Explosive Blast Injuries: Principles and Practices 981192855X, 9789811928550

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Zhengguo Wang Jianxin Jiang Editors

Explosive Blast Injuries Principles and Practices

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Explosive Blast Injuries

Zhengguo Wang • Jianxin Jiang Editors

Explosive Blast Injuries Principles and Practices

Editors Zhengguo Wang Research Institute of Surgery Daping Hospital Chongqing, China

Jianxin Jiang Research Institute of Surgery Daping Hospital Chongqing, China

ISBN 978-981-19-2855-0    ISBN 978-981-19-2856-7 (eBook) https://doi.org/10.1007/978-981-19-2856-7 © People’s Medical Publishing House, PR of China 2023 This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the whole or part of the material is concerned, specifically the rights of reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publishers, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publishers nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publishers remain neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Singapore Pte Ltd. The registered company address is: 152 Beach Road, #21-01/04 Gateway East, Singapore 189721, Singapore

Preface

Blast injuries are characterized by high incidence rate, occurrence among the masses, and difficulty in prevention whether in wartime or in peacetime. Such explosions usually result in multiple critical injuries, high infection rates, treatment difficulty, and high mortality. Along with changes in combat styles and extensive application of various explosive weapons, blast injuries have become the main injury category in modern warfare, accounting for more than 70% of total injuries. In peacetime, frequent terrorist bombings and various explosions have caused a large number of casualties. Since the “September 11 attacks,” terrorist bombings around the world have become increasingly rampant, and serious and vicious incidents with hundreds of casualties have become more frequent. Such terrorist bombings constitute a major issue facing the international community today and a top priority for world security. Therefore, it is of far-reaching military and social significance to strengthen the research on blast injury and improve protection and treatment of such injuries. As the name suggests, blast injury is mechanical damage caused by various kinds of explosions. Its presence is closely related to gunpowder, one of the four great inventions of China. The black powder was invented as early as the beginning of the Western Han Dynasty. According to historical records, during the process of refining medicinal pills, ancient Chinese alchemists discovered that the mixture of nitrate, sulfur, and charcoal could burn and explode, thus giving birth to gunpowder. Close to the end of the Tang Dynasty at the beginning of the tenth century, gunpowder came to be used in warfare. Early gunpowder weapons did not explode with much power and were mainly used in ignition. In the thirteenth century, gunpowder was introduced to Arab countries by merchants through India, and then made its way to Europe. In the 1860s, Alfred Bernhard Nobel invented what is now trinitrotoluene, also known as nitroglycerin. The widespread use of gunpowder and gunpowder weaponry is a turning point in the world history of weapons, after which the military operation has undergone tremendous transformation, and armies transitioned from cold weaponry into the era of hot weaponry. In the future of IT-based warfare, not only will explosive weapons become the main combat force, but various types of new explosive weapons with greater lethality will also continue to be developed and play greater roles in winning conflicts against enemies. Although warfare has already ushered in the age of hot weapons as early as the nineteenth century, research on blast injury really was only started after World War II. In August 1945, the United States dropped two atomic bombs on the Japanese cities of Hiroshima and Nagasaki. The whole world was shocked by their destructive power as hundreds of thousands of people were killed and injured, while huge parts of the cities fell into ruins. After World War II, the U.S. military took the lead in launching international research on blast injuries due to concerns about the emergence of nuclear warfare. The research on blast injury in China began in the late 1970s. Academician Zhengguo Wang, as the founder of blast injury research in China, mainly conducted early blast injury researches during nuclear tests. Through a large number of animal field experiments, he has successively summarized and compiled the monographs such as Nuclear Weapon Injuries to Personnel and Its Protection, Nuclear Blast Injuries, and other related works, which laid the foundation for systematic research on blast injuries at the later stages. In 1984, the former Institute of Field Surgery of the Third Military Medical University

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established the first and also so thus far the world’s largest and the most advanced bio-shock tube laboratory in China, opening a new era in which blast injury research may be carried out in labs. In spite of the late start of blast injury research in China compared to the United States and the former Soviet Union, Chinese blast injury research has been advancing rapidly since the 1980s, having solved a series of worldwide challenges in the field of blast injury treatment and becoming an international leader in blast injury research in one fell swoop. In the 1980s, Academician Zhengguo Wang wrote the first international monograph Blast Injury. In recent decades, with the frequent occurrence of various explosion incidents and consequently the increasingly serious threats to society, blast injuries have garnered widespread attention, and considerable efforts are being committed to related research as people have begun to truly understand the severity of injuries caused by such explosions and the necessity of proper treatment. To better respond to the medical rescue needs of various explosion incidents, further improve the national awareness, and enhance the level of blast injury prevention and treatment, we have brought together 61 well-known national experts in trauma surgery, field surgery, coal mine medicine, anti-terrorism medicine, explosion physics, and other fields for the compilation of the book Principles and Practices of Explosive Blast Injury, which is in fact an updated version and expansion of the monograph Blast Injury. The book presents a systematic summary on the series of achievements of blast injury research and new progress in injury treatment in China and related international developments over the past 30 years. It not only includes methods to deal with various conventional injuries inflicted by explosive weapon and nuclear explosion commonly seen in modern warfare, but also systematically covers injuries caused by various explosion accidents (such as coal mine gas explosions and chemical explosions) and terrorist bombing. It also offers a comprehensive introduction to knowledge and injury theory about explosive shock waves, prevention and treatment of various explosion blast injuries and their complications. It is regarded as the only monograph that systematically expounds various types of blast injuries in peacetime and wartime, reflecting the highest level of research and treatment of blast injuries in the world today. Containing a wide variety of contents, the book is very practical as many segments are dedicated to elaborate on the causes of various types of explosion and impact injuries, as well as protection and treatment measures. This book serves not only as an important basis and technical support for military health service support in modern warfare, but is also extremely important in providing practical value in peacetime disaster prevention, mitigation, and relief and embodies great military and social significance for promoting the construction of a world-class army and propelling socio-­ economic development. While the Principles and Practices of Explosive Blast Injury awaits publication, I would like to express my sincere gratitude to the experts who have participated in the compilation of this book, to whose great support and efforts that the debut of this book largely owes to. At the same time, my sincere thanks go to the People’s Medical Publishing House for the guidance and scrutiny for this book. As this book covers a wide range of disciplines with relatively complex content, I hereby implore readers to put forth valuable criticisms and suggestions on any inadequacies. Chongqing, China Chongqing, China  August 15, 2019

Zhengguo Wang Jianxin Jiang

Contents

Part I General Introduction I ntroduction and Epidemiology�����������������������������������������������������������������������������������������   3 Zhengguo Wang, Jihong Zhou, and Zhihuan Yang Explosion Physics ���������������������������������������������������������������������������������������������������������������  15 Tong Liu  xplosion and Injuring Factors�����������������������������������������������������������������������������������������  63 E Jianxin Jiang and Zhengguo Wang I njury Principles and Mechanisms of Shock Wave���������������������������������������������������������  81 Zhengguo Wang, Zhihuan Yang, and Haibin Chen  echanical Mechanisms and Simulation of Blast Wave Protection �����������������������������  89 M Zhuang Zhuo and Zhanli Liu Biological Shock Tube���������������������������������������������������������������������������������������������������������  99 Haibin Chen  efense Against Blast Injury��������������������������������������������������������������������������������������������� 117 D Ce Yang  iagnosis of Blast Injury ��������������������������������������������������������������������������������������������������� 143 D Lianyang Zhang  edical Treatment in Echelons of Blast Injury��������������������������������������������������������������� 153 M Zhaohui Huang  irst Aid Techniques for Blast Injury������������������������������������������������������������������������������� 167 F Zhaowen Zong  last Injury Management and Treatment in ICU����������������������������������������������������������� 187 B Hao Tang and Dongpo Jiang Blast Trauma Care������������������������������������������������������������������������������������������������������������� 193 Lei Liu, Haiyan He, and Xiuhua Yang  sychological Intervention and Therapy After Blast Injury������������������������������������������ 203 P Zhengzhi Feng Part II Key Complications and Their Treatment Hemorrhagic Shock ����������������������������������������������������������������������������������������������������������� 211 Liangming Liu I nfection and Sepsis ����������������������������������������������������������������������������������������������������������� 227 Huaping Liang and Jun Yan

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Trauma-Induced Coagulopathy����������������������������������������������������������������������������������������� 253 Su Liu and Liyong Chen  ultiple Organ Dysfunction Syndrome��������������������������������������������������������������������������� 265 M Jian Zhou  tress Disorder After Blast Injury������������������������������������������������������������������������������������� 281 S Jie Gao and Yamin Wu Part III Local Blast Injury  last Lung Injury��������������������������������������������������������������������������������������������������������������� 295 B Bo Zhang  earing Damage Through Blast ��������������������������������������������������������������������������������������� 301 H Dejing Meng and Jichuan Chen  last-Induced Traumatic Brain Injury����������������������������������������������������������������������������� 319 B Minhui Xu  cular Blast Injury������������������������������������������������������������������������������������������������������������� 327 O Nian Tan and Jian Ye  eart Blast Injury��������������������������������������������������������������������������������������������������������������� 349 H Qianjin Zhong  bdominal Blast Injury����������������������������������������������������������������������������������������������������� 357 A Song Zhao, Xiongbo Guo, and Weidong Tong Part IV Combined Blast Injury  urn-Blast Combined Injury��������������������������������������������������������������������������������������������� 375 B Jihong Zhou and Jun Qiu  rojectile-Blast Combined Injury������������������������������������������������������������������������������������� 391 P Jianmin Wang  ombined Radiation-Blast Injury������������������������������������������������������������������������������������� 397 C Yongping Su and Tao Wang  oxin-Blast Composite Injury������������������������������������������������������������������������������������������� 417 T Maoxing Yue Part V Blast Injury in Special Environments  lateau Blast Injury����������������������������������������������������������������������������������������������������������� 431 P Zuoming Yin, Bo Kang, and Hao Yin  nderwater Blast Injury ��������������������������������������������������������������������������������������������������� 451 U Shengxiong Liu and Zhiyong Yin  abin Blast Injury ������������������������������������������������������������������������������������������������������������� 465 C Xinan Lai Part VI Different Types of Blast Injuries  uclear Blast Injury����������������������������������������������������������������������������������������������������������� 487 N Yang Xu, Cheng Wang, Chunmeng Shi, Binghui Lu, and Zhou Jihong

Contents

Contents

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I njuries from Conventional Explosive Weapons ������������������������������������������������������������� 505 Jianmin Wang, Jing Chen, Jihong Zhou, Jun Qiu, and Yuan Yao  and Mine Blast Injury����������������������������������������������������������������������������������������������������� 549 L Bingcang Li  last Injuries from Mining Gas����������������������������������������������������������������������������������������� 559 B Mingxiao Wang  last Injuries from Explosion of Chemicals��������������������������������������������������������������������� 579 B Aimin Luo  errorist Blast Injuries������������������������������������������������������������������������������������������������������� 605 T Min Yu, Jiashu Li, and Xianghong Zhang Explosion Incidents������������������������������������������������������������������������������������������������������������� 623 Liang Zhang Index������������������������������������������������������������������������������������������������������������������������������������� 633

Contributors

Haibin Chen  Army Medical Center of PLA, Chongqing, China Jichuan Chen  Army Medical Center of PLA, Chongqing, China Jing Chen  Army Medical Center of PLA, Chongqing, China Liyong Chen  Army Medical Center of PLA, Chongqing, China Zhengzhi Feng  Army Medical University, PLA, Chongqing, China Jie Gao  Army Medical Center of PLA, Chongqing, China Xiongbo Guo  Army Medical Center of PLA, Chongqing, China Haiyan He  Army Medical Center of PLA, Chongqing, China Yinghui Huang  Army Medical University, PLA, Chongqing, China Zhaohui Huang  Army Medical University, PLA, Chongqing, China Dongpo Jiang  Army Medical Center of PLA, Chongqing, China Jianxin Jiang  Army Medical Center of PLA, Chongqing, China Bo Kang  General Hospital of the People’s Liberation Army in Tibet Military District, Tibet Autonomous Region, China Xinan Lai  Army Medical Center of PLA, Chongqing, China Huaping Liang  Army Medical Center of PLA, Chongqing, China Bingcang Li  Army Medical Center of PLA, Chongqing, China Jiashu  Li The Academy of Military Medical Sciences of the PLA Academy of Military Science, Beijing, China Dengqun Liu  Army Medical University, PLA, Chongqing, China Lei Liu  First Affiliated Hospital of Army Medical University, PLA, Chongqing, China Liangming Liu  Army Medical Center of PLA, Chongqing, China Shengxiong Liu  Chongqing University of Technology, Chongqing, China Su Liu  Army Medical Center of PLA, Chongqing, China Tong Liu  South University of Science and Technology, Sichuan, China Zhanli Liu  Tsinghua University, Beijing, China Binghui Lu  Army Medical University, PLA, Chongqing, China Aimin Luo  China Academy of Safety Science and Technology, Beijing, China Dejing Meng  Army Medical Center of PLA, Chongqing, China xi

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Jun Qiu  Chongqing Emergency Medical Center, Chongqing, China Chunmeng Shi  Army Medical University, PLA, Chongqing, China Yongping Su  Army Medical University, PLA, Chongqing, China Nian Tan  Army Medical Center of PLA, Chongqing, China Hao Tang  Army Medical Center of PLA, Chongqing, China Weidong Tong  Army Medical Center of PLA, Chongqing, China Cheng Wang  Army Medical University, PLA, Chongqing, China Jianmin Wang  Army Medical Center of PLA, Chongqing, China Mingxiao Wang  Emergency General Hospital, Beijing, China Tao Wang  Army Medical University, PLA, Chongqing, China Zhengguo Wang  Army Medical Center of PLA, Chongqing, China Yamin Wu  Army Medical Center of PLA, Chongqing, China Minhui Xu  Army Medical Center of PLA, Chongqing, China Yang Xu  Army Medical University, PLA, Chongqing, China Ce Yang  Army Medical Center of PLA, Chongqing, China Xiuhua Yang  Army Medical Center of PLA, Chongqing, China Zhihuan Yang  Army Medical Center of PLA, Chongqing, China Jun Yan  Army Medical Center of PLA, Chongqing, China Yuan  Yao 903 Hospital of the People’s Liberation Army Joint Logistic Support Force, Jiangsu, China Jian Ye  Army Medical Center of PLA, Chongqing, China Hao Yin  Shanghai Medical College of Fudan University, Shanghai, China Zhiyong Yin  China Automotive Engineering Research Institute Co., Ltd., Chongqing, China Zuoming Yin  General Hospital of the People’s Liberation Army in Tibet Military District, Tibet Autonomous Region, China Maoxing Yue  PLA Strategic Support Force Special Medical Center, Beijing, China Min Yu  The Academy of Military Medical Sciences of the PLA Academy of Military Science, Beijing, China Bo Zhang  Army Medical Center of PLA, Chongqing, China Liang Zhang  Army Medical Center of PLA, Chongqing, China Lianyang Zhang  Army Medical Center of PLA, Chongqing, China Xianghong Zhang  Fuxing Hospital Affiliated to Capital Medical University, Beijing, China Song Zhao  Army Medical Center of PLA, Chongqing, China Qianjin Zhong  Army Medical Center of PLA, Chongqing, China Jian Zhou  Army Medical Center of PLA, Chongqing, China Jihong Zhou  Army Medical Center of PLA, Chongqing, China Zhuo Zhuang  Tsinghua University, Beijing, China Zhaowen Zong  Army Medical University, PLA, Chongqing, China Editor-In-Chief Assistant: Cai Qingli

Contributors

About the Editors

Zhengguo  Wang  is one of the first batch of academicians, researcher, doctoral supervisor of the Department of Medicine and Health of the Chinese Academy of Engineering, academic leader of field surgery, first-level professor of the Chinese People’s Liberation Army Special Medical Center, editor-inchief of the Chinese version of Chinese Journal of Traumatology, deputy director of the Military Medical Science and Technology Committee. He is one of the main founders of blast injury, wound ballistics, and traffic medicine research in China, the academic leader of the national key discipline — field surgery, and the first doctoral supervisor of the discipline. He has been engaged in blast injury research since 1970, has entered the nuclear blast zones eight times, visited the front line in Yunnan twice, participated in field tests of weapon explosion, and frequented scenes of accident more than ten times to observe injuries caused by various explosives for investigation and gathering of related first-­hand information on blast injury. He has also conducted a large number of animal experiments. In 1984, in coordination with the Institute of Mechanics of Chinese Academy of Sciences, he helped develop the first bio-shock tube in China to simulate indoor shock waves generated by the explosion of different equivalents of explosives, thus enabling the performance of laboratory shock injury research for the first time in China. He also carried out systematic researches on lethal effects of shock wave, dose-effect relationship, safety standards and protection, etc., and he is the first in the world to systematically clarify the shock wave injury mechanism (overdraft effect theory). He put forward the principle of diagnosis and treatment, especially the use of perfusion, casting, freezeetching, morphometric measurement, molecular biology, and other technologies for the first time, benefitting innovative studies on lung blast injuries. He also proposed a new pathological classification method for lung blast injuries. Regarding the traditional understanding that fluid infusion therapy for pulmonary shock injury would aggravate pulmonary edema and worsen the injury, after in-depth research, he put forward the treatment principle of “sufficient fluid supplementation and monitoring,” providing a strong basis for clinical treatment of pulmonary shock injuries. In 1992, as the person in charge of the “development and application of a series of biological shock tubes,” he won the first prize of State Scientific and Technological Progress xiii

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About the Editors

Award; and then the second prize of State Scientific and Technological Progress Award in 2005 with “Research on the Mechanism and Prevention Measures of Lung, Eye and Brain Shock Injuries.” He has published more than 200 papers as first author, written and edited 39 monographs, and participated in the editing of more than ten books. He has won one first prize, five second prizes, four third prizes of the State Scientific and Technological Progress Award, and one third prize of the National Invention Award. He was also a winner of the Science Technology Progress Award by Ho Leung Ho Lee Foundation, the Mikael Debakey International Military Surgeons Award, the TKK Science Awards, and the Guanghua Engineering Science and Technology Prize. Jianxin Jiang  is an Academician of the Division of Medicine and Health of the Chinese Academy of Engineering, researcher, doctoral supervisor, and specialist in field and trauma surgery. He is also the Director of the State Key Laboratory of Trauma, Burns and Combined Injuries, Director of the War Injury Treatment of the Field Surgery Research Department of the Army Special Medical Center of Army Medical University, as well as Director of Key Laboratory of Combined Injuries in Military Field. Throughout the years he has also been concurrently holding various academic posts including the East Asia Regional President of the International Traffic Medicine Association, Secretary General of Asian Trauma Society, Member of the Discipline Appraisal Group of Academic Degree Commission of the State Council, Chairman of Traumatology Society of Chinese Medical Association, Chairman of Trauma Medicine Branch of China International Exchange and Promotive Association for Medical and Healthcare, Vice Chairman of Tissue Repair and Regeneration Society of Chinese Medical Association, Editor-in-chief of the Chinese Journal of Traumatology, etc. He has also been elected as a deputy to the 13th National People’s Congress. He is mainly engaged in study on the treatment of high explosive weapon injury and wound infection in the field of war trauma and has presided over the completion of more than 30 scientific research projects including the National Basic Research Program (973 Program) and major military projects. He has pioneered studies in the molecular genetics of sepsis in modern explosive weapons wounds and trauma, established modern explosive weapon injury theory, solved the problem of injury mechanism and protection caused by explosive shock wave, and realized the preventable and treatable facts of explosion injury. He has uncovered endogenous infection as a significant pathway of critical injury complicated infection and the mechanism of immune escape infection by pathogenic bacteria, put forward new mechanism such as “trauma sensitization” of trauma sepsis and molecular genetics, established a new technical system for diagnosis and treatment of wound infection, and realized early warning identification and precise prevention and treatment of trauma infection, significantly enabling China to reach an inter-

About the Editors

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national advanced level in the prevention and treatment of severe sepsis. He is the winner of four second prizes of State Scientific and Technological Progress Award, Science Technology Progress Award by Ho Leung Ho Lee Foundation, Wu Jieping Medical Innovation Award, Military Outstanding Professional Technical Talent Award, Outstanding Contribution Award for Western Development of China Association for Science and Technology, and Chongqing Outstanding Talent Award. He has also been selected into the New Century Millions of Talents Project, as well as the first batch of Military Highlevel Scientific and Technological Innovation Talent Project. He is the chief editor of seven monographs including Trauma Infection Studies and Chinese Trauma Intensive Medicine Studies, among others.

