3

Pathophysiology of Blast Injury and Overview of Experimental Data

This chapter reviews what is known about the mechanisms of blast injury. It begins with an explanation of blast physics. Next is a discussion of how blast waves interact with the body directly and indirectly and how exposure to blast can affect multiple systems in the body and can cause systemic effects on the autonomic nervous, vascular, and immune systems. That discussion is followed by a description of models used to study blast-injury mechanisms and the challenges involved in using models. The chapter ends with a summary of the results of experimental studies conducted in blast-exposed animal models. The committee used the information presented here to understand the mechanisms of blast injury, to discern clues about possible long-term health effects in humans, and to help to identify data gaps in the evidence base.

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). A blast wave generated by an explosion starts with a single pulse of increased air pressure that lasts a few milliseconds. The negative pressure or suction of the blast wave follows the positive wave immediately (Owen-Smith, 1981). The duration of the blast wave—that is, the time that an object in the path of the shock wave is subjected to the pressure effects—depends on the type of explosive and the distance from the point of detonation (Clemedson, 1956). Table 3-1 summarizes the safety zones—that is, the standoff distances—for various types of bomb explosions.



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3 Pathophysiology of Blast Injury and Overview of Experimental Data T his chapter reviews what is known about the mechanisms of blast injury. It begins with an explanation of blast physics. Next is a discussion of how blast waves interact with the body directly and indirectly and how exposure to blast can affect multiple systems in the body and can cause systemic effects on the autonomic nervous, vascular, and immune systems. That discussion is followed by a description of models used to study blast-injury mechanisms and the challenges involved in using models. The chapter ends with a summary of the results of experimental studies conducted in blast-exposed animal models. The committee used the information presented here to understand the mechanisms of blast injury, to discern clues about possible long-term health effects in humans, and to help to identify data gaps in the evidence base. 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). A blast wave generated by an explosion starts with a single pulse of increased air pressure that lasts a few milliseconds. The negative pressure or suction of the blast wave follows the positive wave immediately (Owen-Smith, 1981). The duration of the blast wave—that is, the time that an object in the path of the shock wave is subjected to the pressure effects— depends on the type of explosive and the distance from the point of detona- tion (Clemedson, 1956). Table 3-1 summarizes the safety zones—that is, the standoff distances—for various types of bomb explosions. 33

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34 TABLE 3-1  Safety Recommendations for Standoff Distances from Different Types of Exploding Bombs Container or Vehicle Maximum Explosives Maximum Evacuation Description Capacity Lethal Air-Blast Range Distance Falling-Glass Hazard Pipe 2 × 12 in 5–6 lb 850 ft (259 m) Pipe 4 × 12 in 20 lb Pipe 8 × 24 in 120 lb Bottle 2 L 10 lb Bottle 2 gal 30 lb Bottle 5 gal 70 lb Boxes or shoebox 30 lb Briefcase or satchel bomb 50 lb 1,850 ft (564 m) 1,250 ft (381 m) 1-ft3 box 100 lb Suitcase 225 lb 1,850 ft (564 m) 1,250 ft (381 m) Compact sedan 500 lb in trunk 100 ft (30 m) 1,500 ft (457 m) 1,250 ft (381 m) Full-size sedan 1,000 lb in trunk 125 ft (38 m) 1,750 ft (534 m) 1,750 ft (534 m) Passenger van or cargo van 4,000 lb 200 ft (61 m) 2,750 ft (838 m) 2,750 ft (838 m) Small box van 10,000 lb 300 ft (91 m) 3,750 ft (1,143 m) 3,750 ft (1,143 m) Box van or water or fuel truck 30,000 lb 450 ft (137 m) 6,500 ft (1,982 m) 6,500 ft (1,982 m) Semitrailer 60,000 lb 600 ft (183 m) 7,000 ft (2,134 m) 7,000 ft (2,134 m) NOTE: Table compiled from several publications of the Advanced Technical Group for Blast Mitigation and Technical Support Working Group. SOURCE: Reprinted with permission from Charles Stewart, MD, EMDM, MPH (Stewart, 2014).

