning within 90 days after the injury. All the subjects had primary blast exposure plus another, blast-related mechanism of injury (e.g., being struck by a blunt object or injured in a fall or motor vehicle crash). Controls consisted of 21 military personnel who had blast exposure and other injuries but no clinical diagnosis of traumatic brain injury. Abnormalities revealed on DTI were consistent with traumatic axonal injury in many of the subjects with traumatic brain injury. None had detectable intracranial injury on computed tomography. As compared with DTI scans in controls, the scans in the subjects with traumatic brain injury showed marked abnormalities in the middle cerebellar peduncles (P<0.001), in cingulum bundles (P=0.002), and in the right orbitofrontal white matter (P=0.007). In 18 of the 63 subjects with traumatic brain injury, a significantly greater number of abnormalities were found on DTI than would be expected by chance (P<0.001). Follow-up DTI scans in 47 subjects with traumatic brain injury 6 to 12 months after enrollment showed persistent abnormalities that were consistent with evolving injuries. DTI findings in U.S. military personnel support the hypothesis that blast-related mild traumatic brain injury can involve axonal injury. However, the contribution of primary blast exposure as compared with that of other types of injury could not be determined directly, since none of the subjects with traumatic brain injury had isolated primary blast injury. Furthermore, many of these subjects did not have abnormalities on DTI. Thus, traumatic brain injury remains a clinical diagnosis. (Funded by the Congressionally Directed Medical Research Program and the National Institutes of Health; ClinicalTrials.gov number, NCT00785304.).

Authors' reply: abdominal trauma in primary blast injury (Br J Surg 2011; 98: 168–179)

Authors' reply: abdominal trauma in primary blast injury (<i>Br J Surg</i> 2011; 98: 168–179)

Abdominal trauma in primary blast injury (Br J Surg 2011; 98: 168–179)

Abdominal trauma in primary blast injury (<i>Br J Surg</i> 2011; 98: 168–179)