Part I General Introduction

Introduction and Epidemiology Zhengguo Wang, Jihong Zhou, and Zhihuan Yang

1 Overview of Explosive Blast Injury When high explosives or nuclear weapons detonate, a tremendous amount of energy is released at an instant, and the pressure and temperature at ground zero soar in a dramatic fashion. The explosive force then rapidly spreads in all directions through surrounding media (e.g., air, water, soil, steel sheets), forming a high-pressure and high-speed energy wave, and this is explosion shock wave (blast wave). The abrupt movement of high-pressure gas from the firing of a cannon, supersonic flight, explosions from gas leaks, shock tube experiment, and other instances also generate similar shock waves. Bodily injuries caused by shock waves are hereinafter referred to as “explosive blast injury.” In clinical context, “explosion blast injury” usually refers to primary injury caused directly by shock waves in air or water. Injuries caused by shock wave in a solid (e.g., deck of a warship), or mechanical trauma from objects thrown by shock wave or other indirect effects (e.g., collapse of structures) may be categorized as “blast injuries” but are usually not called “explosive blast injuries.” In modern warfare, belligerents might adopt carpet bombing strategy and drop a huge number of large bombs in densely populated cities, or use bombs that mainly cause destruction through shock wave such as aerosol bomb or fuel-air explosive bomb, which are more likely to result in blast injuries. Take for example an equivalent to a 5-megaton nuclear weapon, the shock wave could injure personnel exposed on the ground surface within an area of over 800 km. This is only the direct kill zone, and if the indirect impacts of shock wave are taken into account, the area of effect would enlarge by one to two folds. Shock wave is one of the primary destructive elements that cause injury and damage in the use of a nuclear weapon. In August 1945, some 70% of injuries in the atomic bombings of Japan resulted from shock

Z. Wang (*) · J. Zhou · Z. Yang Army Medical Center of PLA, Chongqing, China e-mail: [email protected]

wave. At Hiroshima, among the deaths early on, 60% were attributed to blast injury. Among victims of moderate and severe injuries that survived after the first day of detonation, those afflicted by blast injuries accounted for 36.6%. In conventional warfare, shock wave is one of the primary destructive elements essential to the different types of explosive weapons. For instance, among the 1303 cases of patients severely wounded by explosion treated at the former Yugoslav Academy of Military Medical Sciences, 51.0% resulted from blast injuries. In skirmishes along the border in southwestern China, among a group of 166 persons injured by artillery and mines, 22.3% resulted from blast injuries. Outside of the battlefield, many have been injured or killed from explosions in weapon factories, munition depots, chemical plants, mines, or other areas, not to mention victims of terrorist attacks. Bombings account for approximately 75% of terrorist attacks, and blast injury is one of the most common types of injuries caused by such attacks. With advancements in explosive production and technology, explosives become increasingly diverse and powerful. Some common types of explosives include black powder, ammonium nitrate, nitroglycerine gelignite, TNT, RDX, Composition C and other plastic explosives, emulsion explosives and liquid explosives, to name but a few. In recent years, Composition C plastic explosive has risen as the weapon of choice for terrorist bombing. For example, Composition C plastic explosives were used in two series of bombings in Indonesia, respectively at tourist district on the island of Bali in 2002 and at upscale hotels in the business district of capital Jakarta in 2009. Explosive devices are becoming smaller and smarter, and less metals are being used. Some explosives are made to look like toys, toothpaste, and other daily items, while others convert cameras, radios, and other objects into small bombs. Methods of detonation have also diversified from safety fuse to electrical, mechanical and chemical means, and even methods like remote control, temperature control, light control, or sound control. On July 9th, 2007, a bombing in Jinan

© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 Z. Wang, J. Jiang (eds.), Explosive Blast Injuries, https://doi.org/10.1007/978-981-19-2856-7_1

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shocked the nation, as perpetrator used remote control to detonate an explosive device planted inside a car. Thus, it can be seen that blast injury is not only a matter crucial to military medicine, but also a type of injury and emergency commonly seen in hospitals. In addition, it should also be pointed out that most vulnerable to the typical blast injury (as in what is frequently referred to as “explosive blast injury”) are auditory apparatus and organs, in particular the lungs because of its high content of air. Many victims meanwhile do not exhibit obvious signs of injury on the surface. In the early phase of injury, the vital signs (e.g., breathing, circulation) of the injured might appear normal because of the body’s natural tendency to compensate, but soon after the situation would quickly deteriorate. At the same time, blast injuries might be accompanied by other injuries (i.e., burns or other mechanical injuries), or bodily damage might manifest as multiple trauma. Prompt diagnosis and corresponding treatments are mandatory so as not to miss the best opportunity for medical intervention, otherwise the consequence could be dire or might even result in death.

2 Physical Parameters and Biomechanical Mechanisms of Injury from Blast Wave

Z. Wang et al.

consists of two parameters, i.e., pressure peak and positive pressure duration, and it is more accurate and suitable in describing the relationship between a blast wave and the severity of injuries caused. In particular, for blast injuries that happen underwater, pressure peak is high but positive pressure duration is short; or for composite blast injuries that occur inside enclosed spaces such as that of a tank or armored vehicle, impulse can better explain the relationship between the shock wave’s physical parameters and the resulting blast injuries. 4. Duration of pressure increase. Duration of pressure increase refers to the length of time starting when pressure acts on a certain point on the body until reaching its peak value. It is measured in millisecond (ms) or second (s). Duration of pressure increase reflects the rate at which pressure rises on a point affected by the shock wave, and when other conditions are constant, the shorter the duration of pressure increase, the faster the rate of pressure increase, the more severe the blast injury.

2.2 Biomechanical Mechanisms of Injury from Blast Wave

Main physical parameters of injury from blast wave include: peak value of shock wave pressure, duration of positive pressure, impulse, duration of pressure increase, etc.

Blast wave injuries mainly result from the direct effect of blast wave, the indirect effect from the displacement of objects caused by the blast, and being thrown and collided against other objects due to dynamic pressure. Injury mechanism behind shock wave can be simplified as either a direct or indirect result of the shock wave. The biomechanical mechanisms, however, are not completely understood, particularly with regard to the effects of the overpressure and negative pressure from a blast wave.

1. Peak value of shock wave pressure. Peak value of shock wave pressure refers to the highest value of pressure in a blast wave and may be categorized as overpressure peak, negative pressure peak, and dynamic pressure peak. It is measured in kilopascal (kPa). A blast wave’s pressure peak is the main parameter that causes blast injury, and it positively correlates with severity of injury. In other words, the higher the peak value of the shock wave at the site of explosion, the more severe the injury. 2. Duration of positive pressure. Duration of positive pressure refers to the length of time of positive pressure caused by shock wave in the pressure zone. It is measured in millisecond (ms) or seconds (s). Within a certain length of time and under the same peak pressure, the longer the duration of positive pressure, the more severe the injury. 3. Impulse. Impulse refers to the sum of the value of instantaneous pressure within the duration of pressure, or in other words, the integral of the force of pressure with respect to time. It is measured in kPa/s or kPa/ms. Impulse

1. Direct effects of blast wave refers to injury arising from the pressure of a blast wave (overpressure and negative pressure). Such injuries are called primary blast injury or pure blast injury, and are chiefly manifested in injuries to air-filled organs such as lungs, gastrointestinal tracts, and auditory apparatus, in addition to possible bleeding in some more solid organs. Strong overpressure on the human body could cause rupture in organs and fractures in bones such as ribs and ossicles, but usually does not cause direct injury on the surface. At present, there is general agreement that direct shock wave injury mechanisms mainly include: (a) Implosion: When a shock wave propagates through a liquid medium that contains bubbles or air pockets, the overpressure of shock wave would cause the compressible air to compress drastically, while liquids and solids would not be compressed nearly as much. The shock wave’s overpressure is followed by negative pressure, which would cause the compressed

2.1 Physical Parameters of Injury from Blast Wave

Introduction and Epidemiology

air bodies to expand immensely, much like many mini explosions that release energy in all directions and injure tissues in their surroundings. Implosion-­ induced injuries usually occur in tissues of air-filled organs such as the lungs and gastrointestinal tract. (b) Pressure differential: When pressure on two sides of a tissue differ, such pressure differential could directly injure said tissue. Therefore, when a shock wave propagates and as it reaches a certain tissue or organ, the tremendous difference in pressure at a local area within a split instance caused by the high pressure on one side and ambient pressure on the other side could directly injure said tissue or organ. For instance, eardrum rupture caused by overpressure is the outcome of pressure differential. Another example happens in the lungs, when shock wave hits a body, pressures rise in both the liquid (blood inside vessels) and gas (air in pulmonary alveoli), but pressure rises more in liquid, and the massive pressure difference between liquid and gas would rip apart the capillaries, resulting in blood flowing into pulmonary alveoli and pulmonary hemorrhage. (c) Overtension: When air-filled organs in the body are hit by a blast wave, during the pressure-decreasing and negative pressure phases, these air-filled organs could change from being under pressure to being expanded, as in tissues changing from being compressed to being inflated and extended, and these tissues have to bear tensile strain and tension stress arising from such inflation. In most cases, tissues can withstand much more compression than extension, and when tensile strain reaches a certain point, microvascular endothelial cells and alveolar epithelial cells would become more permeable, which would result in edema and bleeding. Worst, when tensile strain exceeds the limits of the tissue’s capacity, more serious edema and bleeding would occur as the tissues and blood vessels rupture. During the course of pressure decrease, the higher the pressure peak and the shorter the duration of pressure decrease (i.e., faster rate of pressure decrease), the more obvious the overtension and the more serious the injury. (d) Spalling (fragmentation): When a blast wave propagates through the body from a compact tissue into loose tissue, reflections take place at the interface between compact tissue and loose tissue. This type of reflected wave could cause a sudden rise in  local pressure in the compact tissue, leading to injuries such as alveolar laceration and bleeding, subendocardial bleeding, and bladder mucosal bleeding. (e) Inertia: When the same shock wave acts on two tissues with different densities, the two tissues accelerate and decelerate at markedly different rates,

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and this difference causes tremendous shear stress on the interface between the two tissues, resulting in laceration where the two connect. For examples, rib and intercostal tissue lacerations and bleeding, intestinal and mesenteric tissues lacerations and bleeding are both attributed to shock wave inertia. (f) Negative pressure: Immediately following the overpressure of a blast wave is negative pressure. The speed at which pressure drops, the duration of negative pressure and peak value of negative pressure are the chief parameters in injury, of which, negative pressure peak value plays the biggest role. Negative pressure could result in severe injuries to the lungs, such as widespread pulmonary hemorrhage and edema. Worth noting is that the negative pressure peak value needed to cause such severe injury is much less than overpressure peak value. (g) Hemodynamics: After a blast wave’s overpressure acts on the body, the pressure pushes against the soft abdominal wall, causing pressure inside the abdominal cavity to rise rapidly, in turn pressing the diaphragm upward, causing blood in the superior vena cava to abruptly rush into the heart and lungs, sharply increasing blood volume in these organs. At the same time, the shock wave’s overpressure also presses against the chest cavity, decreasing the volume of the space behind the chest, and since the thoracic cage is relatively harder than the abdomens, the pressure increase in the chest cavity is relatively delayed, resulting in subsequent rush of blood toward the head and sharp increase in blood volume inside the head. Right after overpressure is negative pressure, and the retraction due to pressure decrease would cause the abdominal cavity and thoracic cage to enlarge. This kind of rapid compression and expansion generates huge hemodynamic changes, resulting in injuries to the heart, lungs, and distant vascular tissues (such as that of the brain). 2. Indirect effects of blast wave: Indirect and secondary injuries caused by projectiles and other elements resulting from the dynamic pressure of a blast wave are collectively known as indirect blast wave injuries. Indirect injury effects of blast wave mainly include: (a) Secondary projectiles: Not only does the dynamic pressure of a blast wave turn fragments and shrapnel of a shell into projectiles that could injure the human body, but also imbues other objects (e.g., glass, stone) with kinetic energy and turns them into damaging projectiles. Bombing investigations and statistical data acquired after the atomic bombings of Japan show that the majority of different kinds of open wounds were caused by these secondary pro-

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jectiles. In cities, industrial sites, and residential areas, most secondary projectiles are glass shards from windows, in open spaces meanwhile rocks and even dust or dirt could be “weaponized” as projectiles. (b) Throw and displacement: When dynamic pressure is strong enough, it could manifest as an impact force or projection force. When the dynamic pressure of a blast wave hits a human body, the person could be displaced or thrown high in the air, and then land from a high altitude or impacted against another solid object, resulting in injury. Injuries due to being thrown or displaced are similar to traumas from falling or traffic accident, such as skin abrasion, contusion of subcutaneous tissue, internal organ bleeding and rupture, and bone fracture. (c) Crush and collision from the collapse of structure: Blast wave often causes a portion or an entirety of structures or fortifications on the ground surface to collapse, crushing or burying people within, leading to surface soft tissue and internal organ injuries alongside bone fractures, with crush injuries and crush syndrome appearing in the more severe cases. When fortifications covered in dirt collapse, people within might be buried and even die from suffocation. (d) Other concurrent injuries: During the course of an explosion, often times there are other injury causes such as flash, fire, poisonous gas, dust, drowning, radioactive substance, virus, and other pathogens, which could lead to corresponding injuries to the human body.

3 Types of Blast Injuries Due to the varying metrics systems and standards, blast injuries could be classified using different methods. For instance, methods could be based on blast injury cause, shock wave propagation medium, or body part and organ injured, etc.

3.1 Classification of Blast Injury Cause Classification based on the biomechanics behind blast injury is a method based on the dynamics of how people are injured by a blast wave. In this regard, most classification methods used in China and abroad are based on the method developed by Zuckerman during World War II. This method classifies blast injury into four types: primary blast injury, type II blast injury, type III blast injury, and type IV blast injury, of which, the last three blast injuries are also known as secondary blast injuries.

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1. Primary blast injury refers to injury directly caused by physical factors such as a shock wave’s overpressure, dynamic pressure, or negative pressure, and may be called a pure blast injury. Since air is easily compressed and expanded, primary blast injuries are often seen in the lungs, middle ear, gastrointestinal tracts, and other air-­ filled organs. 2. Type II blast injury refers to bodily injuries caused by projectiles like shrapnel, fragment, broken glass and rock launched by the force of a blast wave. Such injuries are mostly penetration or laceration wounds, and could be seen on any part of the body from the surface and internal organ to the limbs. 3. Type III blast injury refers to collision injuries when people are being thrown by the force of a blast wave, or being struck or crushed by the collapse of structure and fortification. These could result in penetration wound, blunt trauma, bone fracture, traumatic disjunction, crush injury, and crush syndrome on any part of the body. 4. Type IV blast injury refers to any other injuries or diseases related to an explosion but not classified as either primary, secondary, or tertiary blast injury. This miscellaneous group includes bodily harms from flash, fire, toxic gas, dust, drowning, psychological factor, and other issues caused by an explosion, and may afflict any part or organ of the human body.

