G. J. Cooper

The role of stress waves in thoracic visceral injury from blast loading: Modification of stress transmission by foams and high-density materials

Materials have been applied to the thoracic wall of anaesthetised experimental animals exposed to blast overpressure to investigate the coupling of direct stress waves into the thorax and the relative contribution of compressive stress waves and gross thoracic compression to lung injury. The ultimate purpose of the work is to develop effective personal protection from the primary effects of blast overpressure--efficient protection can only be achieved if the injury mechanism is identified and characterized. Foam materials acted as acoustic couplers and resulted in a significant augmentation of the visceral injury; decoupling and elimination of injury were achieved by application of a high acoustic impedance layer on top of the foam. In vitro experiments studying stress wave transmission from air through various layers into an anechoic water chamber showed a significant increase in power transmitted by the foams, principally at high frequencies. Material such as copper or resin bonded Kevlar incorporated as a facing upon the foam achieved substantial decoupling at high frequencies--low frequency transmission was largely unaffected. An acoustic transmission model replicated the coupling of the blast waves into the anechoic water chamber. The studies suggest that direct transmission of stress waves plays a dominant role in lung parenchymal injury from blast loading and that gross thoracic compression is not the primary injury mechanism. Acoustic decoupling principles may therefore be employed to reduce the direct stress coupled into the body and thus reduce the severity of lung injury--the most simple decoupler is a high acoustic impedance material as a facing upon a foam, but decoupling layers may be optimized using acoustic transmission models. Conventional impacts producing high body wall velocities will also lead to stress wave generation and transmission--stress wave effects may dominate the visceral response to the impact with direct compression and shear contributing little to the aetiology of the injury.

Physiologic responses to primary blast.

BACKGROUND Primary blast injuries are produced by the blast shock wave. The critical determinant of survival is pulmonary injury, but acute cardiorespiratory responses to blast exposure are not well understood. The aim of this study was to investigate these changes. METHODS Twenty anesthetized rats were exposed to moderate blast overpressure, 10 animals receiving thoracic and 10 receiving abdominal exposure. Another 9 animals acted as controls. Respiration, heart rate, and blood pressure were recorded continuously before, during, and for 6 hours after blast exposure. RESULTS All animals exposed to thoracic blast demonstrated apnea, bradycardia, and hypotension after blast exposure, followed by a return to preblast values. No significant cardiovascular or respiratory changes were seen in animals in the other groups. CONCLUSION Moderate thoracic blast injury produces a reflex triad of apnea, bradycardia, and hypotension that is not present after abdominal blast. These observations may have important implications for the immediate management of patients with blast injuries.

Protection of the Lung from Blast Overpressure by Thoracic Stress Wave Decouplers

The nature and extent of injury resulting from an explosion, depends on the type of device used and the environment within which it detonates. Explosive devices used by terrorists are frequently improvised devices placed in crowded urban environments--the incidence and severity of penetrating wounds

The Biomechanical Response of the Thorax to Nonpenetrating Impact with Particular Reference to Cardiac Injuries

Sternal injury, gross cardiac pathology, and cardiac dysrhythmias following nonpenetrating impact by a variety of impactors to the sternum of experimental animals are described. The biomechanical response of the chest wall to the impact and the associated transient pressure changes within the heart are presented, and a correlation between injury severity and chest wall displacement is demonstrated. A simple model is then developed to predict chest wall displacement if the mass, velocity, and dimensions of an impactor are known. The model demonstrates the dependence of chest-wall displacement upon preimpact kinetic energy, impact diameter, and target size.

Prolonged permissive hypotensive resuscitation is associated with poor outcome in primary blast injury with controlled hemorrhage.

Objective:To determine the effects of primary blast injury (PBI) on survival and the physiological response to resuscitation after hemorrhagic shock. Background:Air-blast injury is a significant clinical problem that can reduce blood oxygenation and modify the response to hemorrhage. PBI has specific physiological effects that have not been fully accounted for in resuscitation strategies. Permissive hypotension is a widely adopted strategy in trauma resuscitation. However, the choice of resuscitation strategy requires a full understanding of the mechanisms of injury and their physiological consequences. Methods:Terminally anesthetized pigs were divided into 4 groups and subjected to either air-blast injury (B) or no blast (S). All received a controlled hemorrhage of 30% blood volume and resuscitation with 0.9% saline to a normotensive (Normot, systolic blood pressure 110 mm Hg) or hypotensive (Hypot, 80 mm Hg) end point for up to 8 hours. (n = 6 in each B and n = 8 in each S subgroup). Results:Survival time was significantly shorter with Hypot (P < 0.0001 Peto log rank). The effect was in the animals subjected to B (P = 0.0005) (mean survival time [95% CI]; BNormot 422 [313–531] vs. BHypot137 [94–181] min), but not those given S (P = 0.06) (SNormot 480 [all survived] vs. SHypot 352 [210–494] min). PBI exacerbated a profound metabolic acidosis during Hypot, possibly due to an overwhelming compromise in tissue oxygen delivery. Conclusions:Prolonged hypotensive resuscitation is not compatible with survival after primary blast. Casualties most likely to be in this category are those injured by blast in confined spaces or by enhanced blast weapons. The risk of rebleeding associated with normotensive resuscitation needs to be balanced with the metabolic derangement associated with hypotensive resuscitation.

