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3 Pathophysiology of Blast Injury and Overview of Experimental Data
Pages 33-84

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From page 33...
... THE PHYSICS OF BLAST This section is taken from the Institute of Medicine report Gulf War and Health, Volume 7: Long-Term Consequences of Traumatic Brain Injury (IOM, 2009)
From page 34...
... 2,750 ft (838 m) Small box van 10,000 lb 300 ft (91 m)
From page 35...
... The blast wave is the main determinant of the primary blast injury and consists of the front of high pressure that compresses the surrounding air and falls rapidly to negative pressure. It travels faster than sound and in few milliseconds damages the surrounding structures.
From page 36...
... 2008. Figure 1-1 New when the shock wave compresses a gas bubble in a liquid medium, raising the pressure in the bubble much higher than the shock pressure; as the pressure wave passes, the bubbles can re-expand explosively and damage surrounding tissue (Benzinger, 1950; Chiffelle, 1966; Phillips, 1986)
From page 37...
... ACUTE BLAST–BODY AND BLAST–BRAIN INTERACTIONS Explosive blast may have five distinct acute effects on the body (see Figure 3-2) : The primary blast mechanism causes injuries as sole consequences of the shock wave–body interaction; the secondary blast mechanism is due to the propulsion of fragments of debris by the explosion and their connection with the body, which causes penetrating or blunt injuries; the tertiary blast mechanism is due to the acceleration and deceleration of the body or a part of the body when the energy released by the explosion propels the body or body part (acceleration phase)
From page 38...
... . Often, especially in the case of moderate to severe blast injuries, the multiple blast effects interact with the body simultaneously; such an injurious environment and related injuries are sometimes called blast-plus (Moss et al., 2009)
From page 39...
... . During the interaction between the blast shock wave (the primary blast)
From page 40...
... SOURCE: Cernak, 2010. involve interwoven mechanisms of systemic, local, and cerebral responses to blast exposure (Cernak et al., 1991, 1996b)
From page 41...
... . Activation of the Autonomic Nervous System When the incident overpressure wave (the initial shock wave that brings a sudden increase in atmospheric pressure)
From page 42...
... Figure 3-4 is a schematic FIGURE 3-4  Overview of vascular mechanisms that are activated by shock-wave propagation through the body, lead to alterations in functions of multiple organs and organ systems, and substantially influence the brain's response to blast. SOURCE: Created by Ibolja Cernak for the Committee on Gulf War and Health: Long-Term Effects of Blast Exposures.
From page 43...
... . Spasm of the cerebral vasculature has frequently been found in moderate or severe blast-induced traumatic brain injury (TBI)
From page 44...
... . Blast exposures have been reported to cause alterations in the neuroendocrine system that involve multiple hypothalamopituitary end axes (Cernak et al., 1999c; Wilkinson et al., 2012)
From page 45...
... First, the researcher should clarify the blast effects to be reproduced. If the choice is primary blast, the researcher should ensure that the animals are fixed so that there will be no blast-induced acceleration of the body and head during the exposure.
From page 46...
... generating a shock wave, the choices of models and their positioning, and the length of the experiment. Thus, on the basis of the research question and the complexity, a choice is made between nonbiologic models and biologic models.
From page 47...
... As with all blast-injury models, applying operationally relevant loading histories is critical for the in vitro and ex vivo models. Only if blast-loading conditions that are realistic and that mimic what would happen at the cellular or tissue level in a person exposed to a militarily relevant blast environment are used can the mechanisms of the energy transfer to the tissue and the resulting biologic response be reliably analyzed (Effgen et al., 2012)
From page 48...
... applicable to sharp-rising blast waves, derived from the analysis of data of 12 mammalian species (excluding guinea pig)
From page 49...
... Experimental Environment of Blast Generation Experimental studies of primary blast-induced biologic responses are performed either in an open environment or in laboratory conditions. In open-field exposure studies, animals are exposed to a blast wave that is generated by detonation of an explosive (Axelsson et al., 2000; Bauman
From page 50...
... After the diaphragm ruptures, the shock wave travels along the driven section with supersonic velocity and interacts with the animal. The blast overpressure duration can be varied by changing the size of the high-pressure chamber (Celander et al., 1955)
From page 51...
