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Kiriu N, Saitoh D, Sekine Y, Yamamura K, Sasa R, Fujita M, Tsuda H, Tomura S, Kiyozumi T. Shock wave damage from the ventral side in primary blast injury: An experimental study in pigs. Injury 2024; 55:111982. [PMID: 39499985 DOI: 10.1016/j.injury.2024.111982] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/02/2024] [Revised: 10/11/2024] [Accepted: 10/21/2024] [Indexed: 12/02/2024]
Abstract
AIM/PURPOSE This study aimed to apply a shock wave from the ventral side of a pig and examine its effect to use the results for new body armor production for humans. METHODS Seven male hybrid pigs were used. Each pig was placed under general anesthesia on the experimental table in a blast tube in the left lateral position to expose the front chest area, and shock waves generated by compressed air at 3.0 MPa were applied. We examined changes in vital signs and arterial blood gas in the hyper-acute phase and computed tomography (CT) images, and autopsies were performed for organ damage after 3 h of observation. Pathological examination was performed for lung damage, which is considered a characteristic of shock wave injury. RESULTS All seven pigs survived. Respiratory arrest occurred in two pigs; however, spontaneous breathing resumed promptly afterward. Hypotension occurred at a frequency of 4. No bradycardia or cardiac arrest was observed in any pig. In the arterial blood gas analysis before and immediately after shock wave exposure and 1 h later, PaO2 decreased immediately but tended to improve thereafter. CT revealed pulmonary contusions and multiple bulla-like lesions on the surface of the lungs. An autopsy showed lung injury in all pigs, particularly in five cases with bulla-like lesions of various sizes on the lung surface across all lobes. Pathological findings showed visceral pleural detachment with elastic fibers from the lung parenchyma, and the cavity lesion on the lung surface comprised bullae. The degree of intra-abdominal hemorrhage varied; however, all but one case showed splenic injury. CONCLUSION None of the pigs exposed to shock waves from the ventral side died; however, most showed multiple bullae on the lung surface with lung contusion and splenic injury, which may have been greater than those exposed from the dorsal side. This may be due to the direct impact of the shock wave proceeding from the epigastrium and subcostal region, which are not protected by the skeletal structure of the thorax. These characteristics should be considered when producing new body armor for humans to protect the body from shock waves.
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Affiliation(s)
- Nobuaki Kiriu
- Division of Traumatology, Research Institute, National Defense Medical College (NDMC), 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan; Department of Traumatology and Critical Care Medicine, NDMC, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan.
| | - Daizoh Saitoh
- Department of Traumatology and Critical Care Medicine, NDMC, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan; Graduate School of Emergency Medical System, Kokushikan University, 7-3-1, Nagayama, Tama, Tokyo 206-8515, Japan
| | - Yasumasa Sekine
- Division of Traumatology, Research Institute, National Defense Medical College (NDMC), 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan; Department of Traumatology and Critical Care Medicine, NDMC, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan
| | - Koji Yamamura
- Department of Oral Surgery, NDMC, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan
| | - Ruka Sasa
- Division of Traumatology, Research Institute, National Defense Medical College (NDMC), 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan
| | - Masanori Fujita
- Division of Environmental Medicine, Research Institute, NDMC, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan
| | - Hitoshi Tsuda
- Department of Basic Pathology, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan
| | - Satoshi Tomura
- Division of Traumatology, Research Institute, National Defense Medical College (NDMC), 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan
| | - Tetsuro Kiyozumi
- Department of Traumatology and Critical Care Medicine, NDMC, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan
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Kiriu N, Saitoh D, Sekine Y, Yamamura K, Fujita M, Mizukaki T, Tomura S, Kiyozumi T. Effectiveness of Body Armor Against Shock Waves: Preventing Blast Injury in a Confined Space. Cureus 2024; 16:e57568. [PMID: 38707053 PMCID: PMC11069021 DOI: 10.7759/cureus.57568] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 04/03/2024] [Indexed: 05/07/2024] Open
Abstract
Introduction Blast injuries in modern society often occur owing to terrorist attacks in confined spaces, particularly in urban settings, indoors, and in vehicles, leading to significant damage. Therefore, it is important to focus on blast injuries in confined spaces rather than in conventional open-field experiments. Materials and methods We used an air-driven shock wave generator (blast tube) established indoors in 2017 and conducted basic research to potentially save the lives of patients with blast injuries. Under general anesthesia, pigs were divided into with body armor (BA) and without BA groups. The pigs were fixed in the measurement chamber with their dorsal chest directly exposed to the shock wave. The driving pressure was set at 3.0 MPa to achieve a mortality rate of approximately 50%. A generated shock wave was directly applied to the pigs. Comparisons were made between the groups with respect to cardiac arrest and survival, as well as apnea, bradycardia, and hypotension, which are the triad of blast lung. Autopsies were performed to confirm the extent of the organ damage. Statistical analysis was performed using Fisher's exact test, and statistical significance was set at p<0.05. The animal experimentation was conducted according to the protocol reviewed and approved by the Animal Ethics Committee of the National Defense Medical College Hospital (approval number 19041). Results Eight pigs were assigned to the BA group and seven pigs to the non-BA group. In the non-BA group, apnea was observed in four of seven cases, three of which resulted in death. None of the eight pigs in the BA group had respiratory arrest; notably, all survived. Hypotension was observed in some pigs in each group; however, there were no cases of bradycardia in either group. Statistical analysis showed that wearing BA significantly reduced the occurrence of respiratory and cardiac arrest (p=0.026) but not survival (p=0.077). No significant differences were found in other vital signs. Conclusions Wearing BA with adequate neck and chest protection reduced mortality and it was effective to reduce cardiac and respiratory arrest against shock wave exposure. Mortality from shock wave injury appears to be associated with respiratory arrest, and the avoidance of respiratory arrest may lead to survival.
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Affiliation(s)
- Nobuaki Kiriu
- Division of Traumatology, Research Institute, National Defense Medical College, Saitama, JPN
- Department of Traumatology and Critical Care Medicine, National Defense Medical College, Saitama, JPN
| | - Daizoh Saitoh
- Graduate School of Emergency Medical System, Kokushikan University, Tokyo, JPN
- Department of Traumatology and Critical Care Medicine, National Defense Medical College, Saitama, JPN
| | - Yasumasa Sekine
- Division of Traumatology, Research Institute, National Defense Medical College, Saitama, JPN
- Department of Traumatology and Critical Care Medicine, National Defense Medical College, Saitama, JPN
| | - Koji Yamamura
- Department of Oral Surgery, National Defense Medical College, Saitama, JPN
| | - Masanori Fujita
- Division of Environmental Medicine, Research Institute, National Defense Medical College, Saitama, JPN
| | - Toshiharu Mizukaki
- Department of Aeronautics and Astronautics, School of Engineering, Tokai University, Kanagawa, JPN
| | - Satoshi Tomura
- Division of Traumatology, Research Institute, National Defense Medical College, Saitama, JPN
| | - Tetsuro Kiyozumi
- Department of Traumatology and Critical Care Medicine, National Defense Medical College, Saitama, JPN
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Bukowski J, Nowadly CD, Schauer SG, Koyfman A, Long B. High risk and low prevalence diseases: Blast injuries. Am J Emerg Med 2023; 70:46-56. [PMID: 37207597 DOI: 10.1016/j.ajem.2023.05.003] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/18/2023] [Revised: 04/29/2023] [Accepted: 05/02/2023] [Indexed: 05/21/2023] Open
Abstract
INTRODUCTION Blast injury is a unique condition that carries a high rate of morbidity and mortality, often with mixed penetrating and blunt injuries. OBJECTIVE This review highlights the pearls and pitfalls of blast injuries, including presentation, diagnosis, and management in the emergency department (ED) based on current evidence. DISCUSSION Explosions may impact multiple organ systems through several mechanisms. Patients with suspected blast injury and multisystem trauma require a systematic evaluation and resuscitation, as well as investigation for injuries specific to blast injuries. Blast injuries most commonly affect air-filled organs but can also result in severe cardiac and brain injury. Understanding blast injury patterns and presentations is essential to avoid misdiagnosis and balance treatment of competing interests of patients with polytrauma. Management of blast victims can also be further complicated by burns, crush injury, resource limitation, and wound infection. Given the significant morbidity and mortality associated with blast injury, identification of various injury patterns and appropriate management are essential. CONCLUSIONS An understanding of blast injuries can assist emergency clinicians in diagnosing and managing this potentially deadly disease.
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Affiliation(s)
- Josh Bukowski
- Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, TX, USA
| | - Craig D Nowadly
- Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, TX, USA.
| | - Steven G Schauer
- US Army Institute of Surgical Research, JBSA Fort Sam Houston, TX; Brooke Army Medical Center, JBSA Fort Sam Houston, TX, USA.
| | - Alex Koyfman
- Department of Emergency Medicine, UT Southwestern, Dallas, TX, USA
| | - Brit Long
- Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, TX, USA.
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Yamamura K, Kiriu N, Tomura S, Kawauchi S, Murakami K, Sato S, Saitoh D, Yokoe H. The cause of acute lethality of mice exposed to a laser-induced shock wave to the brainstem. Sci Rep 2022; 12:9490. [PMID: 35676447 PMCID: PMC9177849 DOI: 10.1038/s41598-022-13826-6] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/11/2022] [Accepted: 05/27/2022] [Indexed: 11/10/2022] Open
Abstract
Air embolism is generally considered the most common cause of death within 1 h of a blast injury. Shock lung, respiratory arrest, and circulatory failure caused by vagal reflexes contribute to fatal injuries that lead to immediate death; however, informative mechanistic data are insufficient. Here we used a laser-induced shock wave (LISW) to determine the mechanism of acute fatalities associated with blast injuries. We applied the LISW to the forehead, upper neck, and thoracic dorsum of mice and examined their vital signs. Moreover, the LISW method is well suited for creating site-specific damage. Here we show that only mice with upper neck exposure, without damage elsewhere, died more frequently compared with the other injured groups. The peripheral oxygen saturation (SpO2) of the former mice significantly decreased for < 1 min [p < 0.05] but improved within 3 min. The LISW exposure to the upper neck region was the most lethal factor, affecting the respiratory function. Protecting the upper neck region may reduce fatalities that are related to blast injuries.
