To evaluate the effect of blast in common war injuries.
One thousand three hundred and three patients injured by explosive munitions and demonstrating extremity wounds without other penetrating injuries were admitted to the Military Medical Academy in Belgrade between 1991 and 1994. Of these, 665 patients (51%) had symptoms and physical signs that were compatible with the clinical diagnosis of primary blast injury, whereas the remaining 658 patients did not.
Random sampling of 65 patients in the blast group during the early posttraumatic period showed statistically significant elevations in blood thromboxane A2 (TxA2), prostacyclin (PGI2), and sulfidopeptide leukotrienes compared with the random sample of 62 patients in the nonblast group. This difference could not be accounted for by differing injury severity between the groups, because the severity of wounds as measured by both the Injury Severity Score and the Red Cross Wound Classification was similar in both groups. Amongst blast patients, 200 patients (30%) had long-term (1 year) symptoms and signs reflecting central nervous system disorders. These symptoms and signs were only sporadically found in 4% of the nonblast patients. These findings indicate that primary blast injury is more common in war injuries than previously thought and that of those affected by blast, a surprisingly high proportion retain long-term neurologic disability. The elevation in eicosanoids could be used to confirm and monitor blast injury.
In relation to the immediate management of patients injured by explosive weapons, it follows that particular attention should be paid to the presence and/or development of blast injury. Our findings indicate that blast is more common in war injuries than previously thought. Eicosanoid changes after blast injury suggest that blast injury causes a major physiologic stress. A variety of effects on the central nervous system suggest that blast injury could be responsible for some aspects of what is now considered to be the posttraumatic stress disorder.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.
"Regardless of the specific outcome, there is growing evidence that noise exposure, either from blast wave or continuous high intensity noise, can have an effect on hippocampal neurogenesis. Previous studies have demonstrated that blast exposure has a significant impact on memory in rodents (Cernak et al., 2001; Ahlers et al., 2012) and cognitive functioning in humans (Cernak et al., 1999; Martin et al., 2008; Cernak, 2010). Our result of a long-term reduction in neurogenesis in the hippocampus following blast exposure may underlie these findings given the implicated involvement of hippocampal neurogenesis in memory and cognitive functioning (Deng et al., 2010). "
"Another hypothesized primary mechanism is that shock waves impact the torso and are then transmitted to the brain causing TBI (27–31). In particular, it has been proposed that, indirect transmission of kinetic energy from the blast shock wave traveling through the large vessels of the body plays a key role in causing TBI. "
[Show abstract][Hide abstract] ABSTRACT: Traumatic brain injury (TBI) due to explosive blast exposure is a leading combat casualty. It is also implicated as a key contributor to war related mental health diseases. A clinically important consequence of all types of TBI is a high risk for development of seizures and epilepsy. Seizures have been reported in patients who have suffered blast injuries in the Global War on Terror but the exact prevalence is unknown. The occurrence of seizures supports the contention that explosive blast leads to both cellular and structural brain pathology. Unfortunately, the exact mechanism by which explosions cause brain injury is unclear, which complicates development of meaningful therapies and mitigation strategies. To help improve understanding, detailed neuropathological analysis is needed. For this, histopathological techniques are extremely valuable and indispensable. In the following we will review the pathological results, including those from immunohistochemical and special staining approaches, from recent preclinical explosive blast studies.
Frontiers in Neurology 04/2014; 5:47. DOI:10.3389/fneur.2014.00047
"Civilian and military personnel exposure to violent explosions , often from improvised explosive devices (IEDs), has burgeoned with recent world events (Aschkenasy- Steuer et al. 2005; Cernak et al. 1999; DuBose et al. 2011). In military populations, a RAND report (Tanielian and Jaycox 2008) estimated that as many as 20% (320,000) of military personnel experienced some form of traumatic brain injury (TBI). "
[Show abstract][Hide abstract] ABSTRACT: Though intrinsically of much higher frequency than open-field blast overpressures, high-intensity focused ultrasound (HIFU) pulse trains can be frequency modulated to produce a radiation pressure having a similar form. In this study, 1.5-MHz HIFU pulse trains of 1-ms duration were applied to intact skulls of mice in vivo and resulted in blood-brain barrier disruption and immune responses (astrocyte reactivity and microglial activation). Analyses of variance indicated that 24 h after HIFU exposure, staining density for glial fibrillary acidic protein was elevated in the parietal and temporal regions of the cerebral cortex, corpus callosum and hippocampus, and staining density for the microglial marker, ionized calcium binding adaptor molecule, was elevated 2 and 24 h after exposure in the corpus callosum and hippocampus (all statistical test results, p < 0.05). HIFU shows promise for the study of some bio-effect aspects of blast-related, non-impact mild traumatic brain injuries in animals.
Ultrasound in medicine & biology 01/2014; 40(5). DOI:10.1016/j.ultrasmedbio.2013.11.023 · 2.21 Impact Factor