3.2 Classification of Shock Wave Propagation Medium Since any blast wave-induced injury to the human body may only occur through some sort of medium, how an explosion causes injury is closely associated with shock waves in different media, including characteristics of propagation, features of injury causes, exposure–response relationship and outcomes. Therefore, classifying blast injury based on the shock wave propagation medium has many merits. Generally speaking, shock wave propagation medium are classified as either air blast injury, underwater blast injury, or solid blast injury. 1. Air blast injury refers to injuries to the body from blast wave propagated through the air. The term “blast injury” predominantly refers to air blast injury. Air blast injury is not only associated with the shock wave parameters discussed before, but also the wavelength and frequency of shock wave in the air. When shock waves in the air have relatively short wavelength and generate high-frequency “cracking” sounds, the number of shock waves that hit the human body is higher per unit of time, which translates into higher probability of injuring the human body. On the contrary, when shock waves in the air have

Introduction and Epidemiology

r­elatively long wavelength and emit low-frequency “boom” or “thud,” usually only a single wave would strike the human body, which in turn means that the probability of harms to the human body is much lower. At high altitudes, where the air is thin and atmospheric pressure is low, the same shock wave with the same force would cause more severe blast injury than at a lower altitude. The author’s laboratory conducted an experiment using BST-II bio-shock tube to study how rats would be injured by blast waves under different atmospheric pressures (53.99  kPa, 61.33  kPa, and 96.60  kPa). Results show that when overpressure peak value (190.40  kPa) and positive pressure duration (10 ms) remain constant, lower atmospheric pressure leads to significant increase in fatality rate and significant rise in lung injury severity. After 6 h, the fatality rate of the three groups of rats were respectively 36.8%, 25.0%, and 0%, area of pulmonary hemorrhage were respectively (653.21  ±  652.25)mm2, (313.50  ±  357.25)mm2, and (63.75  ±  69.01)mm2, and lung volume indices were respectively 1.51%  ±  0.77%, 1.31%  ±  0.65%, and 0.93%  ±  0.21%, indicating that lower atmospheric pressure raises fatality rate and exacerbates lung injuries. In addition, BST-I bio-shock tube and decompression chamber were used to replicate and model the rats’ high-­ altitude blast injuries so as to observe morphological and hemorheological changes. Results indicate that pulmonary hemorrhage and edema were more severe compared with low-altitude injuries, blood viscosity elevated significantly and remained heightened even 6 h after injury. 2. Underwater blast injury refers to injury to people in water due to blast wave generated in the subsurface explosion of bombs, missiles, or other explosive devices and propagated through water. Naval warfare is one of the major battlespaces in the future, which is why underwater blast injury has become one of the focal points of modern blast injury research, which take into full account the characteristics of shock wave propagation and injury causes in water. The physical properties of underwater shock wave vary markedly from shock waves in the air, and therefore, injuries also differ vastly. Some of the main differences include: (1) Increased speed of propagation (usually three to four times faster than in the air); (2) propagated relatively farther, and area of effect of blast wave in water is almost ten times larger than that in the air; (3) no compression zones or rarefaction zones, and water molecules also do not move as much as air molecules as a shock wave propagates through them; (4) when underwater shock waves reach the interface between the water surface and the air, reflection occurs and creates unique reflected waves, or tensile waves. The tensile waves propagate in directions different from the incident waves, and

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serve to reduce the incident waves (Fig. 1). The closer the point of action to the water surface, the more the incident wave is reduced (Fig. 2). In other words, when there is an underwater explosion, people closer to the water surface would be less severely injured. Clinical features of underwater blast injury are as follows: (1) There are extremely few injuries to the surface of the body. In an underwater explosion, usually there won’t be a large amount of secondary projectiles, and seldom would people be thrown against some sort of hard, solid object. Thus injuries to the surface of the body are rare. (2) Injuries to air-filled organs are severe while injuries to liquid-containing organs are light. The former may be explained by implosion, while the latter is caused by similar density between liquid and soft tissues. Such an experiment has been performed previously: Isotonic saline-filled animal intestine was subjected to an underwater explosion, and no damage to the intestine was observed, even if the intestine was placed near the explosive. However, when there was even a tiny amount of air left inside the intestine, holes could be seen on the intestinal wall right after an explo-

Water surface A

aves ent w

Incid +

b

a Pressure t –

Fig. 1  Formation and action of tensile waves. (a) Incident waves before reaching point A; (b) reduced incident waves when reaching point A; A action point, t time

Water surface

A

Explosive

B

Fig. 2  Different effects of various tensile waves. A Action point, B Action point

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sion. (3) Most head injuries are light. This is because during an underwater explosion, the majority of victims are near the surface and their heads are above water. (4) Most abdominal injuries are severe. For people underwater or floating on the surface, the abdomen is in direct contact with water, and the abdominal wall is relatively soft, which is why when an underwater explosion occurs, organs in the abdomen (gastrointestinal tract for the most part) are more prone to severe injuries compared with an air explosion. (5) The fatality rate is relatively higher. One report indicates that 47 victims out of 118  in an underwater blast died, a fatality rate of 39.8%. Another document reports that 9 victims out of 13 in an underwater blast died, a fatality rate of 69.2%. Meanwhile, in general 90% of air blast injury victims are not severely injured. In order to understand the characteristics of underwater blast injury and the exposure–response relationship between shock wave strength and injury severity, the author’s laboratory carried out the following experiment: 37 mixed-breed dogs anesthetized, floatation devices were attached to their necks so that their heads would stay above water while the bodies and limbs would be underwater perpendicularly to the surface. The dogs were placed on either side of the 3.5 m and 17.5 m in a distance from explosion center (Figs. 1, 2, and 3), TNT explosives ranging from 0.2 to 1.0 kg in quantity were placed 3 m underwater, high-pressure instantaneous detonator was used for detonation, and the survival conditions and pathological changes in the animals were observed on-site and 6 h thereafter. Result shows that (1) the features of physical parameters of underwater shock wave are: high peak pressure value but short duration, as in several hundred microseconds, far shorter than the several or tens of milliseconds in the duration of shock wave in air generated by an explosion. In addition, the duration of pressure increase is measured in microseconds, which is extremely short particularly when com-

Fig. 3 Placement of test animals for underwater blast injury experiment

pared with the 1  ms-range of explosions in the air. Therefore, cause of injury by underwater shock wave can’t be determined simply with using overpressure peak value, and in this regard impulse is more suitable. Preliminary exposure–response relationship analysis indicates that impulse ranges respectively for light, moderate, severe, and extremely severe injuries are 121.1– 14.0 kPa/ms, 142.0–214.3 kPa/ms, 247.8–322.6 kPa/ms, and 322.6–579.8 kPa/ms. (2) The lethal radii for 0.2 kg, 0.5 kg, and 1.0 kg TNT explosions are respectively 5 m, 8.75 m, and 12.5 m from the blast center, much farther than the lethal range of mid-air explosions with the same amount of explosives. The lethal radius of 0.5 kg TNT underwater explosion (8 m) is approximate to 40.0 kg of TNT explosion in mid-air. (3) The fatality rate is high. Of the 37 dogs, ten died on-site (two had collapsed lung and pneumonia before injury, and thus were not counted), and no death was recorded 6  h after injury, registering the final fatality rate of 27%. This result may be attributed to the fact that explosions from the same quantity of explosives at different ranges underwater generate much stronger shock waves when compared to explosions in the air. (4) Lung injury is the most common (83.7%) and most serious, with the majority of on-site deaths associated with severe pulmonary hemorrhage and edema, coronary artery air embolism arising from ruptured lung and pulmonary injury were even observed in some animals. (5) There is a high rate of injury to the intestine, with 29.73% afflicted by small intestine injury and 51.35% afflicted by colon injury, far higher than those caused by mid-air explosions. Colon injury was more common because it contains more air. (6) The rate of injury to solid organs is low. Other than three cases of slight bleeding in the pancreas and one case of ruptured liver, no injuries were found in spleens, kidneys, and filled bladders. (7) There are no injuries on the surface of bodies. 3. Solid blast injury refers to injuries to the body from blast wave propagated through solids. The propagation of blast wave in solid is vastly different from propagation in air or water, specifically, the relatively smaller amplitude and shorter time of the shock wave’s action (usually within a few milliseconds), but also an immensely faster acceleration. Solid blast injuries are often seen when battleships, tanks, or armored vehicles are hit by an explosive, and the blast wave and secondary shock wave thereafter act on the structure, deck and armor of the struck vessel/vehicle, then propagate in the form of flexion wave. This results in two types of motion: First is the slight displacement and acceleration of solid, and second is the subsequent bending, vibration, and other obvious macroscopic motions. The first type of motion would injure body parts that are in contact with the solid, usu-

Introduction and Epidemiology

ally injuries to the lower limb, especially damage to the ankles. This is considered primary injury of and the general definition of solid blast injury. The second type of motion might cause victims to be thrown against other objects and injured, which would be deemed secondary solid blast injury. Main characteristics of solid blast injury include: Mostly injuries to bones and joints in the lower extremities, and this kind of bottom-up impact might result in closed fracture and injury to the heel bone, phalanges, shinbone and lower part of calf bone and ankle joint, with heel bone fracture being relatively frequent. Analysis of information about 50 victims of solid blast injuries shows that 18 suffered from bone fractures in the ankles, with the majority being multiple, comminuted fractures, including 11 victims with heel bone fractures affecting 15 limbs. Body part injured is clearly associated with body position, and the majority of injuries occur on one side of the body. For example, a particularly lower extremity is more easily injured when standing, while the spine is more likely to take damage when sitting. Injuries to solid organs in the abdominal cavity are also quite common, and one possible reason is that the acceleration of the shock wave induces deformation and displacement of internal organs, leading to crushing, collision, retraction, and other injuries when organs interact with bones, muscles, and ligaments. Injuries to the liver and spleen are the most frequent. Indirect injuries happen often, mostly manifested as damages such as soft tissue injury, bone fracture, cerebral concussion arising from sudden acceleration and movement of brain matter caused when a person is thrown or horizontally displaced then struck against something. Of the 50 hospitalized cases, 32 showed loss of consciousness, which resulted from head injuries when they were thrown or displaced.

3.3 Classification of Body Part and Organ Injured Classification based on body part and organ injured is a method that focuses on the specific body part and organ injured by a blast wave. Some common categories are brain blast injury, thoracic blast injury, abdominal blast injury, blast injury of the spinal cord, and blast injury of the extremities. Moreover, blast injuries may also be categorized as injury to the lungs, heart, brain, gastrointestinal tract, liver, auditory apparatus, and other body parts. Among them, blast injuries to the lungs, gastrointestinal tract, and auditory apparatus occur on a more frequent basis. Through body part and organ-based classification, diagnosis can quickly pinpoint the area(s) injured by blast wave, and carry out corresponding diagnosis, prevention

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and research methods based on injury mechanisms and characteristics.

3.4 Classification of Injury Severity 1. Pathological classification: Yelverton, an American scientist, recently introduced an injury scoring system that may be used as basis for judging severity of injury. The main points include: (a) First of all, calculate the overall score of an individual injury including its scope, severity, type, depth, or wound condition; (b) divide the score of said injury by the worst case scenario-score for that type of injury to obtain the ratio score of said injury; (c) add the ratio scores of all individual injuries to find their sum; (d) add scores of pathogenic factors (e.g., pneumothorax, hemothorax, hemoperitoneum, coronary artery air embolism or cerebral vascular air embolism); (e) multiply the score by two if the victim dies; and (f) to determine the level of non-auditory apparatus injury, subtract the ratio score for auditory apparatus injury from the Severity of Injury Index (SII) to obtain the Adjusted Severity of Injury Index (ASII). This methodology is detailed and relatively accurate, but also somewhat complex. 2. Clinical classification (a) Light: General injuries to auditory apparatus, light internal organ contusions (intraplaque hemorrhage), scratches on the surface of the body, etc. (b) Moderate: Relatively large-scale internal organ contusions (patchy hemorrhage or hematoma), relatively light pulmonary edema, large swaths of soft tissue injury, dislocation, rib fracture with no obvious dislocation, cerebral concussion, etc. (c) Severe: Ruptured internal organ, fractured bone (thigh bone, spine, cranial base, and multiple fractured ribs), relatively severe pulmonary edema, pulmonary hemorrhage, etc. (d) Extremely severe: Extremely serious or fatal injuries such as severe cerebral and spinal cord injury, ruptured chest cavity or abdominal cavity, widespread and serious pulmonary hemorrhage or pulmonary edema, ruptured artery, amputation with severe bleeding, etc.

4 Epidemiological Features of Blast Injury Blast injuries differ quite markedly from other kinds of injuries in terms of aspects such as injury causing condition, injury mechanism, on-site environment and treatment. Therefore, the injury characteristics and epidemiological features of blast injury are also quite different from other types of injuries.

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4.1 General Features of Blast Injury

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ous sign of damage. However, the target organs inside, such as the lungs or gastrointestinal tract, might have Since both the direct and indirect effects of a blast wave act already sustained heavy damage, or in other words, light on the body during the course of a blast injury, things can get external injury and severe internal injury. very complicated when injured tissues and organs, injury At the site of major bomb explosion experiment, when mechanisms and processes are all taken into consideration. an animal is closer to the center of explosion (distance The situation is further compounded due to the varying envivaries with respect to explosion equivalent), there might ronments and conditions where injury occurred. Therefore, be visible signs of external injuries to the body surface blast injuries are characterized by features unlike those seen and limbs, but injuries to the internal organs are always in other types of injuries. In general, the features of blast more severe, and most of the times the primary cause of injury include: death. For animals within the range of injury but farther from the center of explosion, there are relatively fewer 1. Complicated injury: The overpressure, negative pressure, and lighter injuries to the body surface and extremities, and dynamic pressure of a blast wave all could cause but internal injuries could still be dire and are even the injury on their own or when acting together, both directly main cause of fatality. and indirectly. This diversity in injury causes and meth- 4. Rapid deterioration of injury. For severe or worst blast ods means that blast injury types and conditions are cominjuries, there is a relatively stable compensatory period plicated. Blast injuries are complicated for the following within a short span right after the injury, but if treatment reasons: Most blast injuries are multiple injuries or injuis not administered promptly, the situation would rapidly ries to multiple body parts, and external and internal injuworsen. In particular, brain injury, pulmonary hemorries to numerous organs and body parts could all happen rhage, pulmonary edema, or other organ injury would furat the same time. Most blast injuries are combined injuther speed up the deterioration. ries such as blast-fragment combined injury, burn-blast During the atomic bombings of Japan in the Second combined injury, and radiation-blast combined injury. World War, there were a relatively few number of victims Blast injuries often include different kinds of injuries recorded as severe or worse blast injuries, which might be such as blunt trauma and penetration wound, or contusion because the condition exacerbated rapidly for many such and rupture on the same body, or edema and hemorrhage badly injured victims, resulting in casualty. At the site of simultaneously. In particular, external injuries caused by explosion experiment, it has been observed that some aniexplosion are often accompanied by relatively serious mals initially showed decent conditions and normal infections due to contact of open wounds with disease-­ movement in a short span after the explosion, but soon causing agents. Thus, many medical professionals natuthey would exhibit difficulty in breathing, shock, and then rally associate blast injury victims with substantial death. Dissection shows that these animals were mostly infection. afflicted by serious pulmonary hemorrhage, pulmonary 2. Blast injuries mostly affect specific, target organs. edema, or ruptured organs liver, spleen and other internal Although blast injuries could damage any part or tissue of organs. the body, because of the features of the shock wave itself and of its propagation medium, most blast injuries affect specific organs. Air-containing tissues and organs are the 4.2 Incidence Rate and Fatality Rate primary victims of air blast injury or underwater blast of Blast Injury injury, which is why injuries to the eardrum in the middle ear, the lungs, and gastrointestinal tract are almost With advancements in modern, hi-tech and high-explosive unavoidable. Solid blast injury meanwhile almost always weaponry, and changes in the mode and method of armed affects body parts in direct contact with the solid medium conflict, modern warfare has seen an increasingly abundant of shock wave propagation, or body parts that the propa- use of various kinds of hi-speed and high-explosive weapons gated shock wave act on longitudinally. Thus, identifying (including improvised explosive devices), and the ratios of the target organ damaged in blast injury is of utmost injuries and casualties from blasts and explosions have conimportance. tinued to rise. 3. Light external injury and severe internal injury. This charTake military actions for instance. Between 2001 and 2014, acteristic is the result of the blast wave’s mechanisms and more than 6700 American soldiers in Afghanistan and Iraq modes of action. When a shock wave acts on the body, have been killed by explosions, and over 50,000 wounded. For injury on the surface often appear light, especially inju- the US forces in Iraq between March 2003 and October 2011, ries caused only by overpressure or negative pressure, improvised explosive device (IED) alone killed around 2200 whereby the body surface might not even have any obvi- American soldiers and injuring another 22,000. During the

Introduction and Epidemiology

two military campaigns in Iraq, the number of deaths and casualties among the Iraqi troops and normal citizens are even more difficult to count or even estimate. In the past several decades, there have been many acts of violence perpetrated through explosives around the world, with terrorist bombings being especially devastating. In Israel alone, nearly 20,000 terrorist attacks were perpetrated between September 2000 and December 2003, resulting in approximately 900 casualties, of which suicide bombings have killed 412, accounting for 45.78% of total. Report from the UNESCO Center for Peace shows that between September 11th, 1993 and September 10th, 2009, across the globe there were 624 terrorist bombings that resulted in multiple injuries and deaths, with casualties amounting to a total of 26,073 victims (an average of 42 killed in each attack). The September 11th attacks in 2001 were a watershed moment, with 68 major terrorist bombings (including 9/11 itself) having been committed in the previous 8 years, resulting in the deaths of 3921 persons; meanwhile 556 major terrorist bombings took place in the next 8 years, killing a total of 22,152 persons, with the number of occurrences and casualties being respectively 8.2 times and 5.7 times more than the first 8 years. Clearly, terrorist attacks around the world have been on the rise, and their destructiveness to the worldwide community is only getting worse. At present, there is not yet a relatively uniform database about bombing-related injuries anywhere in the world. In addition, due to the difficulty in gathering data about explosion-­related injuries in warfare, there is still no report or analysis, at least with a relatively comprehensive scope, on worldwide data about the epidemiology of blast injuries. Most blast injury data available originate from the analysis of data of individual explosions, or data from regional databases or research centers such as the US-based Terrorism Research Center and the Global Terrorism Database. Therefore, no one has an accurate idea about the overall incidence rate and fatality rate of explosion-related blast injuries, and we can only make estimates through investigations and data analysis. 1. Blast injury incidence rate: At present, the atomic bombings of Hiroshima and Nagasaki in 1945 by the USA remain the only use of nuclear weapons in warfare, and some of the earliest statistics and data for analysis of relatively detailed extent also came from these atomic bombings. Post-war info on injury and casualty shows that among the moderately and severely wounded, 36.6% were blast injuries, 60% of early casualties in Hiroshima died from injuries due to blast wave, nearly 70% of the wounded (70% for Hiroshima, 64.3% for Nagasaki) that have survived after 20 days of the bombing were afflicted with combined injury that included blast injury. These wounded obviously suffered from blast injuries coupled

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with some other injuries (e.g., burns, radiation). Due to the limited understanding about and diagnostic capacity for blast injury at the time, it is possible that some others wounded by blast injuries were not tallied. Thus, conservative estimate of blast injury incidence rate for the atomic bombings should be above 70%. In the modernization of weaponry, development in explosive weapon is one of the fastest and most obvious. From simple artillery shells, bombs, mines and cluster bombs, to high-explosive squash head (HESH) projectiles, shaped charges and weapons based on augmented shock waves (e.g., fuel-air explosives), even large atomic bombs and hydrogen bombs, the destruction to equipment and structures and fatality to personnel caused by the blast wave of these weapons are increasingly terrifying. In other words, shock wave is destined to be one of the most important and dangerous cause of injury and death in armed conflicts in the future, whether nuclear or conventional. The USA deployed thermobaric weapon (fuel-air explosives) for the first time during the Vietnam War, and report of data analysis about 101 cases of wounded personnel shows that blast injury incidence rate was 50.4%. Another report indicates that blast injury incidence rate during the First Chechen War in Russia was 30%. When tallying the 1303 cases of patients severely wounded by explosion treated at the former Yugoslav Academy of Military Medical Sciences, it was discovered that blast injury incidence rate was 51.0%. In skirmishes along the border in southwestern China in the 1980s, among a group of 166 persons injured by artillery and mines, blast injury incidence rate was 22.3%. In a research about a certain model of fuel-air explosive carried out by the author’s organization, it was discovered that of the animal deaths caused by said model of fuel-air explosive, the incidence rate of blast injury was a whopping 100%, while that for severely injured animals exceeded 90%. Various types of bombs and improvised explosive devices have become the weapon of choice in terrorist attacks, and blast injuries from these explosives constitute the main cause of injury and death in victims. Analysis of statistics of 647 wounded terrorist attack victims tallied after their arrival at hospital shows that blast injury incidence rate was 29.8%. Analysis of a group of 3357 victims in another terrorist bombing points out that of those that died on-site, blast lung injury alone accounted for 47.0%. In terms of distribution of body parts injured by blast wave, figures from different reports vary. In general, among blast wave survivors, about 10% have injured eyes, 9–47% have damaged auditory apparatus, 3–14% have obvious blast injury to the lungs, while only 0.3– 0.6% suffered from blast injury in the gastrointestinal tract.