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Affiliation(s)
- Koji Yamamura
- Department of Oral and Maxillofacial Surgery, National Defense Medical College, Tokorozawa, Japan.
| | - Nobuaki Kiriu
- Division of Traumatology, Research Institute, National Defense Medical College, Tokorozawa, Japan.,Department of Traumatology and Critical Care Medicine, National Defense Medical College, Tokorozawa, Japan
| | - Satoshi Tomura
- Division of Traumatology, Research Institute, National Defense Medical College, Tokorozawa, Japan
| | - Satoko Kawauchi
- Division of Bioinformation and Therapeutic Systems, Research Institute, National Defense Medical College, Tokorozawa, Saitama, Japan
| | - Kaoru Murakami
- Department of Oral and Maxillofacial Surgery, National Defense Medical College, Tokorozawa, Japan
| | - Shunichi Sato
- Division of Bioinformation and Therapeutic Systems, Research Institute, National Defense Medical College, Tokorozawa, Saitama, Japan
| | - Daizoh Saitoh
- Division of Traumatology, Research Institute, National Defense Medical College, Tokorozawa, Japan.,Department of Traumatology and Critical Care Medicine, National Defense Medical College, Tokorozawa, Japan
| | - Hidetaka Yokoe
- Department of Oral and Maxillofacial Surgery, National Defense Medical College, Tokorozawa, Japan
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Sekine Y, Saitoh D, Yoshimura Y, Fujita M, Araki Y, Kobayashi Y, Kusumi H, Yamagishi S, Suto Y, Tamaki H, Ono Y, Mizukaki T, Nemoto M. Efficacy of Body Armor in Protection Against Blast Injuries Using a Swine Model in a Confined Space with a Blast Tube. Ann Biomed Eng 2021; 49:2944-2956. [PMID: 33686618 PMCID: PMC8510944 DOI: 10.1007/s10439-021-02750-x] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/04/2020] [Accepted: 02/05/2021] [Indexed: 01/04/2023]
Abstract
The purpose of this study was to clarify whether or not body armor would protect the body of a swine model using a blast tube built at National Defense Medical College, which is the first such blast tube in Japan. Seventeen pigs were divided into two groups: the body armor group and the non-body armor group. Under intravenous anesthesia, the pigs were tightly fixed in the left lateral position on a table and exposed from the back neck to the upper lumbar back to the blast wave and wind with or without body armor, with the driving pressure of the blast tube set to 3.0 MPa. When the surviving and dead pigs were compared, blood gas analyses revealed significant differences in PaO2, PaCO2, and pH in the super-early phase. All pigs injured by the blast wave and wind had lung hemorrhage. All 6 animals in the body armor group and 6 of the 11 animals in the control group survived for 3 hours after injury. Respiratory arrest immediately after exposure to the blast wave was considered to influence the mortality in our pig model. Body armor may have a beneficial effect in protecting against respiratory arrest immediately after an explosion.
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Affiliation(s)
- Yasumasa Sekine
- Division of Traumatology, Research Institute, National Defense Medical College (NDMC), 3-2 Namiki, Tokorozawa, 359-8513 Japan ,Dept. of Traumatology and Critical Care Medicine, NDMC, 3-2 Namiki, Tokorozawa, 359-8513 Japan ,Dept. of Emergency and Trauma Care, Saitama Medical University International Medical Center, 1397-1 Yamane, Hidaka, Saitama 350-1298 Japan
| | - Daizoh Saitoh
- Division of Traumatology, Research Institute, National Defense Medical College (NDMC), 3-2 Namiki, Tokorozawa, 359-8513 Japan
| | - Yuya Yoshimura
- Dept. of Traumatology and Critical Care Medicine, NDMC, 3-2 Namiki, Tokorozawa, 359-8513 Japan
| | - Masanori Fujita
- Division of Environmental Medicine, Research Institute, NDMC, 3-2 Namiki, Tokorozawa, 359-8513 Japan
| | - Yoshiyuki Araki
- Dept. of Defense Medicine, NDMC, 3-2 Namiki, Tokorozawa, 359-8513 Japan
| | | | - Hitomi Kusumi
- Dept. of Military Nursing, NDMC, 3-2 Namiki, Tokorozawa, 359-8513 Japan
| | - Satomi Yamagishi
- Dept. of Military Nursing, NDMC, 3-2 Namiki, Tokorozawa, 359-8513 Japan
| | - Yuki Suto
- Division of Traumatology, Research Institute, National Defense Medical College (NDMC), 3-2 Namiki, Tokorozawa, 359-8513 Japan
| | - Hiroshi Tamaki
- Division of Graduate School, Dept. of Academic Affairs, NDMC, 3-2 Namiki, Tokorozawa, 359-8513 Japan
| | - Yosuke Ono
- Department of General Medicine, NDMC, 3-2 Namiki, Tokorozawa, 359-8513 Japan ,Military Medicine Research Unit, Test and Evaluation Command, Japan Ground Self Defense Force, 1-2-24 Ikejiri, setagaya-ku, Tokyo, 154-0004 Japan
| | - Toshiharu Mizukaki
- Dept. of Aeronautics and Astronautics, Tokai University, 4-1-1 Kitakaname, Hiratsuka, Kanagawa 259-1292 Japan
| | - Manabu Nemoto
- Dept. of Emergency and Trauma Care, Saitama Medical University International Medical Center, 1397-1 Yamane, Hidaka, Saitama 350-1298 Japan
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Weppner J, Linsenmeyer M, Ide W. Military Blast-Related Traumatic Brain Injury. CURRENT PHYSICAL MEDICINE AND REHABILITATION REPORTS 2019. [DOI: 10.1007/s40141-019-00241-8] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/24/2022]
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Sharrock AE, Remick KN, Midwinter MJ, Rickard RF. Combat vascular injury: Influence of mechanism of injury on outcome. Injury 2019; 50:125-130. [PMID: 30219382 DOI: 10.1016/j.injury.2018.06.037] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/30/2018] [Revised: 06/05/2018] [Accepted: 06/23/2018] [Indexed: 02/02/2023]
Abstract
BACKGROUND Haemorrhage is the leading cause of death on the battlefield. Seventy percent of injuries are due to explosive mechanisms. Anecdotally, these patients have had poorer outcomes when compared to those with penetrating mechanisms of injury (MOI). We wished to test the hypothesis that outcomes following vascular reconstruction were worse in blast-injured than non blast-injured patients. METHODS Retrospective cohort study. British and American combat casualties with arterial injuries sustained in Iraq or Afghanistan (2003-2014) were identified from the UK Joint Theatre Trauma Registry (JTTR). Eligibility included explosive or penetrating MOI, with follow-up to UK hospital discharge, or death. Outcomes were mortality, amputation, graft thrombosis, haemorrhage, and infection. Statistical analysis was performed using Pearson Chi-Square test, t-tests, ANOVA or non-parametric equivalent, and survival analyses. RESULTS One hundred and fifteen patients were included, 80 injured by explosive and 35 by penetrating mechanisms. Evacuation time, ISS, number of arterial injuries, age and gender were comparable between groups. Seventy percent of arterial injuries resulted from an explosive MOI. The explosive injuries group received more blood products (p = 0.008) and suffered more regions injured (p < 0.0001). Early surgical interventions in both were ligation (n = 36, 31%), vein graft (n = 33, 29%) and shunting (n = 9, 8%). Mortality (n = 12, 10%) was similar between groups. Differences in limb salvage rates following explosive (n = 17, 53%) vs penetrating (n = 13, 76.47%) mechanisms approached statistical significance (p = 0.056). Nine (28%) vein grafted patients developed complications. No evidence of a difference in the incidence of vein graft thrombosis was found when comparing explosive with non-explosive cohorts (p = 0.154). CONCLUSIONS The recorded numbers of vein grafts following combat arterial trauma in are small in the JTTR. No statistically-significant differences in complications, including vein graft thrombosis, were found between cohorts injured by explosive and non-explosive mechanisms.
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Affiliation(s)
- Anna E Sharrock
- Regeneration, repair and development section, National Heart and Lung Institute, Imperial College, London, UK; Royal British Legion Centre for Blast Injury Studies, Imperial College London, UK; Academic Department of Military Surgery and Trauma, Royal Centre for Defence Medicine, Birmingham, UK.
| | - Kyle N Remick
- The Department of Surgery at the Uniformed Services University of the Health Sciences & the Walter Reed National Military Medical Center, Bethesda, MD, USA.
| | | | - Rory F Rickard
- Academic Department of Military Surgery and Trauma, Royal Centre for Defence Medicine, Birmingham, UK.
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Sandlin DS, Yu Y, Huang J, Zhang C, Arteaga AA, Lippincott JK, Peeden EO, Guyton RR, Chen L, Beneke LL, Allison JC, Zhu H, Zhou W. Autonomic responses to blast overpressure can be elicited by exclusively exposing the ear in rats. J Otol 2018; 13:44-53. [PMID: 30559764 PMCID: PMC6291641 DOI: 10.1016/j.joto.2018.01.001] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/07/2017] [Revised: 01/28/2018] [Accepted: 01/30/2018] [Indexed: 11/29/2022] Open
Abstract
Blast overpressure has become an increasing cause of brain injuries in both military and civilian populations. Though blast's direct effects on the cochlea and vestibular organs are active areas of study, little attention has been given to the ear's contribution to the overall spectrum of blast injury. Acute autonomic responses to blast exposure, including bradycardia and hypotension, can cause hypoxia and contribute to blast-induced neurotrauma. Existing literature suggests that these autonomic responses are elicited through blast impacting the thorax and lungs. We hypothesize that the unprotected ear also provides a vulnerable locus for blast to cause autonomic responses. We designed a blast generator that delivers controlled overpressure waves into the ear canal without impacting surrounding tissues in order to study the ear's specific contribution to blast injury. Anesthetized adult rats' left ears were exposed to a single blast wave ranging from 0 to 110 PSI (0-758 kPa). Blast exposed rats exhibited decreased heart rates and blood pressures with increased blast intensity, similar to results gathered using shock tubes and whole-body exposure in the literature. While rats exposed to blasts below 50 PSI (345 kPa) exhibited increased respiratory rate with increased blast intensity, some rats exposed to blasts higher than 50 PSI (345 kPa) stopped breathing immediately and ultimately died. These autonomic responses were significantly reduced in vagally denervated rats, again similar to whole-body exposure literature. These results support the hypothesis that the unprotected ear contributes to the autonomic responses to blast.
