Hemoconcentration Caused by Microvascular Dysfunction After Blast Injuries to the Chest and Abdomen of Rabbits

Zhang, Bin; Wang, Aiming; Hu, Wei; Liang-chao, Zhang; Xiong, Yan; Chen, Jing; Wang, Jianmin

doi:10.1097/ta.0b013e318224595f

Cited by 7 publications

(3 citation statements)

References 35 publications

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“…Therefore, damage to the ear is a primary blast injury. Other organs that are particularly sensitive to primary blast injury include the lung and abdomen [6], [7].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Hearing Loss after Blast Injury to the Ear

et al. 2013

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Given the frequent use of improvised explosive devices (IEDs) around the world, the study of traumatic blast injuries is of increasing interest. The ear is the most common organ affected by blast injury because it is the body’s most sensitive pressure transducer. We fabricated a blast chamber to re-create blast profiles similar to that of IEDs and used it to develop a reproducible mouse model to study blast-induced hearing loss. The tympanic membrane was perforated in all mice after blast exposure and found to heal spontaneously. Micro-computed tomography demonstrated no evidence for middle ear or otic capsule injuries; however, the healed tympanic membrane was thickened. Auditory brainstem response and distortion product otoacoustic emission threshold shifts were found to be correlated with blast intensity. As well, these threshold shifts were larger than those found in control mice that underwent surgical perforation of their tympanic membranes, indicating cochlear trauma. Histological studies one week and three months after the blast demonstrated no disruption or damage to the intra-cochlear membranes. However, there was loss of outer hair cells (OHCs) within the basal turn of the cochlea and decreased spiral ganglion neurons (SGNs) and afferent nerve synapses. Using our mouse model that recapitulates human IED exposure, our results identify that the mechanisms underlying blast-induced hearing loss does not include gross membranous rupture as is commonly believed. Instead, there is both OHC and SGN loss that produce auditory dysfunction.

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“…Therefore, damage to the ear is a primary blast injury. Other organs that are particularly sensitive to primary blast injury include the lung and abdomen [6], [7].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Hearing Loss after Blast Injury to the Ear

et al. 2013

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“…Among these mechanisms, implosion forces are the most consistent with the observed lung response in this study, resulting in rapid compression and expansion of gaseous content. At the alveolar length scale, compression can cause the alveolus to collapse and result in atelectasis [ 48 ], while pneumothorax can occur at the length scale of the lung [ 18 , 19 ]. Rapid lung expansion can cause alveolar and capillary overstretching and rupture, or the driving of extravascular fluid into the alveolar space, causing pulmonary oedema and hemorrhage [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

The dynamic response of human lungs due to underwater shock wave exposure

Bar-Kochba,

Iwaskiw,

Dunn

et al. 2024

PLoS ONE

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Since the 19th century, underwater explosions have posed a significant threat to service members. While there have been attempts to establish injury criteria for the most vulnerable organs, namely the lungs, existing criteria are highly variable due to insufficient human data and the corresponding inability to understand the underlying injury mechanisms. This study presents an experimental characterization of isolated human lung dynamics during simulated exposure to underwater shock waves. We found that the large acoustic impedance at the surface of the lung severely attenuated transmission of the shock wave into the lungs. However, the shock wave initiated large bulk pressure-volume cycles that are distinct from the response of the solid organs under similar loading. These pressure-volume cycles are due to compression of the contained gas, which we modeled with the Rayleigh-Plesset equation. The extent of these lung dynamics was dependent on physical confinement, which in real underwater blast conditions is influenced by factors such as rib cage properties and donned equipment. Findings demonstrate a potential causal mechanism for implosion injuries, which has significant implications for the understanding of primary blast lung injury due to underwater blast exposures.

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“…[7][8][9] In addition, PBI to vascular endothelium may cause diffuse plasma leakage and resultant hemoconcentration and hypovolemic shock, even in the absence of other injuries causing blood loss. 10 Classically, a ruptured TM was seen as a marker for blast severity, and a normal otoscopic examination was thought to identify a patient at low risk for PBI. This concept has not been supported by data from recent incidents.…”

Section: Primary Blast Effectsmentioning

confidence: 99%