... . Blast overpressure results in primary injury to the lungs owing in part to compression of alveolar septa and capillary walls (DePalma et al., 2005)
From page 52...
... The initial study by Brown and colleagues (1993) has served as a platform for validation of blast-induced changes in the lungs in other animal models.
From page 53...
... Repeated low-level blast overpressure exposures of rodents also revealed hemorrhages and ruptured alveolar walls, but the number of blast exposures did not appear to alter the magnitude of pulmonary injury; that is, the pathologic picture after repeated exposures was similar to that after a single exposure and in all cases pathologic changes increased over time (Elsayed and Gorbunov, 2007)
From page 54...
... that used low-level blast waves and blasts restricted to a limb (Chavko et al., 2006; Elsayed and Gorbunov, 2003, 2007; Gorbunov et al., 1997; Ning et al., 2012)
From page 55...
... . Repeated low-level blast exposures result in decreases in vitamins C and E (by 20–60% and 25–40%, respectively)
From page 56...
... 56 GULF WAR AND HEALTH TABLE 3-3  Animal Models Description of Blast Species, Sexa Times Studied Compressed-air-driven shock tube Sprague-Dawley rats 5, 60 min Compressed-air-driven shock tube Sprague-Dawley rats 1, 3, 6, 12, 24 hr Compressed-air-driven shock tube Sprague-Dawley rats 1, 3, 6, 12, 24 hr Compressed-air-driven shock tube Sprague-Dawley 15 min, 1, 3, 6, 12, rats 24, 34, 56 hr Blast to hind limb by commercial Sprague-Dawley rats, male 0.5, 1, 3, 6 hr detonator Compressed-air-driven shock tube Sprague-Dawley rats, male 1, 6, 24 hr Compressed-air-driven shock tube Sprague-Dawley rats, male 2–192 hr NOTES: 3NTyr = 3-nitrotyrosine; BAL = bronchoalveolar lavage; CINC-1 = cytokine chemoattractant-1; HO-1 = heme oxygeanse-1; ICAM-1 = intercellular adhesion molecule-1; IL = interleukin; iNOS = inducible nitric oxide synthase; MCP-1 = monocyte chemoattractant protein-1; MIP-2 = macrophage inhibitory protein-2; MnSOD = manganese superoxide dismutase; MPO = myeloperoxidase; SOD = superoxide dismutase; TNF = tumor necrosis factor. aSome studies do not report gender.
From page 57...
... , damage to endothelium, epithelial cell necrosis, deposition of free iron Increase in TNF-alpha; decrease Alveolar congestion, neutrophil Ning et al., 2012 in SOD, cystathionine gamma- infiltration, hemorrhagic lesions lyase, hydrogen sulfide Vitamins C and E decreased After single blast, multifocal Elsayed and after initial blast by 20–60%; minimal to mild hemorrhage Gorbunov, 2007 lipid peroxidation increased by throughout lobes; by 24 25–60% hr, increased intra-alveolar hemorrhage, ruptured alveolar walls Increases in MPO, CINC- Chavko et al., 2006 1, ICAM-1, iNOS, protein oxidation and nitration, hemeoxygenase-1, MnSOD
From page 58...
... 20 hours before blast exposure, and euthanized 30 minutes after the blast. The blast induced heme-oxygenase-1 mRNA and protein in the lungs, but there were no differences between the treated and vehicle groups, although there was a significant difference in survival rates between the two groups: 35% survival in vehicle controls and 68% in the hemintreated group.
From page 59...
... Such a foundation may prove useful to researchers who are only beginning to decipher the complex pathophysiology of blast lung and its long-term consequences. Abdominal Organs The most popular explanation of primary blast-induced injuries to the abdominal organs involves the transmission of a shock wave's kinetic energy (Clemedson and Criborn, 1955)
From page 60...
... Although the usual interval for perforation after blast exposure is 1–14 days, their study identified patterns of injury and a classification in which no difference was observed in the distribution of histologic grades at the two times. Thus, the authors made TABLE 3-4  Histologic Classification of Primary Intestinal Blast Injuries Mucosal Muscular Serosal Grade of Injury Appearance Appearance Appearance Ia Normal or diffuse Normal Normal bleeding only II Mucosal hematoma Mild edema only Normal without glandular disruption III Marked hemorrhage Marked edema or Normal with glandular minor hemorrhage disruption only IV Gross glandular or Muscular disruption Subserosal hemorrhage mucosal disruption; or major hematoma muscularis mucosae may be disrupted V Complete mucosal Muscular laceration Serosal laceration laceration or disruption aIncludes contusions in which submucosal hematoma is evident without other evidence of mural injury.