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Affiliation(s)
- David S. Sandlin
- Graduate Program in Neuroscience, University of Mississippi Medical Center, Jackson, MS, USA
- School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA
| | - Yue Yu
- Department of Otolaryngology and Communicative Sciences, University of Mississippi Medical Center, Jackson, MS, USA
| | - Jun Huang
- Department of Otolaryngology and Communicative Sciences, University of Mississippi Medical Center, Jackson, MS, USA
| | - Chunming Zhang
- Department of Otolaryngology and Communicative Sciences, University of Mississippi Medical Center, Jackson, MS, USA
- Department of Otolaryngology, First Affiliated Hospital, Shanxi Medical University, 85 Jiefang S Rd, Yingze Qu, Taiyuan Shi, Shanxi Sheng, China
| | - Alberto A. Arteaga
- Department of Otolaryngology and Communicative Sciences, University of Mississippi Medical Center, Jackson, MS, USA
| | - John K. Lippincott
- School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA
| | - Erin O.H. Peeden
- School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA
| | - Ryan R. Guyton
- Graduate Program in Neuroscience, University of Mississippi Medical Center, Jackson, MS, USA
| | - Lan Chen
- Summer Undergraduate Research Experience, University of Mississippi Medical Center, Jackson, MS, USA
| | - Laura L.S. Beneke
- School of Medicine, University of Mississippi Medical Center, Jackson, MS, USA
| | - Jerome C. Allison
- Department of Otolaryngology and Communicative Sciences, University of Mississippi Medical Center, Jackson, MS, USA
| | - Hong Zhu
- Department of Otolaryngology and Communicative Sciences, University of Mississippi Medical Center, Jackson, MS, USA
- Department of Neurobiology and Anatomical Sciences, University of Mississippi Medical Center, Jackson, MS, USA
| | - Wu Zhou
- Department of Otolaryngology and Communicative Sciences, University of Mississippi Medical Center, Jackson, MS, USA
- Department of Neurobiology and Anatomical Sciences, University of Mississippi Medical Center, Jackson, MS, USA
- Department of Neurology, University of Mississippi Medical Center, Jackson, MS, USA
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9
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Awwad HO, Durand CD, Gonzalez LP, Tompkins P, Zhang Y, Lerner MR, Brackett DJ, Sherry DM, Awasthi V, Standifer KM. Post-blast treatment with Nociceptin/Orphanin FQ peptide (NOP) receptor antagonist reduces brain injury-induced hypoxia and signaling proteins in vestibulomotor-related brain regions. Behav Brain Res 2018; 340:183-194. [PMID: 27793733 DOI: 10.1016/j.bbr.2016.10.041] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/31/2016] [Revised: 10/17/2016] [Accepted: 10/24/2016] [Indexed: 12/14/2022]
Abstract
Mild traumatic brain injury (mTBI) diagnoses have increased due to aggressive sports and blast-related injuries, but the cellular mechanisms and pathology underlying mTBI are not completely understood. Previous reports indicate that Nociceptin Orphanin/FQ (N/OFQ), an endogenous neuropeptide, contributes to post-injury ischemia following mechanical brain injury, yet its specific role in cerebral hypoxia, vestibulomotor function and injury marker expression following blast-induced TBI is not known. This study is the first to identify a direct association of N/OFQ and its N/OFQ peptide (NOP) receptor with TBI-induced changes following a single 80psi head blast exposure in male rats. N/OFQ and NOP receptor expression increased in brain tissue and plasma following TBI, concurrent with vestibular dysfunction but preceding hypoxia and appearance of injury markers compared to sham rats. A single post-blast treatment with the NOP receptor antagonist, SB-612111, transiently improved acute vestibulomotor performance. It also prevented increases in markers of TBI-induced hypoxia, pro-apoptotic proteins and injury seen 8-10days post-blast. This study reveals an apparent role for the N/OFQ-NOP receptor system in blast TBI and suggests potential therapeutic utility of NOP receptor antagonists for mTBI.
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Affiliation(s)
- Hibah O Awwad
- Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Oklahoma Center for Neuroscience, Oklahoma City, OK, USA.
| | - Cindy D Durand
- Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
| | - Larry P Gonzalez
- Oklahoma Center for Neuroscience, Oklahoma City, OK, USA; Department of Psychiatry & Behavioral Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
| | - Paul Tompkins
- Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
| | - Yong Zhang
- Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Oklahoma Center for Neuroscience, Oklahoma City, OK, USA
| | - Megan R Lerner
- Department of Surgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK USA; Oklahoma city VA Medical Center, Oklahoma City, OK 73117, USA
| | - Daniel J Brackett
- Department of Surgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK USA
| | - David M Sherry
- Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Oklahoma Center for Neuroscience, Oklahoma City, OK, USA; Department of Cell Biology, College of Medicine, University of Oklahoma Health Sciences Center, USA
| | - Vibhudutta Awasthi
- Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
| | - Kelly M Standifer
- Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Oklahoma Center for Neuroscience, Oklahoma City, OK, USA; Department of Cell Biology, College of Medicine, University of Oklahoma Health Sciences Center, USA
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10
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Skotak M, Alay E, Chandra N. On the Accurate Determination of Shock Wave Time-Pressure Profile in the Experimental Models of Blast-Induced Neurotrauma. Front Neurol 2018; 9:52. [PMID: 29467718 PMCID: PMC5808170 DOI: 10.3389/fneur.2018.00052] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/03/2017] [Accepted: 01/19/2018] [Indexed: 01/04/2023] Open
Abstract
Measurement issues leading to the acquisition of artifact-free shock wave pressure-time profiles are discussed. We address the importance of in-house sensor calibration and data acquisition sampling rate. Sensor calibration takes into account possible differences between calibration methodology in a manufacturing facility, and those used in the specific laboratory. We found in-house calibration factors of brand new sensors differ by less than 10% from their manufacturer supplied data. Larger differences were noticeable for sensors that have been used for hundreds of experiments and were as high as 30% for sensors close to the end of their useful lifetime. These observations were despite the fact that typical overpressures in our experiments do not exceed 50 psi for sensors that are rated at 1,000 psi maximum pressure. We demonstrate that sampling rate of 1,000 kHz is necessary to capture the correct rise time values, but there were no statistically significant differences between peak overpressure and impulse values for low-intensity shock waves (Mach number <2) at lower rates. We discuss two sources of experimental errors originating from mechanical vibration and electromagnetic interference on the quality of a waveform recorded using state-of-the-art high-frequency pressure sensors. The implementation of preventive measures, pressure acquisition artifacts, and data interpretation with examples, are provided in this paper that will help the community at large to avoid these mistakes. In order to facilitate inter-laboratory data comparison, common reporting standards should be developed by the blast TBI research community. We noticed the majority of published literature on the subject limits reporting to peak overpressure; with much less attention directed toward other important parameters, i.e., duration, impulse, and dynamic pressure. These parameters should be included as a mandatory requirement in publications so the results can be properly compared with others.
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Affiliation(s)
- Maciej Skotak
- Department of Biomedical Engineering, New Jersey Institute of Technology, Newark, NJ, United States
| | - Eren Alay
- Department of Biomedical Engineering, New Jersey Institute of Technology, Newark, NJ, United States
| | - Namas Chandra
- Department of Biomedical Engineering, New Jersey Institute of Technology, Newark, NJ, United States
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11
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Abstract
A case of blast injury with tympanic perforation and limb laceration is reported. The classification (into four types), mechanism and pathogenesis of blast injury are discussed. Detection of early air embolism, especially on site, can be very difficult. Victims who appear to have only superficial secondary injuries (by missile fragments) should not be discharged without a careful examination since overt air embolism can occur later. To prevent or reduce air embolism, mechanical ventilation should be avoided.
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Affiliation(s)
| | | | | | - Cw Kam
- Tuen Mun Hospital, Accident and Emergency Department, Tuen Mun, N.T., Hong Kong
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12
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Abstract
Combat-related blast trauma results in massive tissue injury and tends to involve multiple systems. Further, an acute measure of injury severity based on underlying biological mechanisms may be important for the triage and treatment of these types of patients. We hypothesized that urinary biomarkers (UBs) would reflect severity of injury and that they would be elevated for blast injuries compared with gunshot wounds (GSW) in a cohort of combat casualties. We also postulated that UBs would be higher in patients with burns compared with patients with non-burn trauma in a civilian cohort. Among 80 service members who sustained combat-related injuries, we performed generalized estimating equations to compare differences in log-transformed concentrations of the UBs by both injury severity and injury mechanism. Among 22 civilian patients, we performed Kruskal-Wallis tests to compare differences for the UBs stratified by burn and non-burn trauma. In the military cohort, with the exception of IL-18, all UBs were significantly (P <0.05) higher for patients with a severe combat-related injury (Injury Severity Score ≥25). In addition, all crude UBs concentrations were significantly higher for blast versus GSW patients (P < 0.05). After adjusting for injury severity score and time of UB draw, KIM-1 (2.80 vs. 2.31; P = 0.03) and LFABP (-1.11 vs. -1.92; P = 0.02) were significantly higher for patients with a blast mechanism of injury. There were no significant differences in UBs between burn and non-burn civilian trauma patients. Future studies are needed to understand the physiologic response to trauma and the extent that UBs reflect these underlying processes.
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13
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CD43Lo classical monocytes participate in the cellular immune response to isolated primary blast lung injury. J Trauma Acute Care Surg 2017; 81:500-11. [PMID: 27306447 DOI: 10.1097/ta.0000000000001116] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/24/2022]
Abstract
BACKGROUND Understanding of the cellular immune response to primary blast lung injury (PBLI) is limited, with only the neutrophil response well documented. Moreover, its impact on the immune response in distal organs remains poorly understood. In this study, a rodent model of isolated primary blast injury was used to investigate the acute cellular immune response to isolated PBLI in the circulation and lung, including the monocyte response, and investigate distal subacute immune effects in the spleen and liver 6 hours after injury. METHODS Rats were subjected to a shock wave (~135 kPa overpressure, 2 ms duration) inducing PBLI or sham procedure. Rat physiology was monitored, and at 1, 3, and 6 hours thereafter, blood, lung, and bronchoalveolar lavage fluid (BALF) were collected and analyzed by flow cytometry, enzyme-linked immunosorbent assay, and histologic examination. In addition, at 6 hours, spleen and liver were collected and analyzed by flow cytometry. RESULTS Lung histology confirmed pulmonary barotrauma and inflammation. This was associated with rises in CXCL-1, interleukin 6 (IL-6), tumor necrosis factor α and albumin protein in the BALF. Significant acute increases in blood and lung neutrophils and CD43Lo/His48Hi (classical) monocytes/macrophages were detected. No significant changes were seen in blood or lung "nonclassical" monocyte and in natural killler, B, or T cells. In the BALF, significant increases were seen in neutrophils, CD43Lo monocyte-macrophages and monocyte chemoattractant protein-1. Significant increases in CD43Lo and Hi monocyte-macrophages were detected in the spleen at 6 hours. CONCLUSION This study reveals a robust and selective response of CD43Lo/His48Hi (classical) monocytes, in addition to neutrophils, in blood and lung tissue following PBLI. An increase in monocyte-macrophages was also observed in the spleen at 6 hours. This profile of immune cells in the blood and BALF could present a new research tool for translational studies seeking to monitor, assess, or attenuate the immune response in blast-injured patients.
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14
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Horst K, Simon TP, Pfeifer R, Teuben M, Almahmoud K, Zhi Q, Santos SA, Wembers CC, Leonhardt S, Heussen N, Störmann P, Auner B, Relja B, Marzi I, Haug AT, van Griensven M, Kalbitz M, Huber-Lang M, Tolba R, Reiss LK, Uhlig S, Marx G, Pape HC, Hildebrand F. Characterization of blunt chest trauma in a long-term porcine model of severe multiple trauma. Sci Rep 2016; 6:39659. [PMID: 28000769 PMCID: PMC5175194 DOI: 10.1038/srep39659] [Citation(s) in RCA: 43] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/04/2016] [Accepted: 11/24/2016] [Indexed: 12/20/2022] Open
Abstract
Chest trauma has a significant relevance on outcome after severe trauma. Clinically, impaired lung function typically occurs within 72 hours after trauma. However, the underlying pathophysiological mechanisms are still not fully elucidated. Therefore, we aimed to establish an experimental long-term model to investigate physiological, morphologic and inflammatory changes, after severe trauma. Male pigs (sus scrofa) sustained severe trauma (including unilateral chest trauma, femur fracture, liver laceration and hemorrhagic shock). Additionally, non-injured animals served as sham controls. Chest trauma resulted in severe lung damage on both CT and histological analyses. Furthermore, severe inflammation with a systemic increase of IL-6 (p = 0.0305) and a local increase of IL-8 in BAL (p = 0.0009) was observed. The pO2/FiO2 ratio in trauma animals decreased over the observation period (p < 0.0001) but not in the sham group (p = 0.2967). Electrical Impedance Tomography (EIT) revealed differences between the traumatized and healthy lung (p < 0.0001). In conclusion, a clinically relevant, long-term model of blunt chest trauma with concomitant injuries has been developed. This reproducible model allows to examine local and systemic consequences of trauma and is valid for investigation of potential diagnostic or therapeutic options. In this context, EIT might represent a radiation-free method for bedside diagnostics.