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PATHOPHYSIOLOGY OF BLAST INJURY 35 The blast wave progresses from the source of the explosion as a sphere of compressed and rapidly expanding gases, which displaces an equal volume of air at a high velocity (Rossle, 1950). The velocity of the blast wave in air may be extremely high, depending on the type and amount of the explosive used. 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. The blast wind following the wave is generated by the mass displacement of air by expanding gases; it may accelerate to hurricane proportions and is responsible for disintegration, evisceration, and traumatic amputation of body parts. Thus, a person exposed to an explosion will be subjected not only to a blast wave but to the high-velocity wind traveling directly behind the shock front of the blast wave (Rossle, 1950). A hurricane-force wind traveling about 200 km/h exerts overpressure of only 1.72 kilopascal (kPa) (0.25 psi), but a blast-induced overpressure of 690 kPa (100 psi) that causes substantial lung damage and might be lethal travels at about 2,414 km/h (Owen-Smith, 1981). The magnitude of damage due to the blast wave depends on the peak of the initial positive-pressure wave (an overpressure of 414–552 kPa or 60–80 psi is considered potentially lethal), the duration of the overpressure, the medium of the explosion, the distance from the incident blast wave, and the degree of focusing due to a confined area or walls. For example, explosions near or within hard solid surfaces become amplified 2–9 times because of shock-wave reflection (Rice and Heck, 2000). Moreover, vic- tims positioned between the blast and a building often suffer 2–3 times the degree of injury of a person in an open space. Indeed, people exposed to explosion rarely experience the idealized pressure-wave form, known as the Friedlander wave. Even in open-field conditions, the blast wave reflects from the ground, generating reflective waves that interact with the primary wave and thus changing its characteristics. In a closed environment (such as a building, an urban setting, or a vehicle), the blast wave interacts with surrounding structures and creates multiple wave reflections, which, inter- acting with the primary wave and between each other, generate a complex wave (Ben-Dor et al., 2001; Mainiero and Sapko, 1996) (see Figure 3-1). Table 3-2 summarizes the effects of different levels of overpressure on mate- rial surrounding the explosion and unprotected persons exposed to blast. Previous attempts to define the mechanisms of blast injury suggested the involvement of spalling, implosion, and inertial effects as major phys- ical components of the blast-body interaction and later tissue damage (Benzinger, 1950). Spallation is the disruption that occurs at the boundary between two media of different densities; it occurs when a compression wave in the denser medium is reflected at the interface. Implosion occurs

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36 GULF WAR AND HEALTH Complex wave c Pressure Simple free-field wave b Friedlander wave a Time FIGURE 3-1  Explosion-induced shock waves: (a) idealized representation of pres- sure-time history of an explosion in air; (b) shock wave in open air; (c) complex shock-wave features in closed or urban environment. SOURCE: Mayorga, 1997. Reprinted with permission from Elsevier Science, Ltd. 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 pres- sure wave passes, the bubbles can re-expand explosively and damage sur- rounding tissue (Benzinger, 1950; Chiffelle, 1966; Phillips, 1986). Inertial effects occur at the interface of the different densities: the lighter object will be accelerated more than the heavier one, so there will be a large stress at the boundary. Recent results suggest that there is a frequency dependence of the blast effects: high-frequency (0.5–1.5 kHz) low-amplitude stress waves target mostly organs that contain abrupt density changes from one medium to another (for example, the air–blood interface in the lungs or the blood–parenchyma interface in the brain), and low-frequency (<0.5 kHz) high-amplitude shear waves disrupt tissue by generating local motions that overcome natural tissue elasticity (for example, at the contact of gray and white brain matter).