12

Clinically speaking, although incidence rate of abdominal injury from blast wave is not very high, the fatality rate from such injury is relatively high. Analysis of 61 articles and papers between 1966 and 2009 shows that average incidence rate of abdominal blast injury was 3.0% (lowest was 1.3%, highest was 33.0%). Primary blast injury incidence rates in open space and enclosed space are respectively 5.6% and 6.7%. 2. Blast injury fatality rate: Compared with other types of injury, blast injuries are characterized by more complications and more severe injuries, as well as a higher fatality rate. In most cases, death rates of blunt trauma or penetration wound exhibit a classic three-phase distribution, while that of blast injury is characterized by a two-phase distribution, namely a relatively higher rate of instantaneous death, and relatively lower fatality rate later on. Instantaneous death rate is contingent on a myriad of influential factors such as intensity of explosion equivalent, distance from center of explosion, potential number of victims, structural collapse of buildings, and whether environment is open or enclosed. When other conditions are the same, structural collapse of buildings and fortifications, and whether environment is open or enclosed, are relatively more influential on blast injury severity and fatality rate. When buildings and fortifications collapse due to an explosion, death rate of blast injury significantly rises. For example, analysis of blast injury data about 29 groups of explosion victims shows that instantaneous death rate is as high as 25% when there is structural collapse. In addition, explosions in enclosed spaces would lead to a larger number of and more severe primary blast injuries, along with a significant increase in instantaneous death rate. Research report shows that in explosions that occurred in enclosed spaces, death rate fluctuates between 8.3% and 15.8%, whereas fatality rate in open space explosions is merely 2.8–4%. Other experiment and research outcomes also demonstrate that with the same explosion equivalent and same density of animal distribution, primary blast injury incidence rate would reach as high as 78% and death rate 49% in enclosed space. Meanwhile, in open space, primary blast injury incidence rate drops to 34% and death rate merely 7.8%. At the explosion site, victims with light or moderate primary blast injuries usually appear similar to those unwounded persons due to the absence of external injuries, but it is extremely difficult to diagnose and identify any damage to internal organs on-site. In addition, the fatality rate among victims with light or moderate primary blast injuries is very low, which drags down the death rate of blast injuries and can’t truly reflect the

Z. Wang et al.

severity of blast injuries. Therefore, some researchers use death rate from critical injury to reflect the seriousness of blast injury of an explosion and rescue performance level. In most cases, critical blast injury may be categorized as requiring immediate surgery, ICU care, or endotracheal intubation due to acute problems in windpipe, breathing, circulatory system, or nervous system. Death rates of critical blast injury as seen in documents and reports range from 9% to 22%.

5 Principles for Treatment of Blast Injury In order to promptly and effectively perform emergency rescue, diagnosis, evacuation and transportation to hospital, and treatment, first and foremost it is necessary to determine injury severity before carrying out corresponding measures.

5.1 Light Blast Injury Such injuries are mainly light cerebral concussion, light pulmonary hemorrhage, general auditory apparatus injury, cuts and scratches on the surface of the body, among others. Usually this category of victims are the most numerous, accounting for roughly half of all blast injury victims. Due to the lack of obvious internal organ damage or body-wide symptoms, this class of injury does not seriously affect victim’s capacity and does not mandate special treatment.

5.2 Moderate Blast Injury Such injuries are mainly relatively serious cerebral concussion, light pulmonary edema, serious auditory apparatus injury, internal organ intraplaque hemorrhage or patchy hemorrhage or hematoma, and large swaths of soft tissue injury, among others. Clinical symptoms are relatively obvious, usually accompanied by body-wide symptoms. Hemoptysis is common 1–3 days after moderate lung injury, auscultation might discover occasional rale and crepitus, and similar symptoms to other injuries for soft tissue injury and single dislocations. Situations for some victims might worsen because of combination of other injuries or inadequate protection during the evacuation process, but in general there won’t be shocks or life-threatening risks. Most victims would eventually recover rather well, and only a small percentage would experience worsened situation due to other injuries.

Introduction and Epidemiology

13

5.3 Severe Blast Injury

5.4 Extremely Severe Blast Injury

Such injuries are mainly cerebral contusion, relatively serious pulmonary edema or hemorrhage, ruptured or perforated internal organs (i.e., liver, spleen, stomach, intestine, and bladder) and bone fracture (i.e., thigh bone, spine, cranial base and multiple fractured ribs), among others. Cerebral contusion might result in unconsciousness and increase in intracranial pressure. Lung injury might lead to dyspnea and hemoptysis, percussion of the chest may produce dull sounds, and auscultation might discover wide areas of moist rale. Ruptured abdominal organs might result in abdominal pain, abdominal wall tension, pain, pressing pain, rebound tenderness, and other peritoneal irritations. Ruptured liver or spleen might result in serious internal bleeding or shock, while gastrointestinal rupture or perforation might lead to diffuse peritonitis. Bone fractures have similar symptoms as other injuries and should be treated as per other injuries.

Such injuries are mainly multiple severe injuries like severe cerebral and spinal cord injury, chest, abdominal and spine injury, ruptured organ, serious pulmonary edema or hemorrhage, ruptured artery, serious crushing injury to soft tissue and amputation, among others. In addition, such victims might also suffer from serious burns or radiation injury. Victims in this category are mostly located near ground zero, and often die within a short period due to excessive injury. Most deaths early on result from serious cerebral and spinal injuries, ruptured organs resulting from serious hemorrhage (hemorrhagic shock) and multiple fractures (fat embolism). Deaths later on are chiefly attributed to perforation peritonitis, bronchopneumonia, septicemia, and other secondary infections. Serious cerebral injuries and multiple internal organ ruptures have clinical symptoms similar to other injuries and should be treated as general injuries. Most of the extremely severely wounded victims die within a day.

Explosion Physics Tong Liu

1 Basic Knowledge About Explosives

it is relatively safe and convenient to use. However, high explosive does explode, it is very destructive to surrounding 1.1 Types of Explosives medium, which is why it is commonly applied in scenarios that require explosion or brisance. Based on the composition, Explosive is a kind of semi-stable substance that exhibits high explosive may be classified as either single-­compound different levels of chemical reaction (release of heat in the explosive, or multi-compound explosive based on a singleform of deflagration, explosion, and detonation) when initi- compound explosive. Some of the more common singleated by external energy. Substances that are merely explosive compound explosives include: trinitrotoluene or TNT but unstable can’t be called explosives, they are only consid- (C7H5N3O6), triamino-trinitrobenzene or TATB (C6H6N6O6), ered some sort of explosive substance. In recent years, the hexanitrostilbene or HNS (C14H6N6O12), Royal Demolition general consensus is to use the term “energetic material” to Explosive or RDX among other names (C3H6N6O6), octodenote materials that exhibit powerful chemical reaction and gen or HMX (C4H8N8O8), tetryl or CE (C7H5N5O8), pengenerate substantial quantity of heat and gas under certain taerythrite tetranitrate or PETN (C5H8N4O12), nitroglycerin conditions. or NG (C3H5N3O9) and nitrocellulose explosives or NC Categorized according to the scope of application and (C12H16N4O18), among others. Common multi-compound based on the reaction initiated, the form of transformation explosives (if categorized based on main constituent exploand explosion, and how explosion is manifested, explosives sive or special additive) include: hexolite (a mixture of TNT may be classified as primer (primary explosive), high explo- and RDX), octol (a mixture of TNT and HMX), ammonal (a sive (secondary explosive), gun propellant (gunpowder, mixture of TNT and ammonium nitrate), aluminized explobooster), and pyrotechnic composition. These substances all sive (a mixture of high-energy single-compound explosive fall within the definition of the term energetic material. and powdered aluminum) and polymer-bonded explosives Primer is highly sensitive in most cases, and striking with (powdered high-energy explosive as main body, mixed with a pin (impact) or spark (fire) can both cause it to explode. additives such as polymeric binder), among others. Since the time between ignition and detonation is extremely Propellants react to heat, but are relatively insensitive to short (10−8 to 10−6 s), its explosion transformation is usually initiation from other forms of external energy. The explosion detonation and primarily functions as a device responsible transformation of propellant is usually stable laminar burnfor initiating the detonation (deflagration) of other explo- ing, and substantial quantity of high-temperature exhausted sives. Several of the most common primers include: mercury gas substances and propulsion forces are created. Propellants fulminate Hg(ONC)2, lead azide Pb(N3)2, trinitroresor- include explosives used for producing gas in barrel-launched cinol C6H(NO2)3O2Pb  ·  H2O, dinitrodiazophenol or DDNP systems, or rocket propellants that generate propulsion in a C6H2(NO2)2N2O and tetracene C2H8N10O, among others. rocket engine. Some common propellants include: gunpowHigh explosive is relatively less sensitive and requires a der, single-base smokeless powder (nitrocellulose powder), primer’s blast wave or high-speed impact from a metallic double-base smokeless powder (nitroglycerine powder) and object (speed ≥1000 m/s) to detonate. The explosion trans- triple-base smokeless powder (Trail Boss powder), among formation of high explosive is usually detonation. Since low-­ others. Common rocket propellants include: liquid rocket energy initiation usually isn’t enough to cause an explosion, propellants (liquid oxygen/liquid hydrogen, liquid oxygen/ kerosene), solid rocket propellants (HTPB, CTPB, etc.), and hybrid solid/liquid propellants (HTPB/liquid oxygen, etc.). T. Liu (*) Southwest University of Science and Technology, Sichuan, China

© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 Z. Wang, J. Jiang (eds.), Explosive Blast Injuries, https://doi.org/10.1007/978-981-19-2856-7_2

15

16

Based on physical form, explosives may be categorized as solid explosive, liquid explosive, or gas explosive. Based on application, explosives may be categorized as military explosive or civil/industrial explosive.

1.2 Characteristics of Explosives The chemical reaction of explosive is a stimulated/initiated reaction (only reacts when needed), and may be categorized as either thermal decomposition, deflagration, or detonation. Thermal decomposition of explosive is similar to normal organic substance. Explosives decompose at an extremely slow rate in room temperature and may be safely stored for an extensive period. However, the deflagration of explosive is unlike the combustion of normal organic substance. Explosives do not need external source of oxygen to burn, and combusts also faster than normal organic substance, the rate of which hinges on environment temperature and pressure. Detonation is a chemical reaction unique to explosives. Detonation is a rapid reaction, and the high temperature and high pressure generated are unrivaled by other forms of chemical reactions. The exothermicity of reaction, the speed of reaction, and the substantial volume of gases generated are the three major characteristics of explosive. (1) Exothermicity of reaction: For most commonly used high explosives, the heat of explosion generated ranges from 3.71 to 7.53 MJ/kg, while temperature during explosion could reach as high as 3000– 5000  °C, and the heat of explosion is symbolic of how an explosive releases its energy and works externally. (2) Speed of reaction: The speed of propagation of detonation could reach several thousand meters per second, and one way to put it is that all the potential energy before the explosion are contained within the explosive, meaning that the released energy density is extremely high. (3) Substantial volume of gases generated: This is equivalent to volume expansion by a thousand times. Before the explosion, these gases are forcefully compressed within a volume about the size of the original explosive at the instant of explosion, which is why the result generated could become high-­pressure, high-temperature gas several hundred thousand times the pressure of the atmosphere. The potential energy in an explosive is instantaneously transformed into mechanical energy of the blast, which is how it releases its energy and works externally in a powerfully destructive manner. Explosives are also characterized by their relative instability and high energy density. Explosives are comprised of oxygen elements such as O and F, and combustible elements like C, H, Si, B, Mg, and Al. The redox reaction between combustible elements and oxygen elements releases heat, and therefore, the performance and explosion process of an explosive are contingent on the proportion of combustible

T. Liu

elements and oxygen elements in the explosive. To demonstrate the proportionate relationship between combustible elements and oxygen elements in an explosive, the concept of oxygen balance was formulated. Oxygen balance refers to the surplus or shortage of oxygen, measured in grams, contained within 1 g of the explosive itself needed to completely oxidize all combustible elements within said explosive. Oxygen coefficient A is used to illustrate the oxygen saturation level of explosive molecules: When A = 1, there is just enough oxygen in the explosive to completely oxidize all combustible elements, this is said to be zero oxygen balance and this type of explosive is called zero oxygen balance explosive. When A > 1, there is more than enough oxygen in the explosive to completely oxidize all combustible elements, this is said to be positive oxygen balance and this type of explosive is called positive oxygen balance explosive. When A  0 can be < 0 adiabatic line also differs. dv and dv 2 proven, showing how the Hugoniot adiabatic line is a concave curve on the plane (P, v), which is why the line is called the Hugoniot curve. For the same medium, the Hugoniot

20

T. Liu P

P D1

S

D2

H

H - Hugoniot curve S - Isentropic line T - Isotherm

2 D1

D

C0

j

a1

a

D2

P0 , V0 a2

P0

a0

O

O

V0

V

curve reflects the total of downstream states (PH, vH) of the shock wave for the corresponding upstream state (P0, v0). Therefore, the Hugoniot curve is not a line of process. Equation (6) should be modified as:

1  PH  P0   vH  v0  2

(13)

In combination with the first law of thermodynamics, dS it can be proven that at point (P0, v0), dv d3 S meanwhile dv 3

>0 0

0

=0,

d2 S dv 2

=0 0

. In the equation, S represents

entropy, indicating that upstream and downstream of the shock wave, the increase in entropy (S) takes place in third order small quantities, and the isentropic state equation (11) may be applied. The isentropic state equation (11) mirrors the course of changes in the isentropic state, and this is called the isentropic line.

dP d2 P 0 can also be proven, , dv 2 dv

indicating that the isentropic line on plane (P, v) is also a concave curve. The isentropic line is a process line that reflects changes in the state, and for the same upstream state (P0, v0), different entropy (S) value corresponds to different isentropic line (Fig. 3). 3. Relationship between Hugoniot curve, isentropic line, and isotherm line. Thermodynamics theories prove  dPH dPS   dv  dv   0 ,  0

O v/v0

O

Fig. 3  Rayleigh line, Hugoniot curve, and isentropic line of shock wave

Fig. 2  Velocity line of shock wave

H  P,v   eH  e0 

1

 d 2 PH d 2 PS   2  2  0, dv  0  dv

and

 d 3 PH d 3 PS   3  3   0 at point (P0, v0) on the P − v plane, dv  0  dv

demonstrating that Hugoniot curve and isentropic line from the same initiate state [point (P0, v0)] are tangent at second order. Due to the rise in entropy during the shock’s compression, the A in the corresponding Eq. (11) increases, and when specific volume is the same, the pressure of Hugoniot curve is higher than that of the isentropic line, which is why the Hugoniot curve is located above the isentropic line. Meanwhile, the temperature of the isentropic line increases but that of the isotherm line remains the same. The work along the isentropic line is higher than that of the isotherm line, which is also why the isentropic line is located above the isotherm line. Theoretically speaking, under low pressure conditions, the Hugoniot shock adiabatic line and the isentropic line are very close, and during experimentation, due to some uncertainties in measurement, the Hugoniot shock adiabatic line and the isentropic line were difficult to distinguish under the pressure of 20 GPa as measured in actual experiment (Fig. 4). 4. Relationship between shock wave velocity D and particle velocity downstream of the wave uH. Theoretical analysis and empirical experiment show that shock wave velocity D and particle velocity downstream of the wave uH share a linear relationship under a rather broad spectrum of pressure in many different materials.

D  c0   uH (14)

In the equation, c0 and λ are constants. Table 1 shows the ρ0, c0, and λ values of several common materials. 5. Shock wave front structure. When inferring the shock wave front upstream and downstream physical qualities in the above segment, the viscosity and heat transfer of the medium were ignored, holding that the parameters of states and parameters of motions on the front of the shock wave do not exhibit tiered jumps with slope, and considering the front of the shock wave as a plane with abrupt jump in pressure (Fig. 5). However, shock waves in the

Explosion Physics

21

real world do not behave as such, and parameters of states and parameters of motions on the front of the shock wave do actually exhibit tiered jumps due to the influences of the viscosity (internal friction) and heat transfer of the medium, it’s just that the tiers are extremely steep. Therefore, shock wave fronts in the real world are not perfect planes but possess a narrow transition zone with width d (Fig.  6). Using system of molecular dynamics equations that take into consideration heat transfer and viscosity, in tandem with measurements from actual experimentation, it can be shown that the width d of shock wave front and mean free path γ of molecules upstream of the shock wave exist on the same order of magnitude, demonstrating that the transition zone is very narrow (roughly several γ). The patterns of changes of the various physical qualities upstream and downstream of the shock wave front also differ. Figure 7 reflects the distribution of electron temperature T0, ion temperature TH, and density ρ upstream and downstream of shock wave fronts in the real world.