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Affiliation(s)
- K Horst
- Department of Orthopaedic Trauma, RWTH Aachen University, Germany.,Harald Tscherne Research Laboratory, RWTH Aachen University, Germany
| | - T P Simon
- Department of Intensive Care and Intermediate Care, RWTH Aachen University, Germany
| | - R Pfeifer
- Department of Orthopaedic Trauma, RWTH Aachen University, Germany.,Harald Tscherne Research Laboratory, RWTH Aachen University, Germany
| | - M Teuben
- Department of Orthopaedic Trauma, RWTH Aachen University, Germany.,Harald Tscherne Research Laboratory, RWTH Aachen University, Germany
| | - K Almahmoud
- Department of Orthopaedic Trauma, RWTH Aachen University, Germany.,Harald Tscherne Research Laboratory, RWTH Aachen University, Germany
| | - Q Zhi
- Harald Tscherne Research Laboratory, RWTH Aachen University, Germany
| | - S Aguiar Santos
- Chair for Medical Information Technology, Helmholtz-Institute for Biomedical Engineering, RWTH Aachen University, Aachen, Germany
| | - C Castelar Wembers
- Chair for Medical Information Technology, Helmholtz-Institute for Biomedical Engineering, RWTH Aachen University, Aachen, Germany
| | - S Leonhardt
- Chair for Medical Information Technology, Helmholtz-Institute for Biomedical Engineering, RWTH Aachen University, Aachen, Germany
| | - N Heussen
- Department of Medical Statistics, RWTH Aachen University, Germany.,Medical School, Sigmund Freud Private University, Vienna, Austria
| | - P Störmann
- Department of Trauma-, Hand- and Reconstructive Surgery, University of Frankfurt/Main, Germany
| | - B Auner
- Department of Trauma-, Hand- and Reconstructive Surgery, University of Frankfurt/Main, Germany
| | - B Relja
- Department of Trauma-, Hand- and Reconstructive Surgery, University of Frankfurt/Main, Germany
| | - I Marzi
- Department of Trauma-, Hand- and Reconstructive Surgery, University of Frankfurt/Main, Germany
| | - A T Haug
- Experimental Trauma Surgery, Department of Trauma Surgery, Klinikum rechts der Isar, Technical University of Munich, Germany
| | - M van Griensven
- Experimental Trauma Surgery, Department of Trauma Surgery, Klinikum rechts der Isar, Technical University of Munich, Germany
| | - M Kalbitz
- Department of Orthopedic Trauma, Hand-, Plastic-, and Reconstructive Surgery, University of Ulm, Germany
| | - M Huber-Lang
- Department of Orthopedic Trauma, Hand-, Plastic-, and Reconstructive Surgery, University of Ulm, Germany
| | - R Tolba
- Institute for Laboratory Animal Science and Experimental Surgery, RWTH Aachen University, Germany
| | - L K Reiss
- Institute of Pharmacology and Toxicology, RWTH Aachen University, Germany
| | - S Uhlig
- Institute of Pharmacology and Toxicology, RWTH Aachen University, Germany
| | - G Marx
- Department of Intensive Care and Intermediate Care, RWTH Aachen University, Germany
| | - H C Pape
- Department of Orthopaedic Trauma, RWTH Aachen University, Germany
| | - F Hildebrand
- Department of Orthopaedic Trauma, RWTH Aachen University, Germany
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15
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Mishra V, Skotak M, Schuetz H, Heller A, Haorah J, Chandra N. Primary blast causes mild, moderate, severe and lethal TBI with increasing blast overpressures: Experimental rat injury model. Sci Rep 2016; 6:26992. [PMID: 27270403 PMCID: PMC4895217 DOI: 10.1038/srep26992] [Citation(s) in RCA: 77] [Impact Index Per Article: 8.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/01/2015] [Accepted: 04/27/2016] [Indexed: 11/25/2022] Open
Abstract
Injury severity in blast induced Traumatic Brain Injury (bTBI) increases with blast overpressure (BOP) and impulse in dose-dependent manner. Pure primary blast waves were simulated in compressed gas shock-tubes in discrete increments. Present work demonstrates 24 hour survival of rats in 0–450 kPa (0–800 Pa∙s impulse) range at 10 discrete levels (60, 100, 130, 160, 190, 230, 250, 290, 350 and 420 kPa) and determines the mortality rate as a non-linear function of BOP. Using logistic regression model, predicted mortality rate (PMR) function was calculated, and used to establish TBI severities. We determined a BOP of 145 kPa as upper mild TBI threshold (5% PMR). Also we determined 146–220 kPa and 221–290 kPa levels as moderate and severe TBI based on 35%, and 70% PMR, respectively, while BOP above 290 kPa is lethal. Since there are no standards for animal bTBI injury severity, these thresholds need further refinements using histopathology, immunohistochemistry and behavior. Further, we specifically investigated mild TBI range (0–145 kPa) using physiological (heart rate), pathological (lung injury), immuno-histochemical (oxidative/nitrosative and blood-brain barrier markers) as well as blood borne biomarkers. With these additional data, we conclude that mild bTBI occurs in rats when the BOP is in the range of 85–145 kPa.
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Affiliation(s)
- Vikas Mishra
- Center for Injury Biomechanics, Materials and Medicine (CIBM3), Department of Biomedical Engineering, New Jersey Institute of Technology, Newark, NJ 07102-1982, USA
| | - Maciej Skotak
- Center for Injury Biomechanics, Materials and Medicine (CIBM3), Department of Biomedical Engineering, New Jersey Institute of Technology, Newark, NJ 07102-1982, USA
| | - Heather Schuetz
- Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, 68198, NE,USA
| | - Abi Heller
- Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, 68198, NE,USA
| | - James Haorah
- Center for Injury Biomechanics, Materials and Medicine (CIBM3), Department of Biomedical Engineering, New Jersey Institute of Technology, Newark, NJ 07102-1982, USA
| | - Namas Chandra
- Center for Injury Biomechanics, Materials and Medicine (CIBM3), Department of Biomedical Engineering, New Jersey Institute of Technology, Newark, NJ 07102-1982, USA
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16
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Eftaxiopoulou T, Barnett-Vanes A, Arora H, Macdonald W, Nguyen TTN, Itadani M, Sharrock AE, Britzman D, Proud WG, Bull AMJ, Rankin SM. Prolonged but not short-duration blast waves elicit acute inflammation in a rodent model of primary blast limb trauma. Injury 2016; 47:625-32. [PMID: 26838938 DOI: 10.1016/j.injury.2016.01.017] [Citation(s) in RCA: 21] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/30/2015] [Revised: 01/06/2016] [Accepted: 01/14/2016] [Indexed: 02/02/2023]
Abstract
BACKGROUND Blast injuries from conventional and improvised explosive devices account for 75% of injuries from current conflicts; over 70% of injuries involve the limbs. Variable duration and magnitude of blast wave loading occurs in real-life explosions and is hypothesised to cause different injuries. While a number of in vivo models report the inflammatory response to blast injuries, the extent of this response has not been investigated with respect to the duration of the primary blast wave. The relevance is that explosions in open air are of short duration compared to those in confined spaces. METHODS Hindlimbs of adult Sprauge-Dawley rats were subjected to focal isolated primary blast waves of varying overpressure (1.8-3.65kPa) and duration (3.0-11.5ms), utilising a shock tube and purpose-built experimental rig. Rats were monitored during and after the blast. At 6 and 24h after exposure, blood, lungs, liver and muscle tissues were collected and prepared for histology and flow cytometry. RESULTS At 6h, increases in circulating neutrophils and CD43Lo/His48Hi monocytes were observed in rats subjected to longer-duration blast waves. This was accompanied by increases in circulating pro-inflammatory chemo/cytokines KC and IL-6. No changes were observed with shorter-duration blast waves irrespective of overpressure. In all cases, no histological damage was observed in muscle, lung or liver. By 24h post-blast, all inflammatory parameters had normalised. CONCLUSIONS We report the development of a rodent model of primary blast limb trauma that is the first to highlight an important role played by blast wave duration and magnitude in initiating acute inflammatory response following limb injury in the absence of limb fracture or penetrating trauma. The combined biological and mechanical method developed can be used to further understand the complex effects of blast waves in a range of different tissues and organs in vivo.
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Affiliation(s)
| | | | - Hari Arora
- Department of Bioengineering, Imperial College London, UK.
| | | | | | - Mako Itadani
- Department of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
| | - Anna E Sharrock
- National Heart and Lung Institute, Imperial College London, UK.
| | - David Britzman
- Department of Bioengineering, Imperial College London, UK.
| | | | | | - Sara M Rankin
- National Heart and Lung Institute, Imperial College London, UK.
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17
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Miyawaki H, Saitoh D, Hagisawa K, Noguchi M, Sato S, Kinoshita M, Miyazaki H, Satoh Y, Harada N, Sakamoto T. Noradrenalin effectively rescues mice from blast lung injury caused by laser-induced shock waves. Intensive Care Med Exp 2015; 3:32. [PMID: 26662813 PMCID: PMC4675774 DOI: 10.1186/s40635-015-0069-7] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/06/2015] [Accepted: 12/06/2015] [Indexed: 01/08/2023] Open
Abstract
Background Blast lung injuries (BLI) caused by blast waves are extremely critical in the prehospital setting, and hypotension is thought to be the main cause of death in such cases. The present study aimed to elucidate the pathophysiology of severe BLI using laser-induced shock wave (LISW) and identify the initial treatment. Methods The current investigation comprised two parts. For the validation study, mice were randomly allocated to groups that received a single shot of 1.2, 1.3, or 1.4 J/cm2 LISW to both lungs. The survival rates, systolic blood pressure (sBP), heart rate (HR), peripheral oxyhemoglobin saturation (SpO2), and shock index were monitored for 60 min, and lung tissues were analyzed histopathologically. The study evaluated the effects of catecholamines as follows. Randomly assigned mice received 1.4 J/cm2 LISW followed by the immediate intraperitoneal administration of dobutamine, noradrenalin, or normal saline. The primary outcome was the survival rate. Additionally, sBP, HR, SpO2, and the shock index were measured before and 5 and 10 min after LISW, and the cardiac output, left ventricular ejection fraction, and systemic vascular resistance (SVR) were determined before and 1 min after LISW. Results The triad of BLI (hypotension, bradycardia, and hypoxemia) was evident immediately after LISW. The survival rates worsened with increasing doses of LISW (100 % in 1.2 J/cm2 vs. 60 % in 1.3 J/cm2, 10 % in 1.4 J/cm2). The histopathological findings were compatible with those of human BLI. The survival rate in LISW high group (1.4 J/cm2) was highest in the group that received noradrenalin (100 %), with significantly elevated SVR values (from 565 to 1451 dyn s/min5). In contrast, the survival rates in the dobutamine and normal saline groups were 40 and 10 %, respectively, and the SVR values did not change significantly after LISW in either group. Conclusions The main cause of death during the initial phase of severe BLI is hypotension due to the absence of peripheral vasoconstriction. Therefore, the immediate administration of noradrenalin may be an effective treatment during the initial phase of severe BLI.