Blast injury research models

Blast injuries are an increasing problem in both military and civilian practice. Primary blast injury to the lungs (blast lung) is found in a clinically significant proportion of casualties from explosions even in an open environment, and in a high proportion of severely injured casualties following explosions in confined spaces. Blast casualties also commonly suffer secondary and tertiary blast injuries resulting in significant blood loss. The presence of hypoxaemia owing to blast lung complicates the process of fluid resuscitation. Consequently, prolonged hypotensive resuscitation was found to be incompatible with survival after combined blast lung and haemorrhage. This article describes studies addressing new forward resuscitation strategies involving a hybrid blood pressure profile (initially hypotensive followed later by normotensive resuscitation) and the use of supplemental oxygen to increase survival and reduce physiological deterioration during prolonged resuscitation. Surprisingly, hypertonic saline dextran was found to be inferior to normal saline after combined blast injury and haemorrhage. New strategies have therefore been developed to address the needs of blast-injured casualties and are likely to be particularly useful under circumstances of enforced delayed evacuation to surgical care.

Wound ballistics: contemporary and future research.

Wound ballistics research has contributed much to the understanding of the pathophysiology of missile injury that now exists. From this store of knowledge treatment regimes have evolved which have greatly improved the lot of the soldier wounded in war. However, research must keep pace with changes that are taking place in weapons research and development so that the particular needs of the Army Medical Services on a future battlefield can be met. The differing needs of civilian and military medical services are highlighted. The marked differences that exist between the missile wound seen and treated in a late twentieth century hospital and the wounds likely to be encountered on the modern battlefield are enumerated and discussed.

The influence of personal blast protection on the distribution and severity of primary blast gut injury

Primary blast injuries have been recognized since World War I when the most significant reported injury was to the lung. The prevalence of injury to tissues containing air was underlined by the frequency of gut blast injury in underwater explosions mostly reported during World War II. Gut injury is the most likely cause of mortality after the more immediate effects of pulmonary primary blast injury. Effective protection has been achieved for lungs exposed to short duration external blast waves by the placement of stress wave decouplers on to the thoracoabdominal wall in a pig model, thus modifying the energy coupled into the body. A combination of two densities of glass-reinforced plastic plate and Plastazote foam (GRP/PZ) effectively eliminated pulmonary injury in 17 protected animals, compared with the production of severe blast lung in nine unprotected animals (p < 0.001). Partial pulmonary protection was achieved using a plasticized lead and plastazote foam decoupling combination (PbPVC/PZ) in a further group of 10 animals. Peak incident overpressures were not significantly different in any group. Small bowel contusions were highly significantly reduced in the GRP/PZ groups when compared with unprotected animals and with PbPVC protected animals (both p < 0.001); no significant reduction was observed in the summed colonic contusion size in any protected group. Intestinal perforations were also highly significantly reduced in both GRP/PZ groups (p < 0.001). Primary pulmonary blast injury and probably small bowel injury are caused by the propagation of coupled stress waves within the body. Elimination of these injuries implies prevention of stress wave propagation. Because colonic injury was not prevented by the same protection, a different mechanism for the injury is suggested: transmission and propagation of shear waves. These findings have important implications for blast protection and the clinical management of primary blast casualties.

The Surgical Management in War of Penetrating Wounds Contaminated with Chemical Warfare Agents

Military surgeons in a future conflict may face the problem of wounds contaminated with chemical warfare (CW) agents. No useful guidelines for this eventuality exist-nor any assessment of the specific CW risk to such casualties or to the surgical teams operating on them. The principal hazard to surgeons is direct contact with contaminated clothing in the wound. Practices are recommended to reduce this threat significantly. Thorough wound excision augmented by lavage with a specific proprietary hypochlorite solution will provide effective wound decontamination without producing unacceptable tissue damage. The vapour hazard at surgery is very low-respirators are unnecessary but goggles or glasses should be worn to prevent conjunctival splashes of potentially contaminated body fluids.

Cardiovascular distortion in experimental nonpenetrating chest impacts.

High-speed cineradiography and flash radiography were used to determine cardiac distortion and the motion of the heart within the thorax following nonpenetrating chest impact. Maximum ventricular distortion occurred approximately 3 ms after impact which was also the time of maximum chest wall displacement. Between +3 ms and +10 ms the heart moved posteriorly and regained much of its initial shape. Maximal posterior displacement of the body of the heart occurred at approximately +10 ms. Three-dimensional reconstruction showed that the heart moved caudally and to the right, with little rotation. The aortic arch moved cranially with consequent stretching of the thoracic aorta.