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PATHOPHYSIOLOGY OF BLAST INJURY 37 TABLE 3-2  Overpressure Effects on Surrounding Materials and Unprotected Persons Pressure, Pressure, Effects on kPa (psi) Effects on Material kPa (psi) Unprotected Person 0.69–34.47 (0.1–5) Shatter single- 34.47 (5) Slight chance of strength glass eardrum rupture 6.89–13.79 (1–2) Crack plaster walls, 103.42 (15) 50% chance of shatter asbestos eardrum rupture sheet, buckle steel sheet, failure of wood wall 13.79–20.68 (2–3) Crack cinder- 206.84–275.79 Slight chance of lung block wall, crack (30–40) damage concrete block wall 13.79–55.16 (2–8) Crack brick wall 551.58 (80) 50% chance of severe lung damage 34.47–68.95 (5–10) Shatter car safety 689.48 (100) Slight chance of glass death 896.32–1,241.06 50% chance of death (130–180) 1,378.95–1,723.69 Death usual (200–250) SOURCE: Reproduced from Journal of the Royal Army Medical Corps, Hunterian lecture 1980: A computerized data retrieval system for the wounds for war: The Northern Ireland casualties. Owen-Smith, M. S., 127(1):31–54, Copyright 1981, with permission from BMJ Publishing Group Ltd. ACUTE BLAST–BODY AND BLAST–BRAIN INTERACTIONS Explosive blast may have five distinct acute effects on the body (see Fig- ure 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 connec- tion 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) and then the body or body part stops suddenly on hitting the ground or a surrounding object; the quaternary blast mechanism (not depicted in Figure 3-2) includes flash burns caused by the transient but intense heat of the explosion (Mellor, 1988); and the quinary blast mechanism (not depicted in Figure 3-2) is caused by post- detonation environmental contaminants, such as tissue reactions to fuel,

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38 GULF WAR AND HEALTH FIGURE 3-2  Complex injurious environment due to blast. NOTES: Primary blast effects are caused by the blast wave itself (excludes penetrat- ing and blunt-force injury); secondary blast effects are caused by particles propelled by the blast (penetrating or blunt-force injury); tertiary blast effects caused by accel- eration and deceleration of the body and its impact with other objects (penetrating or blunt-force [including “coup-contrecoup”] injury). Quaternary and quinary blast effects are not depicted in this figure but are described in the text. SOURCE: Reprinted with permission from Macmillan Publishers Ltd: Journal of Cerebral Blood Flow and Metabolism, Cernak and Noble-Haeusslein, copyright 2010. metals, and dusts or to bacteria and radiation in dirty bombs (Kluger et al., 2007). 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). When an explosive shock wave strikes a living body, a fraction of the shock wave is reflected and another fraction is absorbed and propagates through the body as a tissue-transmitted shock wave (Clemedson and Criborn, 1955). Different organ and body structures differ in their reac- tions, but two main general types of tissue response are observed: One is

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PATHOPHYSIOLOGY OF BLAST INJURY 39 caused by the impulse of the shock wave and is of longer duration, and the other is caused by the pressure variations of the shock wave and is in the form of oscillations or pressure deflections of shorter duration (Clemedson and Pettersson, 1956). For example, Clemedson and colleagues demon- strated that in rabbits exposed to blast, abdominal organs and costal interspaces (that is, spaces between ribs) responded to the impulse of the shock wave, whereas the rib’s and the hind leg’s response was induced by the pressure variations of the shock wave (Clemedson et al., 1969). During the interaction between the blast shock wave (the primary blast) and a medium—which could be solid, liquid, gas, or plasma—the energy of the shock wave is absorbed or transformed into the kinetic energy of the medium (Tümer et al., 2013). The kinetic energy, in turn, moves and accelerates the elements of the medium from their resting state with a rate that depends on the density of the medium; this leads to rapid physical movement, displacement, deformation, or rupture of the medium (Chu et al., 2005). Consequently, the main mechanisms of the blast–body interac- tion and later tissue damage include spallation, implosion, and inertial effects (Richmond et al., 1967). Spallation is a phenomenon that occurs at the boundary between two media of different densities where a compression wave in the denser medium is reflected at the interface. Implosion occurs in a liquid medium that contains a dissolved gas. As the shock wave passes through such a medium, it compresses the gas bubbles, and this leaves the pressure in the bubbles much higher than the shock pressure; after the pas- sage of the pressure wave, the bubbles can re-expand explosively and dam- age surrounding tissue (Cooper et al., 1991; Richmond et al., 1967, 1968). Inertial effects also occur at the interface of media of different densities: the lighter object will be accelerated more than the heavier one, so there will be a large stress at the boundary (Lu and Wilson, 2003). In addition to the consequences of the kinetic-energy transfer, recent results suggest that the primary blast effects depend on frequency: High- frequency (0.5–1.5 kHz), low-amplitude stress waves target mostly organs that contain media with contrasting densities (for example, the air–blood interface in the lungs or the blood–parenchyma interface in the brain), and low-frequency (<0.5 kHz), high-amplitude shear waves disrupt tissue by generating local motions that overcome natural tissue elasticity (Cooper et al., 1991; Gorbunov et al., 2004) (for example, at the interface between gray and white brain matter). MODIFYING POTENTIAL OF SYSTEMIC CHANGES CAUSED BY BLAST Because of the complexity of the injurious environment—that is, mul- tiple blast effects that may interact with the body—blast injuries often