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Affiliation(s)
- Hiroki Miyawaki
- Department of Traumatology and Critical Care Medicine, National Defense Medical College Hospital, 3-2 Namiki, Tokorozawa, 359-8513, Japan
| | - Daizoh Saitoh
- Division of Traumatology, Research Institute, National Defense Medical College, 3-2 Namiki, Tokorozawa, 359-8513, Japan.
| | - Kohsuke Hagisawa
- Division of Physiology, National Defense Medical College, 3-2 Namiki, Tokorozawa, 359-8513, Japan
| | - Midori Noguchi
- Division of Traumatology, Research Institute, National Defense Medical College, 3-2 Namiki, Tokorozawa, 359-8513, Japan
| | - Shunichi Sato
- Division of Biomedical Information Sciences, National Defense Medical College, 3-2 Namiki, Tokorozawa, 359-8513, Japan
| | - Manabu Kinoshita
- Department of Immunology and Microbiology, National Defense Medical College, 3-2 Namiki, Tokorozawa, 359-8513, Japan
| | - Hiromi Miyazaki
- Division of Traumatology, Research Institute, National Defense Medical College, 3-2 Namiki, Tokorozawa, 359-8513, Japan
| | - Yasushi Satoh
- Department of Anesthesiology, National Defense Medical College, 3-2 Namiki, Tokorozawa, 359-8513, Japan
| | - Nahoko Harada
- Division of Nursing, School of Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, 359-8513, Japan
| | - Toshihisa Sakamoto
- Department of Traumatology and Critical Care Medicine, National Defense Medical College Hospital, 3-2 Namiki, Tokorozawa, 359-8513, Japan
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18
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Courtney A, Courtney M. The Complexity of Biomechanics Causing Primary Blast-Induced Traumatic Brain Injury: A Review of Potential Mechanisms. Front Neurol 2015; 6:221. [PMID: 26539158 PMCID: PMC4609847 DOI: 10.3389/fneur.2015.00221] [Citation(s) in RCA: 51] [Impact Index Per Article: 5.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/02/2014] [Accepted: 10/05/2015] [Indexed: 11/13/2022] Open
Abstract
Primary blast-induced traumatic brain injury (bTBI) is a prevalent battlefield injury in recent conflicts, yet biomechanical mechanisms of bTBI remain unclear. Elucidating specific biomechanical mechanisms is essential to developing animal models for testing candidate therapies and for improving protective equipment. Three hypothetical mechanisms of primary bTBI have received the most attention. Because translational and rotational head accelerations are primary contributors to TBI from non-penetrating blunt force head trauma, the acceleration hypothesis suggests that blast-induced head accelerations may cause bTBI. The hypothesis of direct cranial transmission suggests that a pressure transient traverses the skull into the brain and directly injures brain tissue. The thoracic hypothesis of bTBI suggests that some combination of a pressure transient reaching the brain via the thorax and a vagally mediated reflex result in bTBI. These three mechanisms may not be mutually exclusive, and quantifying exposure thresholds (for blasts of a given duration) is essential for determining which mechanisms may be contributing for a level of blast exposure. Progress has been hindered by experimental designs, which do not effectively expose animal models to a single mechanism and by over-reliance on poorly validated computational models. The path forward should be predictive validation of computational models by quantitative confirmation with blast experiments in animal models, human cadavers, and biofidelic human surrogates over a range of relevant blast magnitudes and durations coupled with experimental designs, which isolate a single injury mechanism.
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Affiliation(s)
- Amy Courtney
- Exponent Engineering and Scientific Consulting, Philadelphia, PA, USA
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19
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Awwad HO, Gonzalez LP, Tompkins P, Lerner M, Brackett DJ, Awasthi V, Standifer KM. Blast Overpressure Waves Induce Transient Anxiety and Regional Changes in Cerebral Glucose Metabolism and Delayed Hyperarousal in Rats. Front Neurol 2015; 6:132. [PMID: 26136722 PMCID: PMC4470265 DOI: 10.3389/fneur.2015.00132] [Citation(s) in RCA: 26] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/28/2015] [Accepted: 05/22/2015] [Indexed: 01/15/2023] Open
Abstract
Physiological alterations, anxiety, and cognitive disorders are strongly associated with blast-induced traumatic brain injury (blast TBI), and are common symptoms in service personnel exposed to blasts. Since 2006, 25,000–30,000 new TBI cases are diagnosed annually in U.S. Service members; increasing evidence confirms that primary blast exposure causes diffuse axonal injury and is often accompanied by altered behavioral outcomes. Behavioral and acute metabolic effects resulting from blast to the head in the absence of thoracic contributions from the periphery were examined, following a single blast wave directed to the head of male Sprague-Dawley rats protected by a lead shield over the torso. An 80 psi head blast produced cognitive deficits that were detected in working memory. Blast TBI rats displayed increased anxiety as determined by elevated plus maze at day 9 post-blast compared to sham rats; blast TBI rats spent significantly more time than the sham controls in the closed arms (p < 0.05; n = 8–11). Interestingly, anxiety symptoms were absent at days 22 and 48 post-blast. Instead, blast TBI rats displayed increased rearing behavior at day 48 post-blast compared to sham rats. Blast TBI rats also exhibited suppressed acoustic startle responses, but similar pre-pulse inhibition at day 15 post-blast compared to sham rats. Acute physiological alterations in cerebral glucose metabolism were determined by positron emission tomography 1 and 9 days post-blast using 18F-fluorodeoxyglucose (18F-FDG). Global glucose uptake in blast TBI rat brains increased at day 1 post-blast (p < 0.05; n = 4–6) and returned to sham levels by day 9. Our results indicate a transient increase in cerebral metabolism following a blast injury. Markers for reactive astrogliosis and neuronal damage were noted by immunoblotting motor cortex tissue from day 10 post-blast in blast TBI rats compared to sham controls (p < 0.05; n = 5–6).
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Affiliation(s)
- Hibah O Awwad
- Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA ; Oklahoma Center for Neuroscience, College of Medicine, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA
| | - Larry P Gonzalez
- Oklahoma Center for Neuroscience, College of Medicine, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA ; Department of Psychiatry and Behavioral Sciences, College of Medicine, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA
| | - Paul Tompkins
- Department of Neurosurgery, College of Medicine, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA
| | - Megan Lerner
- Department of Surgery, College of Medicine, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA ; Oklahoma City VA Medical Center , Oklahoma City, OK , USA
| | - Daniel J Brackett
- Department of Surgery, College of Medicine, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA
| | - Vibhudutta Awasthi
- Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA
| | - Kelly M Standifer
- Department of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA ; Oklahoma Center for Neuroscience, College of Medicine, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA ; Department of Cell Biology, College of Medicine, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA
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20
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Comprehensive Evaluation of Coagulation in Swine Subjected to Isolated Primary Blast Injury. Shock 2015; 43:598-603. [DOI: 10.1097/shk.0000000000000346] [Citation(s) in RCA: 21] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
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21
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Hubbard WB, Lashof-Sullivan MM, Lavik EB, VandeVord PJ. Steroid-Loaded Hemostatic Nanoparticles Combat Lung Injury after Blast Trauma. ACS Macro Lett 2015; 4:387-391. [PMID: 27668129 PMCID: PMC5033257 DOI: 10.1021/acsmacrolett.5b00061] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/29/2022]
Abstract
In response to the lack of therapeutics for internal bleeding following a traumatic event, we synthesized hemostatic dexamethasone nanoparticles (hDNP) to help alleviate internal hemorrhaging. hDNP consist of a block copolymer, poly(lactic-co-glycolic acid)-poly(l-lysine)-poly(ethylene glycol) conjugated to a peptide, glycine-arginine-glycine-aspartic acid-serine (GRGDS). These particles were evaluated as treatment for primary blast lung injury in a rodent model. Animals were randomly placed into test and control groups, exposed to blast and given immediate injection. Recovery was assessed using physiological parameters and immunohistochemistry. We found that dexamethasone-loaded hemostatic nanoparticles alleviate physiological deprivation caused by blast injury and reduce lung injury damage.
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Affiliation(s)
- William B. Hubbard
- School of Biomedical Engineering and Sciences, Virginia Tech University, Blacksburg, VA
| | | | - Erin B. Lavik
- Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH
| | - Pamela J. VandeVord
- School of Biomedical Engineering and Sciences, Virginia Tech University, Blacksburg, VA
- Research Services, Salem VAMC, Salem, VA
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22
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Elder GA, Gama Sosa MA, De Gasperi R, Stone JR, Dickstein DL, Haghighi F, Hof PR, Ahlers ST. Vascular and inflammatory factors in the pathophysiology of blast-induced brain injury. Front Neurol 2015; 6:48. [PMID: 25852632 PMCID: PMC4360816 DOI: 10.3389/fneur.2015.00048] [Citation(s) in RCA: 86] [Impact Index Per Article: 8.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/27/2015] [Accepted: 02/23/2015] [Indexed: 11/13/2022] Open
Abstract
Blast-related traumatic brain injury (TBI) has received much recent attention because of its frequency in the conflicts in Iraq and Afghanistan. This renewed interest has led to a rapid expansion of clinical and animal studies related to blast. In humans, high-level blast exposure is associated with a prominent hemorrhagic component. In animal models, blast exerts a variety of effects on the nervous system including vascular and inflammatory effects that can be seen with even low-level blast exposures which produce minimal or no neuronal pathology. Acutely, blast exposure in animals causes prominent vasospasm and decreased cerebral blood flow along with blood-brain barrier breakdown and increased vascular permeability. Besides direct effects on the central nervous system, evidence supports a role for a thoracically mediated effect of blast; whereby, pressure waves transmitted through the systemic circulation damage the brain. Chronically, a vascular pathology has been observed that is associated with alterations of the vascular extracellular matrix. Sustained microglial and astroglial reactions occur after blast exposure. Markers of a central and peripheral inflammatory response are found for sustained periods after blast injury and include elevation of inflammatory cytokines and other inflammatory mediators. At low levels of blast exposure, a microvascular pathology has been observed in the presence of an otherwise normal brain parenchyma, suggesting that the vasculature may be selectively vulnerable to blast injury. Chronic immune activation in brain following vascular injury may lead to neurobehavioral changes in the absence of direct neuronal pathology. Strategies aimed at preventing or reversing vascular damage or modulating the immune response may improve the chronic neuropsychiatric symptoms associated with blast-related TBI.