From page 61...
... that result from blast exposure range from subcapsular hemorrhage and small foci of parenchymal hemorrhage, to primary or secondary rupture of capsules and parenchymal laceration (Vriese, 1904)
From page 62...
... TABLE 3-5  Distribution of Histologic Grades Between Contusion Groups of Different External Appearance 62 Histologic Grade Significance Contusion Measure I and II III IV and V χ2 d.f.
From page 63...
... TABLE 3-6   Type, Severity, and Frequency of Microscopic Lesions in Key Thoracic and Abdominal Viscera Severe, Severe, Moderate, Moderate, Mild, Mild, Supine (%) Prone (%)
From page 64...
... 64 GULF WAR AND HEALTH FIGURE 3-9  Patterns of blast injury to liver with settings used in Koliatsos et al.
From page 65...
... . Potential chronic consequences of blast exposure for morphologic and functional integrity of kidneys were analyzed in sheep exposed to blast (Casals et al., 2011)
From page 66...
... (2011) used New Zealand rabbits exposed to explosivegenerated blast in laboratory conditions to show that increased permeability, measured by 125I-albumin leakage, and microvessel injury in the lungs and kidneys are among the key outcomes of blast overpressure.
From page 67...
... . In a study that exposed 115 dogs in a shock tube to blast waves with rise times of 12–155 ms, peak overpressures of 52–231 psi, and durations of 0.4–20 s, 11 blow-out fractures (fracture of the walls or floor of the orbit)
From page 68...
... Diffusion-tensor magnetic resonance imaging results demonstrated substantial damage and compensatory plastic changes in some auditory brain regions; most of the changes occurred in the inferior colliculus and medial geniculate body. The authors hypothesized that the lack of important microstructural changes in the corpus callosum could be explained on the grounds that the blast exposure in their experimental setting exerted effects mainly through the auditory pathways rather than through direct impact on the brain parenchyma.
From page 69...
... Neurologic injury to brain visual pathways was observed in male rats that survived blast overpressure exposures of 104–110 kPa and 129–173 kPa. Optic nerve fibers degenerated on the same side as the blast pressure wave.
From page 70...
... The study showed that blast exposure can induce permanent injury to some of the brain's central visual pathways (retinofugal axonopathy)
From page 71...
... and (2) kinetic energy transfer of the primary blast wave to organs and organ systems, including blood in large vessels in the abdomen and chest, reaching the CNS (Irwin et al., 1999; Ohnishi et al., 2001)
From page 72...
... Despite the growing experimental models of BINT, there is a serious need for a well-coordinated, multidisciplinary research approach to clarify injury tolerance in animal models that are relevant to the military experience and to define the injury mechanisms that underlie acute and chronic consequences of blast exposure.
From page 73...
... 2012. Time dependent changes of protein biomarker levels in the cerebrospinal fluid after blast traumatic brain injury.
From page 74...
... 2010. Traumatic brain injury: An overview of patho biology with emphasis on military populations.
From page 75...
... 1999c. Neuroendo crine responses following graded traumatic brain injury in male adults.
From page 76...
... 2011. Visual dysfunction following blast-related traumatic brain injury from the battlefield.
From page 77...
... 2012. Mechanics of blast loading on the head models in the study of traumatic brain injury using experimental and computational approaches.
From page 78...
... 2009. Gulf War and Health, Volume 7: Long-Term Conse quences of Traumatic Brain Injury.
From page 79...
... 2009. Skull flexure from blast waves: A mechanism for brain injury with implications for helmet design.
From page 80...
... 2010. Increase in blood-brain barrier permeability, oxidative stress, and activated microglia in a rat model of blast-induced traumatic brain injury.
From page 81...
... 2000. Blast exposure causes redistribution of phosphorylated neurofilament subunits in neurons of the adult rat brain.
From page 82...
... 2012. Neuro-glial and systemic mecha nisms of pathological responses in rat models of primary blast overpressure compared to "composite" blast.
From page 83...
... 2012. Primary blast injuries: An updated concise review.


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