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40 GULF WAR AND HEALTH FIGURE 3-3  Simultaneous activation of systemic, local, and cerebral responses to blast exposure and interactive mechanisms that cause or contribute to the blast- induced neurotrauma. NOTES: ANS = autonomous nervous system; BBB = blood brain barrier; CBF = cerebral blood flow; E = epinephrine; NE = norepinephrine; PNS = parasympathetic nervous system; SNS = sympathetic nervous system. SOURCE: Cernak, 2010. involve interwoven mechanisms of systemic, local, and cerebral responses to blast exposure (Cernak et al., 1991, 1996b) (see Figure 3-3). Even when multiorgan responses are mild, systemic changes substantially modify the original organ damage and influence its severity and outcome. Air emboli, activation of the autonomic nervous system (ANS), vascular mechanisms, and systemic inflammation are among the most important systemic altera- tions that could modify initial injuries due to blast. Air Emboli Air emboli develop as a consequence of the shock wave’s passing through media in the body that have different densities: gas, such as air; fluid, such as blood; and solid, such as parenchyma. Experimental studies published by Mason et al. (1971) and Nevison et al. (1971) used an ultra- sonic Doppler blood-flow detector in dogs subjected to blast in a shock tube and showed air emboli passing through the carotid artery. The embolus

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PATHOPHYSIOLOGY OF BLAST INJURY 41 detector showed cyclic release of air emboli: Release occurred over the first 10 seconds after the blast, ceased for a time, and was then noted about 2 minutes and 12 minutes after the blast. It is noteworthy that the air-emboli release occurred in parallel with a drastic decrease in blood-flow velocity and with seizure that was prob- ably due to hypoxia or anoxia. Similar experimental findings have been described by others (Chu et al., 2005; Clemedson and Hultman, 1954; Kirkman and Watts, 2011) and have been noted in clinical studies (Freund et al., 1980; Tsokos et al., 2003a,b). Indeed, a massive compressed-air embolism of the aorta and multiple air spaces in the interstitium compress- ing the collecting tubules in the kidneys (Freund et al., 1980) and venous air embolism in the lungs (Tsokos et al., 2003a) were reported in victims of severe blast injuries. It is expected that the rate of the air-emboli release is dependent on the intensity of blast, and the subsequent changes in blood flow and oxygenation concentration are also graded (that is, when the rate of the air-emboli release increases with the increase of blast intensity, the intensity of the pathological changes in blood flow and oxygenation con- centration also increases). Activation of the Autonomic Nervous System When the incident overpressure wave (the initial shock wave that brings a sudden increase in atmospheric pressure) is transmitted through the body, it increases the pressure in organs (Clemedson and Pettersson, 1956). The later sudden hyperinflation of the lungs (Cernak et al., 1996b; Zuckerman, 1940) stimulates the juxtacapillary (J) receptors that are located in the alveolar interstitium and innervated by vagal fibers (Paintal, 1969). The resulting vagovagal reflex leads to apnea followed by rapid breathing, bradycardia, and hypotension, which are frequently observed immediately after blast exposure. Moreover, hypoxia and ischemia due to damaged alveoli, air emboli, or a triggered pulmonary vagal reflex can activate a cardiovascular decompressor Bezold-Jarish-reflex, which involves a marked increase in vagal (parasympathetic) efferent discharge to the heart (Zucker, 1986). That effect causes a slowing of the heart (bradycardia), dilation of the peripheral blood vessels, and an ensuing drop in blood pressure, which could contribute further to cerebral hypoxia (Cernak et al., 1996a,b). Axelsson and colleagues (2000) showed in pigs that the blast-induced brief apnea correlated with flattening of the electric activity of the brain. Other experimental studies demonstrated the importance of vagally mediated cerebral effects of blast (Cernak et al., 1996b; Irwin et al., 1999; Ohnishi et al., 2001). The environment in which an explosion occurs is dramatic and may initiate endocrine mechanisms of the classic flight-and-fight stress response