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Affiliation(s)
- Gregory A Elder
- Neurology Service, James J. Peters Department of Veterans Affairs Medical Center , Bronx, NY , USA ; Department of Psychiatry, Icahn School of Medicine at Mount Sinai , New York, NY , USA ; Department of Neurology, Icahn School of Medicine at Mount Sinai , New York, NY , USA ; Friedman Brain Institute, Icahn School of Medicine at Mount Sinai , New York, NY , USA
| | - Miguel A Gama Sosa
- Department of Psychiatry, Icahn School of Medicine at Mount Sinai , New York, NY , USA ; Friedman Brain Institute, Icahn School of Medicine at Mount Sinai , New York, NY , USA ; Research and Development Service, James J. Peters Department of Veterans Affairs Medical Center , Bronx, NY , USA
| | - Rita De Gasperi
- Department of Psychiatry, Icahn School of Medicine at Mount Sinai , New York, NY , USA ; Friedman Brain Institute, Icahn School of Medicine at Mount Sinai , New York, NY , USA ; Research and Development Service, James J. Peters Department of Veterans Affairs Medical Center , Bronx, NY , USA
| | - James Radford Stone
- Department of Radiology and Medical Imaging, University of Virginia , Charlottesville, VA , USA ; Department of Neurosurgery, University of Virginia , Charlottesville, VA , USA
| | - Dara L Dickstein
- Friedman Brain Institute, Icahn School of Medicine at Mount Sinai , New York, NY , USA ; Fishberg Department of Neuroscience, Icahn School of Medicine at Mount Sinai , New York, NY , USA ; Department of Geriatrics and Palliative Care, Icahn School of Medicine at Mount Sinai , New York, NY , USA
| | - Fatemeh Haghighi
- Department of Psychiatry, Icahn School of Medicine at Mount Sinai , New York, NY , USA ; Friedman Brain Institute, Icahn School of Medicine at Mount Sinai , New York, NY , USA ; Research and Development Service, James J. Peters Department of Veterans Affairs Medical Center , Bronx, NY , USA ; Fishberg Department of Neuroscience, Icahn School of Medicine at Mount Sinai , New York, NY , USA
| | - Patrick R Hof
- Friedman Brain Institute, Icahn School of Medicine at Mount Sinai , New York, NY , USA ; Fishberg Department of Neuroscience, Icahn School of Medicine at Mount Sinai , New York, NY , USA ; Department of Geriatrics and Palliative Care, Icahn School of Medicine at Mount Sinai , New York, NY , USA
| | - Stephen T Ahlers
- Department of Neurotrauma, Operational and Undersea Medicine Directorate, Naval Medical Research Center , Silver Spring, MD , USA
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Abstract
Trauma is the leading cause of death during the first four decades of life in the developed countries. Its haemodynamic response underpins the patient's initial ability to survive, and the response to treatment and subsequent morbidity and resolution. Trauma causes a number of insults including haemorrhage, tissue injury (nociception) and, predominantly, in military casualties, blast from explosions. This article discusses aspects of the haemodynamic responses to these insults and subsequent treatment. 'Simple' haemorrhage (blood loss without significant volume of tissue damage) causes a biphasic response: mean arterial blood pressure (MBP) is initially maintained by the baroreflex (tachycardia and increased vascular resistance, Phase 1), followed by a sudden decrease in MAP initiated by a second reflex (decrease in vascular resistance and bradycardia, Phase 2). Phase 2 may be protective. The response to tissue injury attenuates Phase 2 and may cause a deleterious haemodynamic redistribution that compromises blood flow to some vital organs. In contrast, thoracic blast exposure augments Phase 2 of the response to haemorrhage. However, hypoxaemia from lung injury limits the effectiveness of hypotensive resuscitation by augmenting the attendant shock state. An alternative strategy ('hybrid resuscitation') whereby tissue perfusion is increased after the first hour of hypotensive resuscitation by adopting a revised normotensive target may ameliorate these problems. Finally, morphine also attenuates Phase 2 of the response to haemorrhage in some, but not all, species and this is associated with poor outcome. The impact on human patients is currently unknown and is the subject of a current physiological investigation.
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Affiliation(s)
- E Kirkman
- Biomedical Sciences Department, Defence Science and Technology Laboratory, Porton Down, Salisbury, UK
| | - S Watts
- Biomedical Sciences Department, Defence Science and Technology Laboratory, Porton Down, Salisbury, UK
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Kovacs SK, Leonessa F, Ling GSF. Blast TBI Models, Neuropathology, and Implications for Seizure Risk. Front Neurol 2014; 5:47. [PMID: 24782820 PMCID: PMC3988378 DOI: 10.3389/fneur.2014.00047] [Citation(s) in RCA: 45] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/15/2014] [Accepted: 03/26/2014] [Indexed: 12/31/2022] Open
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.
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Affiliation(s)
- S Krisztian Kovacs
- Laboratory of Neurotrauma, Department of Neurology, Uniformed Services University of the Health Sciences , Bethesda, MD , USA
| | - Fabio Leonessa
- Laboratory of Neurotrauma, Department of Neurology, Uniformed Services University of the Health Sciences , Bethesda, MD , USA
| | - Geoffrey S F Ling
- Laboratory of Neurotrauma, Department of Neurology, Uniformed Services University of the Health Sciences , Bethesda, MD , USA
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Hamele M, Poss WB, Sweney J. Disaster preparedness, pediatric considerations in primary blast injury, chemical, and biological terrorism. World J Crit Care Med 2014; 3:15-23. [PMID: 24834398 PMCID: PMC4021150 DOI: 10.5492/wjccm.v3.i1.15] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/15/2013] [Revised: 11/21/2013] [Accepted: 12/09/2013] [Indexed: 02/06/2023] Open
Abstract
Both domestic and foreign terror incidents are an unfortunate outgrowth of our modern times from the Oklahoma City bombings, Sarin gas attacks in Japan, the Madrid train bombing, anthrax spores in the mail, to the World Trade Center on September 11(th), 2001. The modalities used to perpetrate these terrorist acts range from conventional weapons to high explosives, chemical weapons, and biological weapons all of which have been used in the recent past. While these weapons platforms can cause significant injury requiring critical care the mechanism of injury, pathophysiology and treatment of these injuries are unfamiliar to many critical care providers. Additionally the pediatric population is particularly vulnerable to these types of attacks. In the event of a mass casualty incident both adult and pediatric critical care practitioners will likely be called upon to care for children and adults alike. We will review the presentation, pathophysiology, and treatment of victims of blast injury, chemical weapons, and biological weapons. The focus will be on those injuries not commonly encountered in critical care practice, primary blast injuries, category A pathogens likely to be used in terrorist incidents, and chemical weapons including nerve agents, vesicants, pulmonary agents, cyanide, and riot control agents with special attention paid to pediatric specific considerations.
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Tompkins P, Tesiram Y, Lerner M, Gonzalez LP, Lightfoot S, Rabb CH, Brackett DJ. Brain Injury: Neuro-Inflammation, Cognitive Deficit, and Magnetic Resonance Imaging in a Model of Blast Induced Traumatic Brain Injury. J Neurotrauma 2013; 30:1888-97. [DOI: 10.1089/neu.2012.2674] [Citation(s) in RCA: 49] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/13/2022] Open
Affiliation(s)
- Paul Tompkins
- Department of Neurosurgery, University of Oklahoma, HSC, Oklahoma City, Oklahoma
| | - Yasvir Tesiram
- Advanced Magnetic Resonance Center, Free Radical Biology and Aging Research Program, MS21, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma. (Current address: Center for Advanced Imaging, The University of Queensland, St. Lucia, Australia.)
| | - Megan Lerner
- Department of Surgery, University of Oklahoma, HSC and the Veterans Medical Administration Center, Oklahoma City, Oklahoma
| | - Larry P. Gonzalez
- Department of Psychiatry and Behavioral Sciences, University of Oklahoma, HSC, Oklahoma City, Oklahoma
| | - Stan Lightfoot
- Department of Pathology, University of Oklahoma, HSC and the Veterans Medical Administration Center, Oklahoma City, Oklahoma
| | - Craig H. Rabb
- Department of Neurosurgery, University of Oklahoma, HSC, Oklahoma City, Oklahoma
| | - Daniel J. Brackett
- Department of Surgery, University of Oklahoma, HSC and the Veterans Medical Administration Center, Oklahoma City, Oklahoma
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27
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Couret D, de Bourmont S, Prat N, Cordier PY, Soureau JB, Lambert D, Prunet B, Michelet P. A pig model for blunt chest trauma: no pulmonary edema in the early phase. Am J Emerg Med 2013; 31:1220-5. [DOI: 10.1016/j.ajem.2013.05.028] [Citation(s) in RCA: 10] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/24/2013] [Revised: 05/03/2013] [Accepted: 05/20/2013] [Indexed: 10/26/2022] Open
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Skotak M, Wang F, Alai A, Holmberg A, Harris S, Switzer RC, Chandra N. Rat injury model under controlled field-relevant primary blast conditions: acute response to a wide range of peak overpressures. J Neurotrauma 2013; 30:1147-60. [PMID: 23362798 DOI: 10.1089/neu.2012.2652] [Citation(s) in RCA: 61] [Impact Index Per Article: 5.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/22/2022] Open
Abstract
We evaluated the acute (up to 24 h) pathophysiological response to primary blast using a rat model and helium driven shock tube. The shock tube generates animal loadings with controlled pure primary blast parameters over a wide range and field-relevant conditions. We studied the biomechanical loading with a set of pressure gauges mounted on the surface of the nose, in the cranial space, and in the thoracic cavity of cadaver rats. Anesthetized rats were exposed to a single blast at precisely controlled five peak overpressures over a wide range (130, 190, 230, 250, and 290 kPa). We observed 0% mortality rates in 130 and 230 kPa groups, and 30%, 24%, and 100% mortality rates in 190, 250, and 290 kPa groups, respectively. The body weight loss was statistically significant in 190 and 250 kPa groups 24 h after exposure. The data analysis showed the magnitude of peak-to-peak amplitude of intracranial pressure (ICP) fluctuations correlates well with mortality rates. The ICP oscillations recorded for 190, 250, and 290 kPa are characterized by higher frequency (10-20 kHz) than in other two groups (7-8 kHz). We noted acute bradycardia and lung hemorrhage in all groups of rats subjected to the blast. We established the onset of both corresponds to 110 kPa peak overpressure. The immunostaining against immunoglobulin G (IgG) of brain sections of rats sacrificed 24-h post-exposure indicated the diffuse blood-brain barrier breakdown in the brain parenchyma. At high blast intensities (peak overpressure of 190 kPa or more), the IgG uptake by neurons was evident, but there was no evidence of neurodegeneration after 24 h post-exposure, as indicated by cupric silver staining. We observed that the acute response as well as mortality is a non-linear function over the peak overpressure and impulse ranges explored in this work.