P

P

PH

P0

O

X

Fig. 5  Pressure jump in ideal shock wave P

H H - Hugoniot curve S - Isentropic line T - Isotherm

d

S

T PH

PO

(P0 , V0 ) O

O

V

X

Fig. 6  Pressure jump in real shock wave

Fig. 4  Hugoniot curve, isentropic line, and isotherm

Table 1  ρ0, c0, and λ values of several common materials Materials Organic glass Al Cu W

ρ0/(g · cm−3) 1.19 2.79 8.466 19.2

c0/(mm · μs−1) 3.16 5.44 3.94 4.049

λ 1.25 1.34 1.47 1.215

Applicable range 104 ba 6–37 22–180 50–270 30–450

T. Liu

22

The front of the shock wave moves at subsonic velocity, and any disturbance behind the shock wave front could catch up to the front and change its power.

T

TH

Before wave

rH T Behind wave

r0 T0 0

X

Fig. 7  Temperature and density distribution of shock wave

The purpose of expounding the structure of shock wave front is to explain that the relationships between physical qualities upstream and downstream of the shock wave front established in the above segment are only applicable to the state of medium upstream and downstream of the shock wave front. To study about the changes in states of medium in the transition zone, it is necessary to also take into full account the influences of the viscosity and heat transfer. 6. Relationship between shock wave front velocity and sound velocity. The velocity of sound is the speed of propagation of micro disturbances. The process of propagation of the velocity of sound is an isentropic process, and in a polytropic gas, sound velocity may be expressed as:

c = kRT

(15)

In the equation, k denotes the polytropic index of the isentropic equation of the polytropic gas. By applying (15) to the relational expression for physical quantities upstream and downstream of shock wave front, it can be demonstrated that relative to undisturbed medium (upstream of wave):

D  u0  c0 (16)

The front of the shock wave moves at supersonic velocity, and the front can catch up to any disturbances propagating ahead. After a shock wave propagates through a medium, the medium obtains the same velocity that moves in the same direction as the propagation of the wave, as in u  −  u0  >  0, and relative to the disturbed medium (downstream of wave):

D  uH  cH (17)

2.2.2 Basics About Detonation Wave 1. The Chapman-Jouguet theory about detonation wave. Results from studies about disastrous gas explosions in coal mines between the end of the nineteenth century and the start of the twentieth century formed the foundation for classical theory of detonation wave fluid dynamics. In order to explain why different ignition conditions in experiment resulted in massive differences in the velocity of the propagation of flame inside channels filled with flammable gas that ranged from several meters per second to several thousand meters per second, Chapman (in 1899) and Jouguet (in 1905) respectively put forth the notion to simplify the detonation process into a one-­ dimensional propagation of strong discontinuity surface that includes chemical reaction, and they referred to this strong discontinuity surface as the detonation wave. The Chapman-Jouguet theory, or the C-J theory, is a fluid dynamics theory about detonation wave that simplifies the detonation wave into a strong discontinuity surface that includes chemical reaction. The C-J theory holds that detonation occurs on an infinitely thin shock wave front at an instant, it is unnecessary to account for chemical reaction process, the laws of conservation are still satisfied upstream and downstream of the wave front, effects of chemical reaction are summarized as an external and added energy, which is reflected in the fluid dynamics energy equation as the thermal effect at the termination state of the reaction. Thus, a detonation wave is a powerful shock wave that has a chemical reaction zone and that propagates as supersonic velocity. (a) Basic relational expression of detonation wave: The C-J theory simplifies the detonation wave into a strong discontinuity surface that includes chemical reaction, and may be understood as a kind of strong shock wave that propagates within the explosive medium. The mass conservation and momentum conservation relationships in physical quantities upstream and downstream of shock wave front are also applicable to detonation wave, but the difference is that the powerful impact and compression generate high temperature and high pressure, which in turn cause chemical changes in the explosive medium. The energy released in chemical reaction maintains and guides the shock wave’s self-sustaining propagation inside the explosive. In terms of the relationship of conservation of energy, it is necessary to consider the heat of reaction in the products of the chemical reaction (detonation products).

Explosion Physics

Similar to the analysis method for the front of shock wave, the origin of coordinates is set on the front of detonation wave, which means using stationary relative coordinates established on the detonation wave front (Fig. 8). With the propagation velocity of detonation wave established as D, in this coordinates system the velocity of incoming detonation wave is D, while the velocity of the outgoing detonation wave is (D − uH), meaning that the physical quantities upstream and downstream of the shock wave front obey the conservation laws of mass, momentum, and energy.

 H  D  uH    0 D

(18)



 H  D  uH   PH  0 D 2  P0

(19)

2

PH rH uH eH

Reaction zone

23

Detonation zone



PH  P0 v0  vH

(21)

Then remove uH in the equation of mass conservation and energy conservation equation to obtain the Rayleigh line: 1

 1 1   D   PH  P0     0  0  H  2 0

(22)

2

Since ρ = 1/v and v is specific volume, the above equation may be rewritten as PH  P0 

v0  vH 2 D v02

(23) 1/ 2

 P  P0  Or rewrittenas : D  v0  H   v0  vH 



(24)

The Rayleigh line of detonation wave does not include energy, and its nature is identical to the Rayleigh line of shock wave. Based on the constancy hypothesis of the detonation process, D is constant, Eq. (23) is expressed as a straight line with slope −

D2 that passes by the points (P0, v0) on the plane v0

(P, v). This is called the detonation wave’s Rayleigh line or velocity equation of the waves. For the same state upstream of the wave (P0, v0), different shock wave velocities D will show straight lines with differ-

D

u0 e0 Unreacted zone

Fig. 8  C-J detonation model

 PH   P  1 1 2   H  D  uH   Q  H  PH   D  uH    0  0 D 2  P0  D   1 2    1 2  

uH   v0  vH 

P0 r0

(20)

ent slopes, as in the higher the shock wave velocity D, the steeper the straight line. When D  =  0 the straight line is horizontal, and when D  =  ∞ the straight line is vertical, as in an instantaneous explosion. When uH and D are removed from Eq. (20), and when the other two conservation conditions are applied, then the Hugoniot adiabatic line of the detonation wave may be obtained: 1 eH  PH ,vH   e0  P0 ,v0    PH  P0   v0  vH   Q (25) 2 In the equation, eH is the specific internal energy of the products downstream of the reaction zone; e0 is the specific internal energy of the explosive; and Q is the heat released by the explosive of a unit mass, equating to the specific heat QPv released by chemical reaction under constant pressure (P  =  P0) and constant volume (v = v0). (b) Hugoniot curve of detonation wave: The Hugoniot adiabatic line of the detonation wave is a concave line on the plane (P, v), and is also known as the Hugoniot curve of the detonation wave. For the same medium, Hugoniot curve of a detonation wave reflects the total of downstream states (PH, vH) under the effects of the detonation wave for the corresponding upstream state (P0, v0). Although the Hugoniot curve of a detonation wave and the Hugoniot curve of a shock wave look similar, they are completely different in terms of physical significance. The Hugoniot curves of shock

24

T. Liu P waves always begin at (P0, v0), but the right side of Eq. (25) includes the release of chemical energy, and I II the Hugoniot curve of a detonation wave expresses the curve of the state of energy increase in the detoS Hugoniot curve nation products. Therefore, it is located above the Hugoniot curve of shock wave, which does not possess chemical reaction, and does not necessarily pass through the point (P0, v0). Since the impact compression provides an activation energy that can initiate a reaction, when the explosive medium in a non-­ C Rayleigh line A reaction layer is impacted and compressed by detoB W nation wave from the layer above, it would be P1 activated from its initiation state at point A (P0, v0) to D IV III point C (P1, v1) in the intermediate state of the shock wave Hugoniot curve, then undergoes chemical reacV tion along the Rayleigh line of the detonation wave. V1 O Heat of reaction is released (heat of explosion Q), and the chemical reaction final state point B (P2, v2) Fig. 10  Hugoniot curve branches of detonation wave of this layer of explosive is the tangent point between the Hugoniot curve of the detonation wave and the Rayleigh line of the detonation wave (Fig. 9). When effects of the detonation wave for the corresponding the chemical reaction of this layer of explosive finupstream state (P0, v0). Upstream states (P0, v0) are ishes, it would activate chemical reaction in the next graphed as vertical line and horizontal line, and they layer of explosive. Therefore, energy released in respectively cross the Hugoniot curve at the points A chemical reaction maintains and guides the shock and B (Fig. 10). Then graph two straight lines from wave’s self-sustaining propagation inside the point (P0, v0) that are tangent to the Hugoniot curve explosive. respectively at the points C and D. Next, let us discuss about the physical significance At point A, with vH  =  v0 and Eq. (24), it can be of the various branches of the Hugoniot curve of detknown that D → ∞ corresponds to specific volume onation wave. In accordance with the previous analydetonation. sis, the Hugoniot curve of a detonation wave reflects At point B, with PH = P0 and Eq. (24), it can be the total of downstream states (PH, vH) under the known that D  =  0 corresponds to specific pressure combustion.

P

Hu

HD

(D)

Hu - Hugoniot curve of undetonated explosives HD - Hugoniot curve of detonation products R - Rayleigh line

(C) R

(B)

O

(E)

(A)

V

Fig. 9  Hugoniot curve of detonation wave. (A) Initiate state of unreacted explosive; (B) state of reaction product of explosion; (C) jump conditions of impact and compression that did not initiate explosive reaction; (D) Hugoniot state of product; and (E) Hugoniot state of product when pressure decreases and volume increases

 dP   dP   PH  P0  At point C, with  dv    dv    v  v  ,  H  S  H 0  R the subscripts “H,” “S,” and “R” respectively denote the Hugoniot curve, isentropic curve, and Rayleigh line. Point C is the point of common tangent between the three lines, and since it corresponds to C-J detonation, it is generally referred to as the C-J detonation point. For area PH > P0, vH  0, u > 0, direction of motion of products is identical to the direction of propagation of detonation wave, and it is a detonation state known as detonation branch. Detonation branch may be sub-­divided into strong detonation branch and weak detonation branch. At the segment CS, PH > PCJ is called strong detonation branch, and at segment CA, PH  >  PCJ is called weak detonation branch.

Explosion Physics

25

 PH  P0   dP  Point D,   corresponds to C-J    dv  H  vH  v0  R combustion point. For area PH  v0 above point B of detonation wave Hugoniot curve, with (21) and (24) it can be known that D > 0, u   vCJ is called strong combustion branch, and at segment DB, vH    P0, vH   D, detonation wave velocity is subsonic compared to the P

H H - Hugoniot curve D - Rayleigh line S - Strong solution W - Weak solution C - C-J point

uS

DS S

DCJ

uj

DW C

uw

medium downstream, and this is called strong detonation. • A “weak” solution W: Given uH + cH  D, the rarefaction wave downstream of the detonation wave will catch up to the wave front, causing unsteady motion in the wave front. Detonation at this phase is unsteady, until uH + cH = D, when a steady state could be maintained downstream of the wave front. Weak detonation is actually a kind of undercompressed detonation state. Due to uH + cH 6 10–50 >50

4. Extremely severe RCBI: Extremely severe radiation injury associated with each degree of blast injury, or severe radiation injury associated with moderate or severe impact injury is extremely severe combined radiationblast injury. Acute radiation injury often has a clear dose–effect relationship, features a gradual increase in exposure dose, a significantly grown mortality, correspondingly shortened survival time, and remarkable differences in clinical manifestations and prognosis. The classification and degree of acute radiation sicknesses are referred to in Table 27.1.

3 Clinical Features and Pathological Basis of Combined Radiation-Blast Injuries The comprehensive reactions between different factors and between different causes and the bodies after the body is subjected to two or more different injury contributors are known as “combined effects” of a combined injury. Combined effects are the main feature of combined injuries different from single injury contributors other than single injury factors plus the resultant effects; different factors, injury contributors, and bodies can interact with each other. Usually, radiation injury often plays a dominant role in RCBI, and the basic pathological changes are mainly the lesions of the radiation injury. But in many cases it shows a “mutual aggravation” effect (1 + 1 > 2), so that the performance of the original single injury is not exactly the same as the effect of a single injury, and the overall injury becomes more complex and more difficult to treat. The effect can also not be aggravated, or even mitigated (1 < 1 + 1 < 2, 1 + 1 < 1, etc.). The clinical features and pathological basis of RCBI injuries can be described in three aspects: overall effect, cell-tissue-organ effect, and combined effects of important pathophysiological processes.

3.1 Overall Effect Overall effect mainly reflects the occurrence and development of the injury, course and stage of the disease, mortality,

average survival time, dose effect, incidence and extent of main signs, and sequelae and outcome. The overall effect of RCBI is characterized by the following:

3.1.1 Severity of Injuries Depends Largely on Radiation Dose The severity of lesion and disease course and the prognostic outcome are bound up with the radiation dose, that is, the injury severity and mortality increase while the survival time contracts with the increasing exposure dose. For example, the animal effect of a nuclear test showed that when comparing the animals with acute intestinal radiation sickness accompanied by severe blast injuries to those with mild blast injuries or without injuries, the difference in survival time and major clinical signs was insignificant, reflecting the fast progression of acute intestinal radiation sickness. 3.1.2 Course of Diseases has Radiation Sickness Characteristics As a rule, there is a staged course of shock (initial phase), pseudo-recovery (latent phase), crisis (critical phase), and convalescence (recovery phase), but the critical phase of RCBI is earlier, longer, and has a shorter latent phase. 3.1.3 Mortality Mortality is a visual concentration of the overall effect and outcome. Severe CRBI often shows a significant increase in mortality. The studies in mice have revealed that the skin wound making up 15% of the body surface area does not lead to death, and the total body irradiation of Co60 γ-ray alone kills 35% of the mice; the combination of the two results in mortality as high as 85%, indicating a noteworthy synergistic exacerbated damage effect. Different wounding sequences however will affect the overall mortality, with the aforementioned pre-injury irradiation model showing an obvious aggravation effect and a remarkable increase in mortality, whereas a study found that the mortality in mice was greatly reduced if skin wound occurred 24 h before irradiation. But it should be noted that the above model of γ-ray combined skin wound is a strain of combined radiation-blast injuries that responds to the combined effects of the shock wave’s secondary effect and the radiation injury. Some investigators have earlier addressed the direct shock wave effects on the lung associated with the injuries caused by different radiation doses are different and found that X-rays at 0.25 Gy, 0.5 Gy, 1.0 Gy, 2.0 Gy, 3.0 Gy, 4.0 Gy, and 5.0 Gy, when associated with the low, medium, and high shock waves, have no significant impact on the body weight and mortality of the animals within 30 days of injury, but the combined radiation-blast injuries of 6.0 Gy irradiation associated with high shock waves show higher animal mortality than that of one-cause injuries, indicating that the overall effect of CRBI

Combined Radiation-Blast Injury

is influenced by the doses of both the radiation injury and the blast wave, i.e., a dose–effect relationship, but the combined effects of mutual aggravation are unapparent as far as mortality is concerned.

3.1.4 Survival Time Survival time reflects a combination of changes and sequelae in the body’s response to injury, including resistance and repair. A certain survival time is necessary to ensure the implementation of life-saving treatment and influenced by both life-saving treatment and the result of the body’s response to life-saving treatment. Therefore, survival time can reflect the combined effects more objectively. The survival time of RCBI is generally shorter than that of the injury from a corresponding radiation dose. 3.1.5 Dose Effect From the comparison of the radiation dose effects of the radiation injury and the combined radiation injury, it can be seen that the radiation dose required to meet the corresponding mortality after the combined radiation injury is lower than that of the radiation injury. The higher the drop, the greater the combined effects. The 30d LD50/30 of the mice exposed to radiation is 9.63 Gy, but reduced to 8.20 Gy after combined burns and to 7.61 Gy after combined trauma, demonstrating a significant accentuation effect of both the combined radiation-burn injury and combined radiation-blast injury. The lowered radiation dose caused by the equivalent radiation injuries associated with other damages is the “equivalent dose” resulting from such injury, which is an important index for studying combined effects.

3.2 Cellular, Tissue, and Organ Effects The combined effects of various tissues and organs after an RCBI vary in performance, most of them showing a mutual aggravation, and the degree of damage is greater than the total of single injuries, some greater than individual injuries, but lesser than the sum of individual injuries. Such differences are related to the response characteristics of specific injury-causing factors in different tissues.

3.2.1 Bone Marrow Bone marrow is an organ sensitive to ionizing radiation, and the inhibitory effect of radiation injury on hematopoietic function is obvious. The hematopoietic disorder is one of the prominent changes of radiation injury and the first problem of the whole disease course, and the destruction and regeneration of hematopoietic tissues can better reflect the severity of radiation injury. When the radiation injury is associated with different injuries, the performance varies at different times according to different doses of exposure and the sever-

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ity of the injury. In radiation-trauma combined injuries, the post-injury peripheral white blood cells and platelet levels are 57% and 33% lower than those in the radiation injury group; the DNA damage in the (lineage negative, lin−) hematopoietic stem cells of the bone marrow is reduced instead (γ-H2AX formation rate is lowered). These studies demonstrate the complex effects on bone marrow hematopoiesis following radiation injuries associated with trauma injuries.

3.2.2 Small Intestine Intestinal mucosa features quick renewal and high radiosensitivity. In radiation injury conditions, cryptic epithelium apoptosis is obvious, and proliferation inhibition is notable, usually resulting in intestinal epithelial necrosis and shedding, villus shortening and bareness, and seriously impaired gut barrier function. Through nuclear tests, the animal effect data show that the dose required for the occurrence of intestinal radiation sickness from a combined injury is smaller than that of the intestinal radiation sickness alone; for instance, the threshold dose for the occurrence of intestinal radiation injury in dogs with radiation injuries is 8.6 Gy and 6.8 Gy with combined injuries (down by 20% or so). Within the range of crossover doses for intestinal and myeloid types, the majority is myeloid in case of radiation diseases alone and intestinal in case of radiation combined injuries. The studies of radiation-trauma combined injuries suggest that the mice with radiation injuries (9.75 Gy γ-ray irradiation) associated with skin wounds (15% of the body surface area) sustained earlier and more severe pyohemia than those with radiation injuries alone at the same dose, indicating increased permeability and reduced barrier function of the small intestine when accompanied by skin wounds. 3.2.3 Lungs Shock waves can cause serious damage to the body, especially to fluid- and gas-containing cavities such as the lungs, heart and blood vessels, digestive tract, and ears, due to their implosion and traction effects, making the lungs an important target organ of the shock wave, the injury-causing factor. Shock waves can lead to remarkable pathological changes such as pulmonary hemorrhage, edema, rupture, bulla, atelectasis, and emphysema. It can be inferred that a combined radiation-blast injury manifests as a more severe lung injury.

