Blast injury to the brain is the predominant cause of neurotrauma in current military conflicts, and its etiology is largely undefined. Using a compression-driven shock tube to simulate blast effects, we assessed the physiological, neuropathological, and neurobehavioral consequences of airblast exposure, and also evaluated the effect of a Kevlar protective vest on acute mortality in rats and on the occurrence of traumatic brain injury (TBI) in those that survived. This approach provides survivable blast conditions under which TBI can be studied. Striking neuropathological changes were caused by both 126- and 147-kPa airblast exposures. The Kevlar vest, which encased the thorax and part of the abdomen, greatly reduced airblast mortality, and also ameliorated the widespread fiber degeneration that was prominent in brains of rats not protected by a vest during exposure to a 126-kPa airblast. This finding points to a significant contribution of the systemic effects of airblast to its brain injury pathophysiology. Airblast of this intensity also disrupted neurologic and neurobehavioral performance (e.g., beam walking and spatial navigation acquisition in the Morris water maze). When immediately followed by hemorrhagic hypotension, with MAP maintained at 30 mm Hg, airblast disrupted cardiocompensatory resilience, as reflected by reduced peak shed blood volume, time to peak shed blood volume, and time to death. These findings demonstrate that shock tube-generated airblast can cause TBI in rats, in part through systemic mediation, and that the resulting brain injury significantly impacts acute cardiovascular homeostatic mechanisms as well as neurobehavioral function.

Blast Overpressure in Rats: Recreating a Battlefield Injury in the Laboratory

The extensive oxygen gradient between the air we breathe (Po2 ~21 kPa) and its ultimate distribution within mitochondria (as low as ~0.5–1 kPa) is testament to the efforts expended in limiting its ...

Defining Physiological Normoxia for Improved Translation of Cell Physiology to Animal Models and Humans

A thoracic mechanism of mild traumatic brain injury due to blast pressure waves.

Working toward exposure thresholds for blast-induced traumatic brain injury: thoracic and acceleration mechanisms.

The US government has initiated the largest coordinated research programs ever in neurotrauma. The specific focus is to get insight in mechanisms and to provide better treatment for blast induced traumatic brain injuries (BINT, Blast Induced Neuro Trauma) (Ling et al., 2009). The background should probably be well known for anyone working in the field of traumatic brain injuries (TBI). The asymmetric warfare in the recent military conflicts in Iraq and Afghanistan has resulted in numerous attacks with Improvised Explosive Devices (IED) and large losses in terms of deaths and wounded soldiers (Warden, 2006; Terrio et al., 2009). TBI has been identified as major health problem in military personnel returning from service. The injuries range from severe multitrauma to a number of mild TBI that still has to be settled. A large number of research groups with different backgrounds contribute to this effort. In addition, a number of other countries have also ongoing research programs on blast induced brain injuries.

The current research programs are so large and well coordinated so that it is tempting to compare with Apollo Program about 50 years ago. Apart from putting man on the moon that program had several positive spinoff effects in many areas, i.e in electronics. Similar spinoff effects might come in from the current programs. It would be logical that these programs can generate important new knowledge in treatment of mildTBI, diffuse axonal injuries (DAI), the role of inflammation in TBI, neuroprotection, rehabilitation of TBI and acute oedema treatment. Many groups are working with advanced computerized mathematical models of the head to provide understanding of propagation of blast waves. Such models will also be important for the design of better injury prevention in road traffic accidents. More detailed criteria for different types of TBI would also be important tools for improvements of safety in vehicles. We can also expect a lot of data from research on more specific biomarkers for TBI (Wang et al., 2005; Agoston et al., 2009) and evaluation of digital EEG to indentify functional changes. New imaging techniques may get an increasing power to identify DAI and regional vascular perfusion defects after TBI.

To mention a few of the specific problems in BINT:


Propagation of blast waves is very complex. It could involve both direct propagation through the skull and indirect propagation via blood vessels (Cernak and Noble-Haeusslein, 2010). If the latter mechanism is important, we could expect effects from vascular disturbance. Several lines of evidence seem to point in that direction.


Is BINT a specific type injury that will require specific and new types of treatment? Or is, for example, the mild TBI from blast exposure more like a classical type of concussion injury (Hoge et al., 2009)?


Is it possible to identify a reliable borderline between mild BINT and posttraumatic stress syndrome (PTSD)? Many of the symptoms are similar and many patients might suffer from both TBI and PTSD (Jaffee and Meyer, 2009).


Is BINT an entirely new problem? The shellshock syndrome (Anderson, 2008) that was seen after the enormous artillery battles during World War I had similarities to BINT and post BINT symptoms, but for many years it has been regarded as PTSD rather than physical injuries. The new situation with IED is that the explosive often detonates at short distance and that improved body armour and helmets protect much better against penetration from fragments. Could the new body armour also change the physical parameters of the blast wave, in a similar way that is described as BABT (behind armour blunt trauma) (Drobin et al., 2007).