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Affiliation(s)
- Maciej Skotak
- Department of Mechanical and Materials Engineering, University of Nebraska-Lincoln, Nebraska, USA
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29
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Wang Y, Pan L, Fan W, Zhou Z, Zhu L, Wang Y, Hu R. Influence of vagal injury on acute traumatic reaction after blast injury. Eur J Trauma Emerg Surg 2013; 39:385-92. [PMID: 26815399 DOI: 10.1007/s00068-013-0277-3] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/07/2012] [Accepted: 03/12/2013] [Indexed: 10/27/2022]
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30
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Xydakis MS, Ling GSF, Mulligan LP, Olsen CH, Dorlac WC. Epidemiologic aspects of traumatic brain injury in acute combat casualties at a major military medical center: A cohort study. Ann Neurol 2012; 72:673-81. [DOI: 10.1002/ana.23757] [Citation(s) in RCA: 34] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/02/2012] [Revised: 07/12/2012] [Accepted: 08/03/2012] [Indexed: 11/09/2022]
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31
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Masel BE, Bell RS, Brossart S, Grill RJ, Hayes RL, Levin HS, Rasband MN, Ritzel DV, Wade CE, DeWitt DS. Galveston Brain Injury Conference 2010: Clinical and Experimental Aspects of Blast Injury. J Neurotrauma 2012; 29:2143-71. [DOI: 10.1089/neu.2011.2258] [Citation(s) in RCA: 27] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/13/2022] Open
Affiliation(s)
- Brent E. Masel
- Transitional Learning Center, Galveston, Texas; Department of Neurology, The University of Texas Medical Branch, Galveston, Texas
| | - Randy S. Bell
- Department of Neurosurgery, National Naval Medical Center, Bethesda, Maryland
| | - Shawn Brossart
- Project Victory, The Transitional Learning Center, Galveston, Texas
| | - Raymond J. Grill
- Department of Integrative Biology and Pharmacology, The University of Texas Medical School at Houston, Houston, Texas
| | - Ronald L. Hayes
- Department of Physical Medicine and Rehabilitation, Baylor College of Medicine, Houston, Texas
| | | | | | | | - Charles E. Wade
- Department of Surgery, The University of Texas Medical School at Houston, Houston, Texas
| | - Douglas S. DeWitt
- Department of Anesthesiology, The University of Texas Medical Branch, Galveston, Texas
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Hemoconcentration caused by microvascular dysfunction after blast injuries to the chest and abdomen of rabbits. ACTA ACUST UNITED AC 2012; 71:694-701. [PMID: 21909001 DOI: 10.1097/ta.0b013e318224595f] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/27/2022]
Abstract
BACKGROUND One of the important causes of death after blast injuries is reduced blood volume, which typically results from hemorrhage but may also result from nonhemorrhagic causes. Hemoconcentration is one such alternate cause of reduced blood volume, but its mechanism is unclear. Because blood is condensed after chest-abdomen blast injuries in rabbits, a series of experiments was conducted to clarify this phenomenon. METHODS Chest-abdomen blast injuries from different distances (10 cm, 15 cm, 20 cm, and 30 cm) were induced in male rabbits. ¹²⁵I-albumin was injected into the blood, and its concentration in different organs was tested at various times after the blast injury. The residual radioactivity in different organs and the pre- and postinjury hematocrit was also tested. Histologic evaluations were conducted to detect the injuries to the different organs. RESULTS After injury, ¹²⁵I-albumin leaked out of the vessels into organs such as the lungs, liver, and kidneys. The volume of leakage was highly correlated with the distance from the blast. At a distance of 10 cm, the rate of leakage was the highest. The hematocrit was higher for 30 minutes and 3 hours after the injury; 6 hours after the injury, the hematocrit began to return to normal levels. The residual radioactivity of ¹²⁵I-albumin was increased in the heart, brain, lungs, and kidneys, especially at a distance of 10 cm. Histologic evaluation results showed that the cells, microvessels, and organelles of the microvessel endothelial cells in the vital organs, such as the kidneys, were damaged. CONCLUSION The preliminary results indicate that microvessels in the lungs and kidneys are the key targets of blast injuries. The damage to the microvessels leads to leakage of albumin, which is one of the important reasons for hemoconcentration in the absence of active bleeding after a blast injury. Treatment should be initiated in victims of blast injuries who are severely wounded as soon as possible after the explosion during the earliest stages of the injury to avoid the occurrence of shock or other severe complications.
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Wu N, Wang W, Tian Y, Zou X, Maffeo M, Niezrecki C, Chen J, Wang X. Low-cost rapid miniature optical pressure sensors for blast wave measurements. OPTICS EXPRESS 2011; 19:10797-10804. [PMID: 21643336 DOI: 10.1364/oe.19.010797] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 05/30/2023]
Abstract
This paper presents an optical pressure sensor based on a Fabry-Perot (FP) interferometer formed by a 45° angle polished single mode fiber and an external silicon nitride diaphragm. The sensor is comprised of two V-shape grooves with different widths on a silicon chip, a silicon nitride diaphragm released on the surface of the wider V-groove, and a 45° angle polished single mode fiber. The sensor is especially suitable for blast wave measurements: its compact structure ensures a high spatial resolution; its thin diaphragm based design and the optical demodulation scheme allow a fast response to the rapid changing signals experienced during blast events. The sensor shows linearity with the correlation coefficient of 0.9999 as well as a hysteresis of less than 0.3%. The shock tube test demonstrated that the sensor has a rise time of less than 2 µs from 0 kPa to 140 kPa.
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Affiliation(s)
- Nan Wu
- Department of Electrical and Computer Engineering, University of Massachusetts Lowell, 1 University Avenue, Lowell, Massachusetts 01854, USA
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Abstract
PRIMARY OBJECTIVE A volumetric blood surge (rapid physical movement/displacement of blood) is hypothesized to cause the non-impact, mild TBI and battlefield PTSD induced by a blast over-pressure wave. RESEARCH DESIGN Systematic review of the literature. METHODS AND PROCEDURES Articles relating to the fields of blast injury, brain injury and relevant disorders were searched between the years 1968-2010 for keywords such as 'brain injury', 'post-traumatic stress disorder' and 'blast pressure wave'. Articles found through journal and Internet databases were cross-referenced. MAIN OUTCOMES AND RESULTS The blood surge, which is driven by elevated overall pressure in the ventral body cavity after exposure of the torso to blast wave, may move through blood vessels to the low-pressure cranial cavity from the high-pressure ventral body cavity. It dramatically increases cerebral perfusion pressure and causes damage to both tiny cerebral blood vessels and the BBB. CONCLUSIONS Three factors may be critical to the induction of blast-induced brain injuries: (1) the difference in pressure between the ventral body cavity and cranial cavity; (2) blood that acts as a transmission medium to propagate a pressure wave to the brain; and (3) the vulnerability of cerebral blood vessels and the BBB to a sudden fluctuation in perfusion pressure.
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Affiliation(s)
- Yun Chen
- Tripler Army Medical Center, Honolulu, HI, USA.
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35
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Kirkman E, Watts S. Characterization of the response to primary blast injury. Philos Trans R Soc Lond B Biol Sci 2011; 366:286-90. [PMID: 21149364 DOI: 10.1098/rstb.2010.0249] [Citation(s) in RCA: 32] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/09/2023] Open
Abstract
Lung injuries, predominantly arising from blast exposure, are a clinical problem in a significant minority of current military casualties. This special feature consists of a series of articles on lung injury. This first article examines the mechanism of the response to blast lung (primary blast injury to the lung). Subsequent articles examine the incidence of blast lung, clinical consequences and current concepts of treatment, computer (in silico) modelling of lung injury and finally chemical injuries to the lungs. Blast lung is caused by a shock wave generated by an explosion causing widespread damage in the lungs, leading to intrapulmonary haemorrhage. This, and the ensuing inflammatory response in the lung, leads to a compromise in pulmonary gas exchange and hypoxia that can worsen over several hours. There is also a characteristic cardio-respiratory effect mediated via an autonomic reflex causing apnoea (or rapid shallow breathing), bradycardia and hypotension (the latter possibly also due to the release of nitric oxide). An understanding of this response, and the way it modifies other reflexes, can help the development of new treatment strategies for this condition and for the way it influences the patient's response to concomitant injuries.
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Affiliation(s)
- E Kirkman
- Biomedical Sciences, Dstl Porton Down, Salisbury SP4 0JQ, UK
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36
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Working toward exposure thresholds for blast-induced traumatic brain injury: Thoracic and acceleration mechanisms. Neuroimage 2011; 54 Suppl 1:S55-61. [DOI: 10.1016/j.neuroimage.2010.05.025] [Citation(s) in RCA: 53] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/01/2009] [Revised: 05/10/2010] [Accepted: 05/11/2010] [Indexed: 12/28/2022] Open
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37
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Cernak I, Merkle AC, Koliatsos VE, Bilik JM, Luong QT, Mahota TM, Xu L, Slack N, Windle D, Ahmed FA. The pathobiology of blast injuries and blast-induced neurotrauma as identified using a new experimental model of injury in mice. Neurobiol Dis 2010; 41:538-51. [PMID: 21074615 DOI: 10.1016/j.nbd.2010.10.025] [Citation(s) in RCA: 195] [Impact Index Per Article: 13.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/05/2010] [Revised: 10/05/2010] [Accepted: 10/27/2010] [Indexed: 12/24/2022] Open
Abstract
Current experimental models of blast injuries used to study blast-induced neurotrauma (BINT) vary widely, which makes the comparison of the experimental results extremely challenging. Most of the blast injury models replicate the ideal Friedländer type of blast wave, without the capability to generate blast signatures with multiple shock fronts and refraction waves as seen in real-life conditions; this significantly reduces their clinical and military relevance. Here, we describe the pathophysiological consequences of graded blast injuries and BINT generated by a newly developed, highly controlled, and reproducible model using a modular, multi-chamber shock tube capable of tailoring pressure wave signatures and reproducing complex shock wave signatures seen in theater. While functional deficits due to blast exposure represent the principal health problem for today's warfighters, the majority of available blast models induces tissue destruction rather than mimic functional deficits. Thus, the main goal of our model is to reliably reproduce long-term neurological impairments caused by blast. Physiological parameters, functional (motor, cognitive, and behavioral) outcomes, and underlying molecular mechanisms involved in inflammation measured in the brain over the 30 day post-blast period showed this model is capable of reproducing major neurological changes of clinical BINT.
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Affiliation(s)
- Ibolja Cernak
- Biomedicine Business Area, National Security Technology Department, Johns Hopkins University Applied Physics Laboratory (JHU/APL), Laurel, MD 20723, USA.
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Effects of fluid resuscitation with hypertonic saline dextrane or Ringer's acetate after nonhemorrhagic shock caused by pulmonary contusion. ACTA ACUST UNITED AC 2010; 69:741-8. [PMID: 20938261 DOI: 10.1097/ta.0b013e3181ea4e6e] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
Abstract
BACKGROUND Injured lungs are sensitive to fluid resuscitation after trauma. Such treatment can increase lung water content and lead to desaturation. Hypertonic saline with dextran (HSD) has hyperosmotic properties that promote plasma volume expansion, thus potentially reducing these side effects. The aim of this study was to (1) evaluate whether fluid treatment counteracts hypotension and improves survival after nonhemorrhagic shock caused by lung contusion and (2) analyze whether resuscitation with HSD is more efficient than treatment with Ringer's acetate (RA) in terms of blood oxygenation, the amount of lung water, circulatory effects, and inflammatory response. METHODS Twenty-nine pigs, all wearing body armor, were shot with a 7.62-mm assault rifle to produce a standardized pulmonary contusion. These animals were allocated into three groups: HSD, RA, and an untreated shot control group. Exposed animals were compared with animals not treated with fluid and shot with blank ammunition. For 2 hours after the shot, the inflammatory response and physiologic parameters were monitored. RESULTS The impact induced pulmonary contusion, desaturation, hypotension, increased heart rate, and led to an inflammatory response. No change in blood pressure was observed after fluid treatment. HSD treatment resulted in significantly less lung water (p < 0.05) and tended to give better Pao2 (p = 0.09) than RA treatment. Tumor necrosis factor-α release and heart rate were significantly lower in animals given fluids. CONCLUSION Fluid treatment does not affect blood pressure or mortality in this model of nonhemorrhagic shock caused by lung contusion. However, our data indicate that HSD, when compared with RA, has advantages for the injured lung.