3.3 Combined Effects of Important Pathological and Physiological Processes Combined radiation-blast injuries can reflect more intricate combined effects in terms of important pathological and physiological processes such as shock, infection, and tissue repair.

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3.3.1 High Incidence of Shock In the early phase, blast injuries, due to the positive and negative pressure of shock waves, result in pulmonary alveolar rupture and fusion, vascular endothelial damage, and secondary pulmonary edema that affect the gas exchange of the lungs and lead to systemic organ ischemia, hypoxia, and shock; radiation injuries only cause vascular endothelial permeability to increase, and early shock is rarely seen. However, if the radiation injury is associated with the trauma that does not cause shock, shock can occur. Therefore, radiation combined injuries are more likely to complicate shock. The higher the radiation dose, the more serious the injury, the higher the incidence of shock, and the more serious the course of the disease. Most of the shock in radiation combined injuries occurs in the early post-injury period. This is a combination of severe impairments to the neurological, endocrine, circulatory, and metabolic functions of the body following the intense action of combined killing factors, wherein the reduction of effective circulating blood volume (ECBV) often becomes an important link in the development of shock and constitutes the main cause of death in the initial phase. Therefore, in severe cases, the initial phase of injury is actually the shock phase, clinically characterized by mental excitement, agitation, restlessness, soon shifting to inhibition, slow response, indifferent expression, or even blurred consciousness. At the same time, there are corresponding time-phase changes in respiration, pulse, and blood pressure, as well as fast blood concentration, blood volume reduction, and biochemical metabolism changes. This type of shock is often characterized by a prolonged excitation period and a shortened inhibition period, which, if left unattended, may affect the timely diagnosis of shock and lead to delayed treatment. Once the inhibition period is entered, the effect of anti-shock measures is significantly reduced. Experimental studies have shown that there are two types of blood pressure changes when shock occurs due to severe combined injuries: one drops after the excitation period, but rises slowly, and can maintain for a period (which is called the compensation stage). At this point, if there is no timely and effective treatment, the blood pressure will fall again (which is known as the exhaustion stage); the other type has no obvious compensation stage after the excitation period, i.e., it enters the exhaustion stage directly after the excitation period, and the blood pressure keeps falling and never rises again. It is worth pointing out that in a few animals with radiation combined injuries, a steep drop in blood pressure can occur with only a very mild trauma after irradiation, i.e., a small amount of trauma can result in decompensated shock. During wartime, the function of vital organs is generally normal at first in cases of shock from a single injury. However, the function of more than one vital organ may be

Y. Su and T. Wang

impaired at the beginning of the radiation combined injury, and the course becomes more pronounced as the injury progresses. This not only allows for great variation in the clinical changes and types of shock, but also has a marked effect on prognosis. Some experimental studies have shown that the mortality of the animals with radiation combined injuries in the shock phase increases significantly. The shock from combined injuries occurs partly in the critical phase, or after the initial shock phase enters the critical phase again through the latent phase, its process characteristics are different from the initial shock, but similar to the toxic shock. Clinically, it is common that the body temperature and blood pressure drop greatly at the same time; without timely and effective treatment, the consequences are serious, and the mortality is high. The incidence of shock from RCBI injuries is high, and the cause of its exacerbation is unclear. Some researches suggest that it may be related to the following: 1. The important role of the nervous system in the occurrence and development of shock has long been highlighted. Various parts of the nervous system are damaged to varying degrees during the radiation injury, accompanied by the functional disorders of the cerebral cortex, subcortical layer, brainstem, and autonomic nervous system among all levels of tissue systems, which affect the function of the blood pressure regulation center (autonomic nervous system). As a result, the tolerance to strong stimuli such as trauma, injury, and bleeding is significantly reduced after the radiation injury. The sensitivity to blood loss is much higher than in non-irradiated animals, the changes in blood pressure are more pronounced, the incidence of shock increases, leading to more serious consequences. Thus, the dysfunction of the nervous system, resulting in increased sensitivity to trauma, may be one of the causes for the aggravation of shock in case of RCBI. 2. The reduction in effective blood volume is a major component in the development of shock. In the event of CRBI, the conditions leading to a reduction in circulating blood volume (CBV) increase, which may be an additional cause of shock exacerbation. Trauma, bleeding, and body fluid loss (of the wound) can cause hemoconcentration and hypovolemia. Both radiation injury-induced v­ omiting and diarrhea can exacerbate fluid loss, electrolyte disturbances, and hypovolemia, thereby promoting the development of shock. In contrast, radiation injury-­ caused functional and structural changes in the microcirculation, such as microvascular dilatation, extravasated blood, slow-flow, intracellular and intercellular edema, disruption of vascular endothelial barrier function, and increased vascular permeability, lead to increased vascular exudate and vascular bed volume, which in turn reduces the effec-

Combined Radiation-Blast Injury

tive CBV and promotes the development and progression of shock. 3. A variety of toxic substances are produced after trauma due to tissue destruction and protein decomposition, and histamine-like toxic substances also appear in the blood immediately after radiation injuries. Some researches have confirmed that the intensity of gas metabolism is weakened greatly during shock from radiation combined injuries, the glycogen decomposition in the body accelerated, and the lactic acid and inorganic phosphate in the blood piled up, etc., all of which are more obvious than single injury-caused shock. Therefore, the increase in toxic substances may also be among the causes of shock aggravation due to RCBI. 4. The poisoning theory has long been argued in the pathogenesis of shock and radiation sicknesses. Experimental researches show that the susceptibility to bacterial toxins raises largely after radiation injury, and the cause of shock aggravation in the critical phase of RCBI may be related to the effects of bacterial infections and toxins, particularly the effects of Gram-negative bacilli, which cannot be ignored.

3.3.2 High Incidence, Early Onset, and Severity of Infection Infections are prominent in both radiation sicknesses and blast injuries and occur earlier, more frequently, and more severely in combined radiation-blast injuries. Why is infection more prominent in RCBI? The analysis can be made in the following ways: 1. Shock is more common and serious in case of CRBI, lowering the systemic resistance to infection. Shock reduces the ability to resist infection, which may be related to the following reasons: (1) hypoxia occurs during shock, and some important organ tissues become degenerative, or even necrotic, leading to functional disturbance, i.e., fewer globulins are synthesized in the liver. (2) Factors such as the damage to capillary endothelial cells due to the extravasated blood and oxygen deficit of the tissue during shock, the effect of decomposition products of damaged tissues such as histamine on the vessel wall, and disruption of mucopolysaccharides in the vascular wall due to radiation injuries increase the permeability of the blood vessel wall. As a result, the intravascular fluid components, even red blood cells, leak out of the blood vessels, and in the meantime, extravascular bacteria easily invade the blood vessels, causing bacteremia and sepsis. 2. The hematopoietic disorder is more serious in case of CRBI, with far fewer neutrophils and lymphocytes, phagocytosis inhibition of the reticuloendothelial system (RES), weakening of specific and non-specific immune functions, and a more significant decrease of serum bac-

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tericidal activity, whereby both cellular and humoral factors of the body against infection are greatly undermined. 3. In case of RCBI, there are not only endogenous infections from the gut, oral cavity, and urinary tract, but also exogenous infections from the wound surface and wound, greatly increasing the chances of infection. The bacteria on the wound surface grow more (millionfold to ten million times) in combined injuries than trauma injuries. This is because the number and function of white blood cells drop greatly, resulting in significantly less phagocytized and killed bacteria; the bacterial endotoxin itself inhibits cellular defense; bacteria can easily grow and multiply in the necrotic tissue. Copious toxic substances (enzymes) produced by bacteria facilitate the spread of bacteria on the wound surface, such as lecithinase, which destroys the cell membranes of red blood cells and other cells, causing hemolysis and necrocytosis; hyaluronidase dissolves the dermal and subcutaneous connective tissue matrix; collagenase dissolves collagen fibers. The necrotic tissue of the wound surface is mostly filled with a large number of cenobium, sometimes complicated by fungal infections. The wound surface bacteria can further spread along the lymphatic vessels and blood vessels, sometimes multiplying in quantity in the lumen, and filling the lumen like a tube, which not only blocks the blood vessels (in this case, it also promotes the diffusion of thrombus) and causes further tissue necrosis, but also leads to local lymph gland infections and systemic blood-­ borne infections. The common clinical manifestations of RCBI-induced infection are wound infections and focal infections. The incidence of infections (wound surfaces and wounds) increases, and the course is severe in case of CRBI. Despite that the bacterial species causing such infections are similar to those in general war wound infections, it often tends to be reduced in Gram-positive cocci (especially staphylococcus) and increased in Gram-negative bacilli. Quantitative bacterial examination reveals that although the number of bacteria in individual and combined wound surfaces is similar in the early post-injury period, as the disease progresses, the number of bacteria in combined wound surfaces increases significantly compared to single injuries, enhancing the chance for the spread of wound infections and invasion of the bloodstream. Special infections common in war wounds, such as gas gangrene, tetanus, and fungal infections that occur after extensive use of antibiotics and hormonal agents, have not received sufficient attention in the studies of radiation combined injuries. Some preliminary reports indicate a high bacterial multiplication rate and morbidity among the animals infected with Bacillus tetani after radiation combined inju-

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ries, as well as accelerated and more severe clinical signs and disease progression than the animals with single injuries. Clinically, focal infections from CRBI are most often seen on the body surface, and in the mouth, and throat, including skin and mucous membrane erosions and ulcers, bedsore infections, gingivitis, tonsillitis, and Ludwig’s angina. The incidence of lesions in the oral-pharyngeal region grew among the casualties of the nuclear attack in Japan. Most of these focal infections appear before the critical phase and can last for several weeks. Clinically, local pain is perceived, affecting speech and swallowing, and there is foreign body sensation, salivation, and local swelling. Such lesions tend to occur in more concentrated areas of lymphoid tissue, and often at the same site as bleeding. In addition, focal infections can occur in internal organs such as the lungs and intestines. Wound infections and focal infections occur at a time when the cellular and humoral factors of the body that have anti-infective functions are significantly reduced. Bacteria can readily take advantage of these sites to invade the blood circulation and cause bacteremia, sepsis, or sapremia. Post-­ injury blood cultures show that the positive rate of blood cultures in animals with radiation combined injuries improves compared to either single traumas or radiation sicknesses. Also, the time of occurrence is earlier. It usually forms right after the wound infection and increases gradually as the disease progresses. In severe cases, there are two peaks in terms of the positive blood culture rate, the first appearing when the wound infection is grave and the necrotic tissue is separated and shed in large pieces, and the second in the critical phase. The first peak is lower and lasts for a shorter period, whereas the second peak is higher and can last longer. The bacteria commonly found in blood cultures are Staphylococcus albus and S. aureus, streptococci, Escherichia coli, and Gram-negative bacilli grow in quantity. There is a trend towards a relatively higher detection rate of streptococci and Gram-negative bacilli, as well as a higher incidence of mixed infections compared to single injuries. It can be seen that the bacterial spectrum of blood cultures and its variations have similarities with these of wound infections. Through detailed analysis, it can also be found that the bacteria detected in blood cultures are often the predominant bacteria present at the site of injury, with only a few being identical to those from other foci of infection. Therefore, it is generally accepted that most of the bacteria present in the blood in case of radiation combined injuries invade the blood circulation via the site of injury. Clinically, septic symptoms often mark the beginning of the critical phase when the casualty feels depressed, sustain generalized weakness, elevated body temperature, sometimes chills (aversion to cold), along with quickened pulse and accelerated breathing, and exacerbation of the wound infection, followed by metabolic disturbances and other

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toxic symptoms. Experimental researches show that fever starts earlier, fluctuates widely, lasts longer, and presents more severe toxic and other symptoms from radiation combined injuries than from individual injuries. The trend and degree of fever are closely related to the decrease in white blood cell counts, wound surface ulceration and infection, and blood cultures. Another feature of infection induced by radiation combined injuries is the high incidence of hypothermia. In severe cases, a low fever may occur at the outset, or suddenly after a high fever. The presence of hypothermia is indicative of critical illness and is often the result of a severe infection with Gram-negative bacilli.

3.3.3 Delayed Wound Healing In case of CRBI, the tissue repair of post-traumatic wounds, wounds, and fractures is difficult, and healing is delayed due to the effects of radiation damage. The degree of this effect depends mainly on the magnitude of the nuclear radiation dose received. If the radiation injury is mild, the local changes of the combined wound are almost the same as those of a single injury; if the radiation injury reaches a moderate degree or above, the effects are obvious, manifesting as weakened inflammatory response, easy complication of infections, increased bleeding tendency, delayed wound healing, and poorer functional recovery. Clinically, the characteristics of delayed wound healing in case of CRBI can be seen from the changes in wound size, the growth of granulation tissues, and the solidity of porosis speed at the fracture site. In the early post-injury period, the early contraction of the wound not only progresses slowly, but also looks paused, and sometimes the wound is even larger than onset. Later on, granulation growth and contraction, epithelial proliferation, and coverage are all delayed than in case of simple trauma. The porosis at the broken end of the fracture is few and slow, and the formation of bone canals is delayed. In general, the more severe the CRBI, the more prominent these characteristics, especially in the critical phase. The reasons for delayed healing of radiation injuries can be explained in the following aspects: Weakened Inflammatory Response In terms of CRBI, it is common to have a small area of the inflammatory response to the wound or injury and a narrow band of inflammatory response around the wound. If a foreign body is present, the response is slight, the formation of an enclosure around the foreign body is delayed, and local bleeding is common at the site of the foreign body in the critical phase. Even when the shallow foreign body is discharged, a fistula that does not heal easily is often left behind. The body prepares the conditions for tissue regeneration and repair by killing and eliminating bacteria and absorbing and removing necrotic tissues through an inflammatory response. Therefore, inflammation is a prerequisite for repair

Combined Radiation-Blast Injury

and healing after tissue injury: during radiation combined injuries, as the hematopoietic tissue is damaged, the white blood cell count declines, the infiltration of inflammatory cells in the wound surface or wound lessens, and the phagocytic function reduces, making bacteria and necrotic tissues not easily phagocytized and removed. At this point, due to increased vascular permeability, there are often excess local fibrin exudates, but because of neutrophils reduction, the proteolytic enzymes released by them also dwindle in numbers. So, the local fibrin is not easily dissolved, but coagulated with the necrotic tissue, making it difficult to fall off and clear away, which not only affects tissue repair, but also easily leads to bacterial growth, and aggravates the infection. This further hinders tissue repair. Local Infection and Hemorrhage Wartime trauma is mostly contaminated by bacteria, but whether it can develop into infection is related to the characteristics of the trauma, the immunity of human bodies, and the situation of bacterial contamination. The systemic and local changes of CRBI are conducive to the occurrence and development of infections. So, the infection is more prominent in case of CRBI, and especially in the critical phase of radiation sickness. Some researches show that during CRBI, the pyogenic infection process of the wound is aggravated, and it is easy to spread and develop cellulitis, osteomyelitis, and septic fistula. The incidence of surgical wound infections is also higher among CRBI patients, which can not only lead to operation failure, but also induce other complications if not treated effectively and promptly. After skin grafting, the already grown and healed skin grafts can become infected. Partially healed wounds can also reopen due to infection. In the event of radiation combined fractures, the overall condition is worsened, in addition to an increased wound infection rate that affects fracture healing, and poor functional recovery of the injured limb. With regard to bleeding, the injured area bleeds mostly in two periods, namely the early post-injury phase, and around the critical phase. The former occurs as a result of trauma-­ induced tissue damage and vascular rupture. The bleeding often has some of the following CRBI characteristics: first, reduced tolerance to blood loss and therefore a severe impact of bleeding; second, slower absorption of blood seeping from the injured area, which affects wound healing and creates conditions for local infection; third, after initial irrigation and debridement, the incidence of hematoma within the wound is significantly higher than in a single injury due to an increased propensity for wound hemorrhage. When systemic hemorrhage occurs due to hematopoietic failure before the critical phase of the CRBI, the bleeding from the wound and wound surface often happens earlier and is more extensive and severe than the bleeding from the body surface skin and mucous membranes. At first, the tendency

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to bleed from the granulation wound increases, followed by small bleeding spots that soon fuse and expand until the granulation surface is extensively overflowing. At this point, the wound surface infection is also particularly severe. The hemorrhage and infection interact with each other, mutually aggravate, and intertwine with the bleeding spots of the skin around the wound. Then, the wound presents a picture of hemorrhagic necrotic infection, characteristic of a radiation combined injury. If the wound is accompanied by vascular damage and not completely healed, it may then split open and bleed again. The consequences are also more serious because the body's tolerance to blood loss is worse in the critical phase of a radiation combined injury. Bleeding not only causes the loss of blood throughout the body, but also reduces or even cuts off the local blood supply to the trauma and burn and discretizes the tissue. The blood coagulation in the tissue provides conditions for bacterial growth. During the observation of the CRBI wound surface, such a development process is frequently seen: in the pseudo-­ healing (latent) phase, the granulation grows well, and looks red, tender, and healthy; after entering the critical phase, the granulation tissue stops growing and becomes pale and stained, prone to infection and bleeding; when entering the recovery phase, the infection and bleeding are controlled and subside, and the granulation tissue and epithelium grow and close up along with the wound surface. This shows that close prevention and control of infection and hemorrhage are extremely important for the acceleration of wound healing. Inhibition of Histiocyte Regeneration Under the effects of nuclear radiation, the regenerative capacity of local tissue cells in the trauma can be directly inhibited, mainly including the regeneration of epithelial cells, fibroblasts, and vascular endothelial cells after skin and soft tissue injuries, division of these cells, collagen synthesis; osteoblast regeneration, and callus formation in case of fractures. In terms of cutaneous and mucosal wounds, only epidermal cells regenerate and cover the wounds in order to destroy them, stop the growth of granulation tissues and allow them to heal. Therefore, the regeneration of epidermal cells and their functions are extremely important for wound healing. In the process of wound healing, the epidermal cells have functions of division, and proliferation, and migration, and cell division is ongoing throughout the repair process. A basilar membrane is formed when the epidermis and connective tissue come into contact. In case of trauma combined radiation injuries, epidermal cell division and migration can be inhibited or even stopped, thus affecting wound healing. During wound healing, the capillary endothelial cells around and at the base of the wound swell, divide, form bud breaks, migrate, and connect to each other. These connected