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42 GULF WAR AND HEALTH (Selye, 1976). For example, recent study (Tümer et al., 2013) showed increased expression of the catecholamine-biosynthesizing enzymes tyro- sine hydroxylase and dopamine hydroxylase in the rat adrenal medulla and increased plasma concentrations of norepinephrine 6 hours after blast injury. Accumulating experimental and clinical evidence suggests that blast induces alterations in ANS activity: instantaneous triggering of the para- sympathetic reflexes followed by neuroendocrine changes due to the activa- tion of the sympathetic nervous system. Vascular Mechanisms One of the most important media for a shock wave’s energy transfer is blood. Veins contain about 70% of total human blood volume (includ- ing the splanchnic system, which accounts for about 20% of that total), compared with 18% in arteries and only 3% in terminal arteries and arte- rioles (Gelman, 2008). In general, veins are 30 times more compliant than arteries; splanchnic and cutaneous veins are the most compliant veins and constitute the largest blood reservoirs in the body. 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.

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PATHOPHYSIOLOGY OF BLAST INJURY 43 representation of the consequences of blast-induced pressure changes and their extremely complex interactions, which form several interconnected loops. The transfer of the shock wave’s energy to the body not only leads to a sudden increase in both abdominal pressure (AbdP) and thoracic pres- sure (ThorP) but causes an increase in intramural central venous pressure (CVP). Hypoxia caused by alveolar damage and later by reduced surface for gas exchange, impaired ventilation and perfusion caused by J-receptor activation, or decreased cardiac output due to activation of the Bezold- Jarish reflex all increase pulmonary arterial resistance, which might increase ThorP (Gelman, 2008). An increase in ThorP amplifies the increase in CVP. Venoconstriction and the mobilization of blood volume depend mainly on the splanchnic circulation, which has a high population of α1- and α2-adrenergic receptors and hence a high sensitivity to adrenergic stimula- tion (Pang, 2001; Rutlen et al., 1979). Thus, it is likely that the initial sud- den drop in systemic arterial pressure caused by blast-induced vagovagal reflexes and the accompanying reduction in the inhibitory influences of the baroreceptors of the carotid sinus and aortic area on the vasomotor center initiate a compensatory increase in sympathetic outflow. The increased sympathetic stimuli constrict venous smooth muscle and lead to mobiliza- tion of blood from the splanchnic vasculature toward the heart (Rutlen et al., 1979). Spasm of the cerebral vasculature has frequently been found in mod- erate or severe blast-induced traumatic brain injury (TBI)—more often than in patients who have TBI of other origins (for example, impact, fall, or acceleration) (Armonda et al., 2006; Ling et al., 2009). It can develop early, often within 48 hours of injury, and can also be manifested later, typically 10–14 days after exposure. It is noteworthy that although cerebral vasospasm is usually prompted by subarachnoid hemorrhage, that is not required for vasospasm in blast-induced TBI (Magnuson et al., 2012). A recent experimental study of theoretical and in vitro models demonstrated that a single rapid mechanical insult is capable of inducing vascular hyper- contractility and remodeling, which are indicative of vasospasm initiation (Alford et al., 2011). Alford and colleagues used in vitro engineered arterial lamellae exposed to high-velocity acute uniaxial stretch to reproduce blast- induced stretch of arterial blood vessels and test whether blast forces can lead to phenotypic switch in vascular smooth muscle cells (VSMCs). The authors measured protein and mRNA expression of two primary markers of contractile VSMCs, smooth muscle myosin heavy chain (SM-MHC) and smoothelin, 24 hours after the injury induction. The results showed that severe (10%) strain decreased expression of smoothelin and decreased mRNA expression of both smoothelin and SM-MHC, suggesting that acute mechanical injury can potentiate a switch away from the contractile pheno- type in VSMCs. The findings support a hypothetical scenario in which the

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