Although the epidemiology of BINT has been established in terms of approximate numbers of injured, it is very difficult to assess the injury mechanisms in individual cases. Complex propagation and reflection of the primary supersonic blast wave, effects from acceleration and rotation, effects from impact of fragments, effects from heating, effects from emitted gases and electromagnetic waves. Well-designed experimental models are required as well as data from acceleration probes and pressure sensors that have been mounted into helmets and body armour will increase the knowledge of the critical mechanisms.



Tragic experience from military conflicts has on previous occasions generated valuable medical knowledge. During the Roman Empire the army physicians learned the lesson not to close contaminated wounds and they also developed an early set of ethical rules, which also included treatment of wounded enemies. We could also mention the Crimean war and its impact on nursing and sanitary principles as well as a war between Russia and Sweden, that resulted in the foundation of the Karolinska institute to provide better training for Army surgeons, exactly 200 years ago. During more recent years, the careful examination of TBI patients from the Vietnam War has generated very important general knowledge (Raymont et al., 2008; Koenigs and Grafman, 2009).

Thus, it is a grand challenge to extract all useful information from the current research program on blast induced brain injuries. We can expect to see a number of articles dealing with that problem in this journal.

/pdf/blast-induced-brain-injuries-a-grand-challenge-in-tbi-4b6sy22e3e.pdf

Blast Induced Brain Injuries - A Grand Challenge in TBI Research

Background:Behind armor blunt trauma (BABT) is defined as the nonpenetrating injury resulting from a ballistic impact on personal body armor. The protective vest may impede the projectile, but some of the kinetic energy is transferred to the body, causing internal injuries and occasionally death. Th

Electroencephalogram, circulation, and lung function after high-velocity behind armor blunt trauma.

The objective of the present study was to investigate the possibility of measuring lung tissue oxygen pressure (PtO2) distributions at the microvascular level, and also if a change in the lung tissue oxygenation could be detected during hypoventilation (50% reduction in ventilatory settings). Experiments were carried out on eight mechanically ventilated ketamine-anaesthetised pigs. A thoracotomy was performed through the third right intercostal space. PtO2 measurements were made using a Clark-type multiwire microelectrode placed onto the pleural surface of the middle lobe. PtO2 was measured during normoventilation, hypoventilation (3 minutes) (reduction of respiratory volume/minute and frequency by 50%), and a second period of normoventilation. Baseline PtO2 was 5.8 (range 4.4 to 10.3) kPa and decreased to 2.9 (range 1.6 to 4.2) kPa during hypoventilation, associated with some PtO2 values close to zero. The PtO2 increased to 5.4 (range 3.6 to 8.4) kPa during the second normoventilatory period, some values still close to zero. This study demonstrates that lung tissue PO2 registrations can be made in a suitable animal (pig) model, and that hypoventilation induced an almost reversible decrease in lung tissue oxygen pressure distributions. In addition, no microscopically visible tissue damage was inflicted by the electrode on the underlying lung surface.

/pdf/microvascular-lung-tissue-oxygenation-a-methodological-study-4l4gl90xup.pdf

Microvascular lung tissue oxygenation--a methodological study in the pig.

The purpose of this paper was to study the effect of peripheral high energy missile trauma on oxygenation of the lung tissue. Eleven pigs were randomised to either high energy gunshot wound of the soft tissues of the thigh or sham exposure. Under anaesthesia and controlled ventilation, the carotid artery and the jugular vein were catheterised and a thoracotomy was performed. A Clark-type multiwire electrode was placed on the surface of the middle lung lobe for registration of the oxygen pressure fields of the lung tissue (PtO2). In animals subjected to missile trauma, an increased heterogeneity was seen in PtO2 1 and 2 hours after exposure, specially under hypoventilatory provocation. Furthermore, PtO2 values did not return to baseline when hypoventilation was followed by normoventilation, in contrast to what was seen in the sham exposed animals. No differences between groups were found in arterial PO2, O2-saturation, PCO2, pH or in pulse frequency. These findings of disturbance in oxygenation of pulmonary tissue, may represent an early phase in the development of a lung injury resembling the post-traumatic adult respiratory distress syndrome seen in man. The initiating events could be release of mediators from traumatised tissue and/or direct effects of the shock waves from missile impact, passing through the body.

B. T. Kjellstrom

Papers

Electroencephalogram, circulation, and lung function after high-velocity behind armor blunt trauma.

Microvascular lung tissue oxygenation--a methodological study in the pig.

Effects of peripheral high energy missile trauma on the oxygenation of lung tissue in the pig.