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protrusions are initially solid and later gradually hollow out, forming lacunas that allow for blood flow. In case of radiation combined injuries, vascular endothelial cells divide and grow slowly, or stop growing, affecting the formation of granulation tissues. The regeneration of lymphatic vessels is slower than that of blood vessels. Fibroblasts play an important role in wound healing. They can swell, elongate, protrude, move in a linear direction, and divide and proliferate, release mucopolysaccharides when mature, and form collagen fibers. Only with the formation of intact collagen fibers can the tensile strength increase after wound healing. In case of radiation combined injuries, both fibroblast division and collagen synthesis can be inhibited, whereby the growth and maturation of granulation tissues are affected. Sometimes the tensile strength is quite low after wound healing. For example, after researchers exposed guinea pigs to 200 C/kg irradiation and rats to 300 C/kg irradiation, suturing was performed immediately after wounds formed on the back, and general histological observations were made on the 7th and 14th days of injury. It was found that there was no significant difference between the animals with combined injuries and single injuries, but the tensile strength of the wound skin was much lower in the animals with combined injuries than with single injuries. The higher the irradiation dose, the more obvious the reduction in skin tightness, and the longer the duration. In rats irradiated with 700 C/kg γ-rays, the collagenation in the wound skin was seen to be 2–3 days later than the control group. if irradiated at a very high dose, the division of fibroblasts, vascular endothelial cells, and epithelial cells stopped, leading to the cease of the healing process. Medium doses of irradiation can slow down the regeneration of broken tissues, set back porosis, and hold up callus modeling. At higher doses, the callus does not grow, resulting in long-lasting fractures or pseudarthrosis. Nuclear radiation can directly inhibit the activity of osteoblasts, slacken the differentiation of osteoblasts into osteocytes, restrain the activity of alkaline phosphatase, and block the calcification process (calcification requires the participation of alkaline phosphatase). In addition, some researchers irradiated rats with X-rays at 400 C/kg and 800 C/kg and found that porosis after fracture was later than in the control group, and the basophilic mast cells began to increase and were later lower than in the control group until the 3rd week of callus formation. These mast cells are associated with mucopolysaccharide synthesis, which is disturbed after irradiation. This may be related to slowed callus formation. In addition, the disruption of the bone marrow blood circulation will affect the vascularization (organization) of fracture end hematoma and the blood supply in the healing process (the vascular system of bone marrow plays an important role in the nutrition of bone tissue).

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These changes affecting fracture union occur mainly during the critical phase of radiation sickness, and fracture union generally proceeds smoothly after entering the recovery phase. Effects of Radioactive Substances on Wound Surfaces and Wounds During surface bursts and low airbursts, the casualties in the explosion zone, especially the personnel exposed in the downwind near zone (similarly, the depleted uranium aerosols formed by depleted uranium munitions, and radioactive substances in dirty bombs), open traumatic wounds may be contaminated by radioactive substances, resulting in two adverse effects, namely delayed local healing and absorption into human bodies. Radioactive substances are adsorbed by local tissues when falling on the wound surface or wound, more so if there is an exudate. The local effects depend mainly on factors such as the intensity of contamination, the time the contaminant remains, and the type of wound. Radioactive contamination locally causes degeneration and progressive necrosis of epithelial cells, connective tissue cells, and muscle cells, and inhibits cell regeneration, especially in the epidermis where the germinal layer cells and fibroblasts are more susceptible to damage. This causes local accumulation of necrotic tissues, delays the process of tissue regeneration, and predisposes to hemorrhage and infection (septic and anaerobic infections). In experiments with domestic rabbits, the incidence of skin-muscle wound suppuration was 11.5%, 22.2% after contamination with radioactive iodine and calcium, and up to 53.8% if the contamination was followed by X-ray exposure. The absorption of radioactive substances through wound surfaces and wounds depends primarily on the physicochemical properties of these substances (e.g., solubility) and the nature of local injuries. Many radioactive substances are almost completely insoluble in the exudate of wounds, such as oxides of heavy metals, peroxides and carbonates, sulfates, and phosphates, whereas hydrochloric acids and nitrates are readily soluble and therefore highly absorbed. Nuclear explosion fallout has a solubility of 10–20, so there will likely be some absorption into the body through blood vessels and lymphatic vessels, and more than a certain amount will be harmful to the organism. It is generally believed that intact skin does not absorb radioactive ­substances or absorbs less; burn wound surfaces with unbroken eschars absorb less, while the wounds with abundant blood circulation and those with broken muscles absorb more. As regards exact data, the laboratory findings vary from a few percent to several tens of percent. From a therapeutic point of view, it is important to treat contaminated wound surfaces and wounds as early and quickly as possible. It has been reported that 20% of the radioactive materials can

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be removed from the surface of the wound by cleansing within 1 h contamination, 10% within 2 h, and only 3–5% later; 30–70% by surgical methods like debridement within 2 h contamination, but surgical and other decontamination approaches are generally not effective after 6 h contamination. Other Factors Neuroendocrine regulation disorders, metabolic disorders, especially systemic changes like protein metabolism disorders, and anemia that appears early in the course of radiation combined injuries are also bound to have adverse effects on local wound healing. The influence of radiation injuries on wound healing mainly occurs in the critical phase. Therefore, efforts should be made to heal or minimize the wound surface or wound as much as possible before the arrival of the critical phase based on systemic treatment, and firm measures should be taken to prevent and control local infections and hemorrhage in the critical phase, not only making for local wound healing, but also creating good conditions for the overall treatment of combined injuries

3.3.4 Aggravation of Hematopoietic Disorder The hematopoietic disorder is a prominent change of radiation injury. The severity of radiation injury is well reflected by the destruction and regeneration of hematopoietic tissues. In acute blast injuries, there is always a decrease in peripheral white blood cells (PWBC), but less severe injuries usually show an elevated leukocyte count response. When the radiation injury is complicated by blast injury, it can accelerate and exacerbate the destruction of hematopoietic tissues and lower and set back their regeneration. The aggravation effect of hematopoietic dysfunction from combined radiation-blast injuries is related to the following aspects: 1. Infections become increasingly serious due to combined injuries, and heavy infections can exacerbate the damage to pre-existing hematopoietic tissues. It is often seen that the white blood cell count (WBC) is falling, but after infection with fever, it drops sharply as the body temperature rises. Sometimes, the hematopoietic function has begun to recover, and the PWBC gradually rises, even by several thousand, indicating that the bone marrow has regenerated. But after the complication of sepsis, the WBC drops sharply; the autopsy reveals that the bone marrow is empty again, that is, the original regenerated bone marrow has been subject to another severe damage. 2. The decline in WBC will also be accelerated by the massive depletion of PWBC from traumatic wounds when the hematopoietic tissue is no longer able to produce and release leukocytes as usual

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3. Toxic substances produced as a result of tissue necrosis due to the combined severe blast injuries may directly inhibit and damage hematopoietic tissues. 4. On the basis of suppressing hematopoiesis, the hemorrhage from the wound, grown blood exudation and hemolysis due to increased vascular permeability, lysis of red blood cells by lecithase and hemolysin infected with bacteria can accelerate the onset of anemia, but in the early stages, the hemolysis, together with congestion and hemorrhage in the GI tract, can result in further destruction and loss of red blood cells. The lesions of the hematopoietic tissue change accordingly in terms of peripheral hematology. The lesions of the hematopoietic tissue change accordingly in terms of peripheral hematology: Changes in Leukocytes Regarding severe radiation combined injuries, the changes in leukocytes are typical and show obvious time-phase alteration. There is mostly a clear rising peak after injury, which can also be seen in a corresponding single injury. Then, it is followed by a rapid drop in the leukocyte count, which reaches the minimum value earlier than in individual radiation sickness, with a low and long-lasting minimum level. In terms of leukocyte classification, the most drastic change happens in neutrophils, followed by lymphocytes. The trends and characteristics of the leukocyte changes in the total count and classification vary according to different types of combined injuries, which can be used as a reference for differential diagnosis. The response of the leukocyte count in the presence of radiation combined injuries is subject to multiple factors. It is generally accepted that, when complicated by radiation injuries, the higher the radiation dose, the more rapid the leukocyte count decrease; the lower the level, the slower the rebound. Some experiments have also demonstrated that the magnitude of the blast wave overpressure also has an appreciable impact on the change of leukocytes when it is complicated by blast injuries. The studies on the radiation sickness and combined radiation-blast injury to dogs have found that the decrease in leukocytes is more pronounced and the animals died earlier after total body irradiation of 3.4 Gy with blast injuries; the leukocyte counts fell quickly and remained at a lower level (less than 40% of normal leukocyte level) for a longer period in animals subject to 1.5 Gy whole-body irradiation and high overpressure (>0.5 kg/cm2), whereas the leukocytes of the animals subject to low overpressure (0.1 × 1012/L, or if peritoneal lavage fluid contains bile, vegetable fiber, feces, or other substances. This test could reach positive rate of more than 97%. (4) Color Doppler ultrasonography: Ultrasonography is convenient, non-invasive and could be done by the bed. It provides real-time and dynamic inspections of changes in organs in the abdominal cavity and offers rather important values in the diagnosis for injuries of solid organs such as the spleen, liver, kidney, and pancreas, as well as retroperitoneal hematoma and abdominal fluid accumulation. (5) Laboratory tests: Serum glutamic pyruvic transaminase (SGPT) activity would raise if liver is ruptured, with figures to surge by four to five folds in 12 h after injury compared with numbers before injury. When the pancreas is injured, elevation of serum amylase and lipase may be observed.

3 Treatment Principles for Plateau Blast Injury After a blast injury occurred, injuries that are life-threatening should be treated firstly, such as ensuring unobstructed airway, maintaining effective circulation, and controlling obvious bleeding. The emergency treatment principle is identical to the first-aid for general traumas. Based on the characteristics of plateau blast injury, and in accordance with the key factors in the treatment of plateau blast injury and composite injury, pay attention to the lungs because these are the main target organs in blast injury. The lungs are extremely vulnerable to the almost incurable hypoxemia, and severely lung injury is one of the primary reasons for death in the early stage. Therefore, emphasizing the treatment and protection of lung injury are especially important. The number one priority in the treatment of plateau blast injury is to maintain respiratory and circulatory function, including keeping airway unobstructed, providing oxygen, and when necessary adopt measures such as tracheotomy and mechanical ventilator-­assisted breathing, as well as blood transfusion, rehydration, and anti-shock treatment.

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3.1 Cautions in Treating Plateau Blast Injury The principles for first-aid, ventilation, hemostasis, wound dressing, shock prevention, and other steps for plateau blast injury are the same as other battlefield traumas. Given the characteristics of plateau blast injury, particular attention should be paid to the following few areas: 1. Swiftly remove victim from the explosion environment, collapsed fortification or building, so that the person is relocated away from the source of explosion. Erratic movement after infliction of blast injury could worsen the situation. If the victim shows respiratory distress, it would be necessary to remove him or her from the battlefield via stretcher. Anyone suspected of suffering from blast lung injury should lie down and rest to lessen stress on the heart and lungs. 2. For victims with breathing difficulties, check to see if his or her mouth and nose are obstructed with foreign obstacles like sand or blood clot and clear out these substances if there are any. For victims exhibiting respiratory distress or coughing up large volume of blood, quickly insert nasopharyngeal airway or oropharyngeal airway, and if necessary, perform tracheal intubation and suck out secretion in order to keep the airway unobstructed. 3. For unconscious victims, pull his or her tongue out from the mouth and tilt head sideway to keep the airway unobstructed. For those with bloody fluid flowing out from nose or mouth, or those with extremely serious breathing difficulty, perform tracheal intubation or tracheotomy, and suck out any liquid inside to keep the airway unobstructed. For victims with breathing difficulty or those with gradually lowering partial oxygen pressure, provide oxygen via nasal cannula or face mask. Use oxygen bubbled through a 50% alcohol solution, administer aminophylline to stop bronchospasm, and when necessary employ mechanical ventilation. For victims showing ARDS during the acute stage, if regular treatments cannot improve his or her condition, apply extracorporeal membrane oxygenation (ECMO). 4. For victims with air embolism, administer pressurized gas at six bar (with oxygen no higher than 2.5 bar) sustained for 2 h, then continue for 36 h at gradually decreasing pressure. 5. When performing resuscitation on the plateau, the lungs cannot bear much liquid, and since the lungs are the chief target organs most sensitive to blast injury, if there is a need to perform resuscitation due to blast composite injury, make appropriate adjustments to the volume and rate of fluid transfusion, prioritize capsules over crystals whenever possible, and monitor hemodynamics carefully,

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otherwise pulmonary edema and other dire consequences could occur extremely easily. 6. Sedation and analgesia of patient after injury; keep the patient’s body temperature normal, prevent pulmonary edema and protect cardiac function; dehydrate, ensure diuresis and strengthen the heart; provide blood and fluid transfusion; and prevent DIC and electrolyte imbalance. Administration of large doses of corticosteroid hormone during the early stage is relatively conducive to defending against interstitial pulmonary edema. 7. Carefully inspect the severity of external wounds and visceral injuries, assess the patient’s conditions, rapidly categorize patient injuries, and strictly uphold the treatment principle of dealing with severe injuries before minor injuries. Carry out systematic inspection prior to surgery, and pay particular attention to injuries of internal organs, especially hollow organs such as the lungs and gastrointestinal tracts. At the same time, do not forget inspections of solid organs like the spleen, liver, kidneys, and bladder to avoid missed diagnosis. 8. After patient condition is stabilized, relocate to a low-­ altitude area for corresponding treatment as soon as possible. If helicopter is used for evacuation, try to lower flight elevation whenever possible to prevent the occurrence of air embolism.

3.2 Treatment Methods for Plateau Blast Lung Injury 3.2.1 Life Support and Regular Symptomatic Treatment Ensure unobstructed airway and normal circulation and provide blood transfusion, rehydration, and anti-shock treatment. For those with hemopneumothorax, perform closed thoracic drainage as soon as possible. Administer hemostatic drugs to reduce bleeding. Administer sufficient amount of antibiotics to prevent pulmonary infections and lower the chances of complications in the lungs. 3.2.2 Mechanical Ventilation The key to treating blast lung injury is to maintain respiratory and circulatory functions, including keeping airway unobstructed, providing oxygen, and when necessary adopt measures such as tracheotomy and mechanical ventilator-­ assisted breathing. When blast lung injury deteriorates into a severe composite injury, the body would initiate strong stress responses, which would easily lead to stress response disorder, including stress ulcer of digestive tract, intestinal infection, hypermetabolism, etc. These could consequently lead to serious pathological harms to organs throughout the body, further complicating patient condition and heightening the difficulty of treatment. Therefore, during the course of treat-

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ing blast lung injury coupled with severe burns, personalized treatment methods should be adopted in accordance with the severity of patient condition. After diagnosis is confirmed, perform tracheotomy right away, establish artificial air circulation and keep airway unobstructed. When airway is blocked by substance like phlegm or blood clot, carry out fibrobronchoscopy immediately, clear out obstruction, and rinse the airway clean. Perform electric coagulation for spots of bleeding in the airway. Take active measures to control infection and prevent the occurrence of pulmonary infection. If breathing difficulty does not improve and hypoxemia continues, apply mechanical ventilator-assisted breathing using the high frequency ventilation or positive end pressure ventilation mode, with the goal of reaching PaO2 > 80 mmHg and SaO2 > 90%. It is suggested to provide ultrasonic atomization inhalation to humidify the airway, promote discharge of phlegm and other liquids, remove stimuli caused by foreign substances, and lessen the effects of various types of inflammatory medium. The utilization of mechanical ventilator should abide by the principle of “early usage, early conclusion, customized application.” When the patient’s spontaneous ventilation ability has returned, he or she can cough powerfully, and arterial blood gas analysis monitoring shows normal and stable status, consider removing mechanical ventilator as soon as possible to prevent the person from reliance on the breathing machine.