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Clapson P, Pasquier P, Perez JP, Debien B. [Blast lung injuries]. REVUE DE PNEUMOLOGIE CLINIQUE 2010; 66:245-253. [PMID: 20933166 DOI: 10.1016/j.pneumo.2010.07.008] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 06/22/2010] [Accepted: 06/28/2010] [Indexed: 05/30/2023]
Abstract
In armed conflicts and during terrorist attacks, explosive devices are a major cause of mortality. The lung is one of the organs most sensitive to blasts. Thus, today it is important that every GP at least knows the basics and practices regarding treatment of blast victims. We suggest, following a review of the explosions and an assessment of the current threats, detailing the lung injuries brought about by the explosions and the main treatments currently recommended.
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Affiliation(s)
- P Clapson
- Service de réanimation, hôpital d'Instruction des Armées Percy, 92140 Clamart, France.
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40
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Cernak I, Noble-Haeusslein LJ. Traumatic brain injury: an overview of pathobiology with emphasis on military populations. J Cereb Blood Flow Metab 2010; 30:255-66. [PMID: 19809467 PMCID: PMC2855235 DOI: 10.1038/jcbfm.2009.203] [Citation(s) in RCA: 290] [Impact Index Per Article: 19.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]
Abstract
This review considers the pathobiology of non-impact blast-induced neurotrauma (BINT). The pathobiology of traumatic brain injury (TBI) has been historically studied in experimental models mimicking features seen in the civilian population. These brain injuries are characterized by primary damage to both gray and white matter and subsequent evolution of secondary pathogenic events at the cellular, biochemical, and molecular levels, which collectively mediate widespread neurodegeneration. An emerging field of research addresses brain injuries related to the military, in particular blast-induced brain injuries. What is clear from the effort to date is that the pathobiology of military TBIs, particularly BINT, has characteristics not seen in other types of brain injury, despite similar secondary injury cascades. The pathobiology of primary BINT is extremely complex. It comprises systemic, local, and cerebral responses interacting and often occurring in parallel. Activation of the autonomous nervous system, sudden pressure-increase in vital organs such as lungs and liver, and activation of neuroendocrine-immune system are among the most important mechanisms significantly contributing to molecular changes and cascading injury mechanisms in the brain.
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Affiliation(s)
- Ibolja Cernak
- National Security Technology Department, Johns Hopkins University Applied Physics Laboratory, Laurel, Maryland 20723, USA.
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ATTENUATION OF PULMONARY INFLAMMATION AFTER EXPOSURE TO BLAST OVERPRESSURE BY N-ACETYLCYSTEINE AMIDE. Shock 2009; 32:325-31. [DOI: 10.1097/shk.0b013e31819c38f1] [Citation(s) in RCA: 43] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
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Abstract
Current trends in global terrorism mandate that emergency medical services, emergency medicine and other acute care clinicians have a basic understanding of the physics of explosions, the types of injuries that can result from an explosion, and current management for patients injured by explosions. High-order explosive detonations result in near instantaneous transformation of the explosive material into a highly pressurized gas, releasing energy at supersonic speeds. This results in the formation of a blast wave that travels out from the epicenter of the blast. Primary blast injuries are characterized by anatomical and physiological changes from the force generated by the blast wave impacting the body's surface, and affect primarily gas-containing structures (lungs, gastrointestinal tract, ears). "Blast lung" is a clinical diagnosis and is characterized as respiratory difficulty and hypoxia without obvious external injury to the chest. It may be complicated by pneumothoraces and air emboli and may be associated with multiple other injuries. Patients may present with a variety of symptoms, including dyspnea, chest pain, cough, and hemoptysis. Physical examination may reveal tachypnea, hypoxia, cyanosis, and decreased breath sounds. Chest radiography, computerized tomography, and arterial blood gases may assist with diagnosis and management; however, they should not delay diagnosis and emergency interventions in the patient exposed to a blast. High flow oxygen, airway management, tube thoracostomy in the setting of pneumothoraces, mechanical ventilation (when required) with permissive hypercapnia, and judicious fluid administration are essential components in the management of blast lung injury.
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Affiliation(s)
- Scott M Sasser
- Department of Emergency Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
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43
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Arciniegas DB, McAllister TW. Neurobehavioral management of traumatic brain injury in the critical care setting. Crit Care Clin 2008; 24:737-65, viii. [PMID: 18929941 DOI: 10.1016/j.ccc.2008.06.001] [Citation(s) in RCA: 29] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/15/2022]
Abstract
Traumatic brain injury (TBI) results in approximately 230,000 hospitalizations annually in the United States. Advances in the acute management of TBI have improved survival after TBI. Many TBI survivors develop neurobehavioral disturbances in the acute post-injury period. Neurobehavioral sequelae present clinical management challenges for critical care professionals. This article defines and describes TBI and reviews its common neuroanatomic and neurobehavioral consequences. These disturbances are organized under the framework of posttraumatic encephalopathy, and the characteristic forms and stages of recovery of this condition are discussed. Recommendations regarding evaluation and management of posttraumatic neurobehavioral problems in the critical care setting are offered.
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Affiliation(s)
- David B Arciniegas
- Brain Injury Rehabilitation Unit, HealthONE Spalding Rehabilitation Hospital, Aurora, CO 80011, USA
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44
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Abstract
BACKGROUND A critical immediate determinant of survival after exposure to blast overpressure (BOP) is cardiovascular and respiratory impairment related to disruption of the alveolar septa and pulmonary capillaries and resulting in acute pulmonary hemorrhage. Hemoglobin (Hb) released from red cells can contribute to lethality by activation of oxidative stress reactions and severe vasoconstriction associated with hypoperfusion in the pulmonary microcirculation. Heme oxygenase-1 (HO-1) is activated by hemin, a product of Hb degradation and may confer protection against hemoglobin-mediated oxidative cell and tissue damage. METHODS Rats were injected intraperitoneally with hemin (50 mg/kg) or phosphate buffered saline (PBS). Twenty hours later, animals were placed in a shock tube and exposed to blast overpressure with mean intensity of approximately 160 kPa. Nonblasted sham-injected animals served as controls. RESULTS HO-1 mRNA and HO-1 protein in lungs was induced by injection of hemin. Exposure to blast resulted in confluent lung hemorrhage and mortality ( approximately 65%). Hemin injection significantly improved the survival rate of animals compared with PBS injected animals (p = 0.01). CONCLUSIONS The protection by hemin against blast may involve antioxidative and vasodilatory effects of HO-1, although, the precise mechanisms of the protection are unknown.
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Courtney AC, Courtney MW. A thoracic mechanism of mild traumatic brain injury due to blast pressure waves. Med Hypotheses 2008; 72:76-83. [PMID: 18829180 DOI: 10.1016/j.mehy.2008.08.015] [Citation(s) in RCA: 80] [Impact Index Per Article: 4.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/31/2008] [Revised: 07/31/2008] [Accepted: 08/03/2008] [Indexed: 10/21/2022]
Abstract
The mechanisms by which blast pressure waves cause mild-to-moderate traumatic brain injury (mTBI) are an open question. Possibilities include acceleration of the head, direct passage of the blast wave via the cranium, and propagation of the blast wave to the brain via a thoracic mechanism. The hypothesis that the blast pressure wave reaches the brain via a thoracic mechanism is considered in light of ballistic and blast pressure wave research. Ballistic pressure waves, caused by penetrating ballistic projectiles or ballistic impacts to body armor, can only reach the brain via an internal mechanism and have been shown to cause cerebral effects. Similar effects have been documented when a blast pressure wave has been applied to the whole body or focused on the thorax in animal models. While vagotomy reduces apnea and bradycardia due to ballistic or blast pressure waves, it does not eliminate neural damage in the brain, suggesting that the pressure wave directly affects the brain cells via a thoracic mechanism. An experiment is proposed which isolates the thoracic mechanism from cranial mechanisms of mTBI due to blast wave exposure. Results have implications for evaluating risk of mTBI due to blast exposure and for developing effective protection.
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Affiliation(s)
- A C Courtney
- Department of Physics, United States Military Academy, West Point, NY 10996, United States.
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Nelson TJ, Clark T, Stedje-Larsen ET, Lewis CT, Grueskin JM, Echols EL, Wall DB, Felger EA, Bohman HR. Close proximity blast injury patterns from improvised explosive devices in Iraq: a report of 18 cases. ACTA ACUST UNITED AC 2008; 65:212-7. [PMID: 17514045 DOI: 10.1097/01.ta.0000196010.50246.9a] [Citation(s) in RCA: 16] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2022]
Affiliation(s)
- Thomas J Nelson
- Forward Resuscitative Surgery System 2 and Shock Trauma Platoon 4, 1st Medical Battalion, 1st Marine Expeditionary Force, Al Anbar, Iraq.
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Bilateral Vagotomy Inhibits Apnea and Attenuates Other Physiological Responses After Blunt Chest Trauma. ACTA ACUST UNITED AC 2008; 64:1420-6. [DOI: 10.1097/ta.0b013e318054e247] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/30/2022]
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Pathobiology of Blast Injury. Intensive Care Med 2007. [DOI: 10.1007/978-0-387-49518-7_92] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/22/2022]
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50
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Abstract
PURPOSE OF REVIEW Blast injuries have always occurred both in civilian life and as acts of war or terrorism. Nowadays, the risk of being involved in an explosion has increased even for those living in countries with no previous experience of such events. It is our intention that this review is of assistance to those providing emergency/critical care to patients who have sustained blast injuries. RECENT FINDINGS Exposure to blast may indirectly produce physiological insults such as bradycardia, hypotension, tissue hypoxia and oxidative stress. The use of early goal-directed therapy might be important in minimizing such insults. Explosions in an enclosed environment are associated with increased risk of pulmonary blast injury and also air and fat embolism. Mechanical ventilation after pulmonary blast injury is associated with barotrauma and the use of lung protective strategies previously recommended in acute lung injury may be beneficial. SUMMARY The potential for blast to cause injury depends on the nature of the explosive and environment in which the blast occurs. Soft tissue injury with environmental contamination is frequent. Optimal antimicrobial cover and strategies such as selective digestive decontamination may be advantageous. Early surgery should follow the principles of 'damage control'. Blast injury often leads to severe sepsis/systemic inflammatory response, multiple organ dysfunction and prolonged critical illness. In this clinical scenario, recent studies have shown improved outcome with the use of activated protein C, steroid replacement and aggressive control of blood glucose but have been less convincing regarding the use of immuno-nutrition.
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Affiliation(s)
- Gavin G Lavery
- Critical Care Services, Theatres and Intensive Care, Royal Hospitals Trust, Belfast, Northern Ireland, UK.
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