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encouraging. Said technique can ensure oxygenation while allowing lung tissues to sufficiently “rest,” thereby buying time for the cardiac and respiratory functions to recover and minimizing damage to the lungs arising from mechanical ventilation. At present, the new technique of ECMO is primarily used for treating acute reversible heart failure, respiratory failure, or cardiopulmonary failure and is praised for its features such as biocompatibility, little damage caused to blood, and prolonged application duration (average of 4–8 days). The underlying mechanism is the use of bio membrane to provide ventilation in lieu of the human lungs. By draining the venous blood of the patient, the artificial lungs can remove CO2 and oxygenate blood, then a specially powered pump returns the blood inside the body through vein or artery, while the lungs “rest” during this process. ECMO also provides the necessary hemodynamics support, so that the heart too can “rest” and increase the chances of lungs and/or heart recovery from reversible pathogenic changes. At present, the new technique of ECMO is primarily used for treating acute reversible heart failure, respiratory failure, or cardiopulmonary failure. Research studies already prove that the adoption of ECMO can provide sufficient oxygenation while imposing no restrictions on ventilation volume of the lungs. Therefore, it is also a great tool for dealing with severe ARDS. ECMO can ensure oxygenation while allowing lung tissues to sufficiently “rest,” while minimizing damage to the lungs arising 3.2.3 Extracorporeal Membrane Oxygenation from mechanical ventilation as well as other complications (ECMO) associated with mechanical ventilation. Quite a number of For normal impulse injury to the lungs, mechanical ventilator-­ clinical studies have proved that the application of ECMO in assisted breathing is the primary method to help breathing treating ARDS patients yields a significantly higher survival and ensure oxygen supply to the body, including treatment rate than subjects in conventional treatment groups using using techniques such as high frequency oscillatory ventila- methods like mechanical ventilation. Therefore, if the new tion (HFOV). However, studies in recent years have revealed technique of ECMO can be applied to treat blast lung injury that although lung-protective ventilation and other treatment victims, especially those suffering from serious blast lung measures have been applied, death rate of victims with injuries, there exists the possibility of helping these seriously ARDS complications still exceeds 40%. In addition, lung-­ injured persons in surviving the most critical phase, winning protective ventilation has its irreparable shortcomings, such precious moments essential to pulmonary function recovery, as rise in CO2 and drop in PH, and the inability to ensure thereby lowering fatality rate and markedly raising blast sufficient oxygenation. In particular, regular treatment meth- injury survival rate. ods seem inadequate to address refractory hypoxemia in cases of severe pulmonary hemorrhage or even when 3.2.4 Hyperbaric Oxygen Therapy mechanical ventilator-assisted breathing is adopted. Fatality Outcomes of experiment by Shan Youan et al. indicate that rate is still rather high when one purely depends on conven- hyperbaric oxygen therapy offers a certain degree of curative tional technologies, in particular the onset of refractory effect for severe blast lung injuries in dogs. Hyperbaric oxyhypoxemia renders regular mechanical ventilator-assisted gen therapy was shown to reduce the fatality rate in the breathing treatment almost fruitless. experimental group, with the control group posting a 40% In recent years, foreign scholars such as Chairperson death rate 24 h after injury, while the death rate of the hyperStein of the Israeli Trauma Association and Mackenzie of the baric oxygen therapy group was only 12.5%. Hyperbaric Queen Elizabeth University and Royal Hospital of the UK oxygen therapy clearly improved arterial blood gas and proposed the utilization of the latest technologies such as hemodynamics indicators in some dogs, raised PaO2 levels, extracorporeal membrane oxygenation (ECMO) to treat vic- and significantly lowered the pulmonary index of the anitims of severe blast lung injury, and the results have been mals within the 24 h-period, offering a certain extent of cura-

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tive effect for animals suffering from severe blast lung injuries.

3.2.5 Anisodamine and dexamethasone Outcomes of experiment by Deng Zhilong et al. indicate that administration of hyperbaric oxygen therapy, anisodamine and dexamethasone, and administration of hyperbaric oxygen therapy and joint usage of anisodamine and dexamethasone, both showed relatively ideal curative effects on patients with plateau blast injury compared to subjects in group that did not receive any treatment. The treated subjects exhibited obvious improvement in arterial blood gas, and death rates dropped by 16.7–26.4%. Of the two treated groups, the one with administration of hyperbaric oxygen therapy and joint usage of anisodamine and dexamethasone produced even better treatment results, providing a certain amount of reference for dealing with plateau blast injuries. The mechanism behind the curative effect of hyperbaric oxygen therapy, anisodamine and dexamethasone on plateau blast injuries might be attributed to the following factors: (1) Hyperbaric oxygen can increase plasma physical oxygen capacity and raise partial pressure of oxygen, in turn ameliorating the lung’s ventilation function and oxygen supply to tissues. At the same time, hyperbaric oxygen therapy can address air embolism arising from severe lung injury and lessen the danger when air embolism does occur. (2) Anisodamine can allay spasms in blood vessels and small airways, contributing to micro circulation and ventilation functions. (3) Dexamethasone has anti-inflammatory, anti-allergy, anti-free radical properties and can stabilize lysosomes, thereby augmenting the body’s stress functions. Research revealed that hyperbaric oxygen therapy, and the use of hyperbaric oxygen therapy in conjunction with anisodamine and dexamethasone, can clearly reduce pulmonary hemorrhage and pulmonary edema compared with the control group. This research result provides beneficial morphological basis for improving arterial blood gas and reducing fatality rate.

3.3 Treatment of Plateau Blast Injury to Abdomen The principles of treating victims of blast injury to the abdomen are identical to treating regular abdominal organ injuries, with top priority being dealing with the most life-threatening problems, such as ensuring airway stays unobstructed and stopping bleeding. Then swiftly carry out a full-body check to determine whether or not abdominal organ injuries exist, or if there are composite injuries involving other body parts. Patients should lie down and rest, refrain from eating or drinking, and reduce pressure on stomach and intestines. Steps need to be taken to minimize stress on the gastrointestinal tract and carefully observe the color,

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form, and property of drainage fluid. Insert catheter, record urine volume, observe urine color, and conduct urine analysis when necessary. For patients that might be suffering from visceral injury, draw blood and conduct cross-matching test right away. For patients that have lost a lot of blood or exhibiting hemorrhagic shock symptoms, perform blood transfusion and rehydration treatment in a timely manner, and take other active steps to ameliorate shocks. For those in critical conditions, exploratory laparotomy should be carried out while administering anti-shock treatments. Broad-spectrum antibiotics should be applied in the early stage to actively defend against infection. Active measures should be taken to prevent bleeding or stress ulcer of digestive tract, and sufficient amount of parenteral nutrition should be provided. For patients confirmed with or suspected of visceral injury, undertake exploratory laparotomy, and restore or remove injured organs, then clear out blood or effusion accumulated in the abdominal cavity or substances in the intestines, so as to prevent severe complications such as abdominal cavity infection.

3.4 Initial Surgical Treatment for Extremity Blast Injuries on Plateau in Peacetime The higher the elevation a particular part of the Earth’s surface, the more solar radiation said part receives. Given thin air, less water vapor, and dust, longer daytime, plateaus receive more radiation than plains. Lhasa, for instance, receives 1.68 times more radiation than plains at the same latitude. Ultraviolet ray constitutes a part of radiation from the sun, and the higher the altitude, the stronger the UV ray. For every hundred meter increased in elevation, UV ray intensity increases by 3–4%. UV radiation at Lhasa is 1.7 times more powerful than that measured at the eastern plain in China (Suzhou), and this increase no doubt intensifies the effects of sunburn. The powerful sunshine and UV radiation on plateaus are important in suppressing the survival and reproduction of bacteria in the environment. Therefore, infection of wounds in a blast injury suffered at such high-­ elevation areas is less severe than those at plains. At the same time, since blast injuries during peacetime usually occur at a single instance, medical care institutions have enough time and human resources to perform relatively thorough debridement, and there are sufficient anti-bacterial medicines sensitive enough to prevent infections. Therefore, if conditions permit, treatment of plateau blast injuries during peacetime should perform primary debridement and suture and primary internal fixation of fractures (Figs.  29.6 and 29.7). Our experimental research and clinical practice both prove this point. Lei Mingquan et al. used local Tibetan dogs to carry out bullet wound experimental research and performed primary

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Fig. 6  Primary debridement and suture and primary internal fixation of fractures in high-altitude explosion blast injuries (image by Yin Zuoming)

ing regular firearm injuries on plateau, and they recorded a grade I healing rate of 97.2%. Since 1991, Yin Zuoming has performed primary internal fixation of fractures for patients of regular gunshot bone fractures on plateau, and all cases reached clinical healing status. In 2002, Yin Zuoming used small pigs to conduct experiments, proving that treatment of plateau firearm injuries during peacetime yields best results when primary debridement and suture and primary internal fixation of fractures are performed within 6–36 h after injury, with wounds showing no obvious redness, swelling or infection, and no shock, multi-organ failure, or other symptoms in the patient. It was noted that during the process it is necessary to thoroughly clean the wound tract, and since the contusion area and concussion zone of firearm injuries on plateau are wider than those on plains, the wound area to be cleaned would also be bigger. It is also suggested to remove inactivated necrotic tissue while minimize harms to the periosteum, retain residual bone tissue, and perform simple internal fixation. In addition, drainage has to be unobstructed and sustained for an adequate period, and full-body support should be provided after the procedure, along with administration of sufficient amount of effective antibiotics. In 2007, Yin Zuoming performed primary debridement and suture to 47 wounds on 11 victims of blast injuries during peacetime, and no infection occurred. However, three wounds ripped because they were not adequately drained. The wounds had grade I healing rate of 91.5%, and the patients were hospitalized an average of 18.6 days. It is worth mentioning that the aforesaid research was completed on plateau during peacetime, and the derived principles are only applicable to plateau blast injuries during peacetime and are currently not yet suitable for use during wartime.

Fig. 7  X-ray scan primary debridement and suture and primary internal fixation of fractures in high-altitude explosion blast injuries (image by Yin Zuoming)

4 Features of Plateau Burn-Blast Combined Injury

debridement and suture, and primary internal fixation of fractures 12, 24, and 36 h after injury. At the same time, bacterial counts were measured, wound infection conditions were observed, and antibiotics were administered for 5 days as per normal protocols. Primary wound healing was achieved for the 14 dogs, stitches were removed after half a month, and X-ray inspection 2 months later reviewed a moderate amount of bone callus growth, while signs of osteomyelitis were not discovered in any subject. This indicates that if infection was not serious within 12–36 h, anti-bacterial procedures were strictly adopted and wounds were thoroughly cleaned, primary internal fixation of gunshot fractures to the limbs may be conducted. Lei Mingquan et  al. undertook primary debridement and suture 24 h after inflict-

Burn-blast combined injury refers to a situation in which the victim is simultaneously or successively afflicted with burns from heat and blast injury from shock wave. If burns are the main injury, then the term would be burn-blast combined injury, and however, if blast injury is the main problem, the term would be blast-burn injury. However, usually the term burn-blast combined injury is used nowadays for both. When the human body is afflicted with burn-blast combined injury, there would be easily observed burn wounds on the surface, but also blast injury to the internal organs that are difficult to see. The victim would not only show obvious burn shock, wound infection and repair, but also serious visceral injury and functional disorder that are hard to see. The two problems promote each other and together aggravate patient condition, bringing about many dilemmas and challenges for

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medical personnel in both diagnosis and treatment. However, the lungs are still the main target organs injured by shock wave. Injury to the respiratory tract is especially serious for victims of large areas of burns and inhalation injury, mainly manifested as airway and lung tissues edema, necrotic shedding of airway mucosa, and gas exchange impairment. Therefore, when blast injury is compounded by large areas of burns and inhalation injury, lung injury would be even more serious and the occurrence of ARDS is almost impossible to prevent. When ARDS occur in victims with blast injury compounded by large areas of burns and inhalation injury, problematic conditions in the lungs would develop quickly. What happen first are changes in one lung segment, and diffused and substantial changes in both lungs within 24 h, along with significant amount of hemorrhagic effusion in the airway. The treatment of this kind of patient is very challenging and the fatality rate is rather high. When plateau blast injury is accompanied by other injuries (burns, shrapnel wound, etc.), injury conditions would be much more severe. Of which, burn-blast combined injury is most obvious, and the reason might be the full-body response to burns, and the bigger impact imparted on the respiratory system, which is the main target in blast injury. Explosions that can result in burn-blast composite injuries are very destructive, have long time of effect, injure many people, and create complicated injuries that are difficult to treat, among other characteristics. Such explosions could occur during times of peace or wartime. This is why burn-­ blast combined injury is difficult to treat, with the key problems being difficulty in diagnosis and in capturing the best timing for treatment.

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sion, with the closer the distance from the center of explosion, the higher the chance of burn-blast combined injury. 3. Burn-blast combined injury is clearly characterized by the mutually worsening effects of the injuries, and the occurrence sequence and injury severity of burns and blast injury affect the development of patient conditions. 4. Numerous injuring factors and complicated victim conditions. Shocks are very common, usually occur relatively early at rather severe levels and could worsen quickly. The pathological and physiological disorders of victims of burn-blast combined injury are often afflicted with multiple, severe, and complicated injuries at different parts of the body. The scope of injury is not only broad but affects numerous body parts and various organs, while local and full-body responses are strong and prolonged. 5. Highly complicated injury mechanism: It is projected that injury mechanism depends on the direct effects of shock wave and heat, and the secondary injuries that they cause. 6. External injuries cover up internal injuries, leading to possible missed or erroneous diagnosis. When a blast injury is coupled with burns or other injuries, injuries on the body surface are obvious, while visceral injuries might be overlooked. However, severity of visceral injury is usually the crux that determines how patient conditions develop. Lack of knowledge in this area could easily lead to missed or erroneous diagnosis or missing the best opportunity for medical rescue. 7. Lung injuries are frequently the bottleneck and focal 4.1 Basic Features of Plateau Burn-Blast point in treatment of burn-blast combined injury. The Combined Injury lungs are some of the most sensitive organs to injuries caused by shock wave and also the main target organs in When burns and blast injury occurring on plateau combine to burns of respiratory tract. When pulmonary functions form burn-blast combined injury, the effects of the two will are seriously endangered, the lungs’ tolerance of fluids add to each other’s severity, causing the body to generate also declines. Therefore, lung injuries should be the boteven stronger stress responses, possibly leading to stress tleneck and focal point in treatment of burn-blast comresponse disorder, stress ulcer of digestive tract, intestinal bined injury. infection, hypermetabolism, etc. These could consequently 8. Infection happened early and in grave severity, with lead to serious pathological harms to organs throughout the simultaneous existence of serious wound/local infection body, further complicating patient condition and heightening of the wound and systemic infection. the difficulty of treatment. 9. Rapid clinical injury conditions development and The main features of plateau burn-blast combined injury extreme difficulty in treatment manifestations include inflicted by explosion include: severe injury, numerous complications, and relatively high fatality rate from sickness and/or injury. 1. Unexpectedness of explosion that caused plateau burn-­ 10. Simultaneous existence of internal injuries and external blast composite injuries, making it more difficult to wounds that affect and overlap each other, further comorganize and direct rescue efforts. plicating and aggravating patient conditions. 2. Rate of occurrence of burn-blast combined injury is con- 11. Usually there exist damages to various organ functions: tingent on a victim’s distance from the center of exploFor instance, the cardiac, circulatory systems, the liver,

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kidneys, nervous and immunity systems, and other damages and functional disorders. 12. The biggest problem in burn-blast combined injury caused by explosion on plateau is how to deal with treatment difficulties and dilemmas arising from the different injuring factors. The crux of the matter of treating burn-­ blast combined injury is addressing the dilemma of transfusion, as treatment of burns requires rapid transfusion, which might run contrary to cautious use of transfusion for plateau blast injuries.

4.2 Clinical Expressions of Burn-Blast Combined Injury Patients of burn-blast combined injury exhibit the various clinical expressions of burns and blast injury at the same time, along with some other general signs and symptoms. These manifestations differ based on the degree of burns and severity of tissues and organs damaged by shock wave.

4.2.1 Clinical Expression of Burns Different degrees of burns have different clinical expressions. When there are burns of the respiratory tract, there are often severe burns around the mouth and nose, burnt nasal hair, swollen lips, red and swollen oral cavity and oropharynx area, white blisters or mucous membranes, irritable cough, dusts of burnt matters in phlegm, scratchy voice, swallowing difficulty or pain, breathing difficulty and/or wheezing, among others. Subsequently, conditions would rapidly deteriorate into tracheobronchitis, "gong-like" sounds and pain during irritable coughs. Burns on the body surface share similar clinical expressions with burns from regular heat source. “Rule of Three Degrees and Four Levels” should be used to estimate burn area based on Chinese Rule of Nines Method. The severity of burns should be further evaluated in accordance with burn area and depth. Burns severity may be categorized as: minor burns, moderate burns, severe burns, and extremely severe burns. 4.2.2 Clinical Manifestation of Blast Injuries (1) Lung injuries from the same intensity of impulse would be more severe if burns also exist, and clinical manifestations would also be more serious. Patients of lung injuries might exhibit sustained lack of breathing for 30–120 s after injury, often times accompanied by bradycardia and hypotension. Minor lung injury might only result in short-term chest pain, chest stuffiness, or sense of suffocation. For those more seriously injured, expressions like cough, hemoptysis, and bloody phlegm might be seen, and a small number might complain about breathing difficulty, and diffused, moist rales might be audible during auscultation. For those with severe lung injuries, manifestations include breathing difficulty,

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cyanosis, large volume of bloody and frothy fluid flowing out from mouth and nose, dull resonance in local areas produced from clinical percussion, weak breathing sounds heard during auscultation, along with widespread moist rales. For patients suffering from pneumothorax or hemothorax, corresponding signs and symptoms might appear. (2) For those with blast injury to the abdomen, the most common clinical expressions are abdominal pain, nausea, vomiting, signs of peritoneal irritation and shock, among others. If internal organ suffers only minor blunt trauma, abdominal pain would usually subside after 3–4 days. If there is ruptured organ, abdominal pain might ameliorate after a short while but would frequently return, accompanied by signs of peritoneal irritation such as tenderness, rebound pain, abdominal muscle rigidity. Hematuria may occur if there is kidney or bladder injury. Rectal bleeding may occur in patients with colon or rectum injury. Perforation of the stomach or intestines could result in symptoms like subphrenic free air, pneumoperitoneum, or disappearance of distinguishing dull sound of liver, and borborygmus might also disappear. (3) When an auditory apparatus blast injury occurs, main signs and symptoms include deafness, tinnitus, vertigo, ear pain, headache, external ear discharge, etc. In a minority of cases, patients might exhibit nausea, vomiting, or vestibular dysfunction, among other signs and symptoms. Inspection might discover eardrum rupture, fracture of auditory ossicles, and temporary or permanent auditory dysfunction. (4) The blast injury to the heart are chiefly manifested as sharp pain in the anterior area of the heart, chest stuffiness, sense of suffocation, cold sweat, and other symptoms of coronary vascular insufficiency, while acute left heart failure may occur in severe cases. Symptoms and signs of acute myocardial infarction may appear in patients with coronary air embolism. In cases where secondary injuries occurred due to ­displacement, collision or other effects caused by dynamic pressure, the most common problem is internal pericardium hemorrhage. If bleeding is profuse, symptoms and signs of cardiac tamponade may be observed. (5) The main symptoms of a blast-induced traumatic brain injury is the loss of consciousness and could also be simultaneously accompanied by various kinds of mental symptoms and signs such as indifference, anxiety, fear, irritation, sleep loss, dizziness, reduced memory capacity, etc. Serious cases may show ataxia, speech disorder, numbness of the limbs, convulsion, and other symptoms and signs of cerebrovascular air embolism. When there is injury to the brain parenchymal, increased cranial pressure or localized symptoms may appear.

4.2.3 Features of Clinical Expressions of Burn-­ Blast Combined Injury While clinical manifestations of burns are obvious, at the same time there would often be auditory capacity loss or auditory apparatus injury, as well as clear clinical expres-

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sions of pulmonary injuries, or even respiratory function disorder. It is common to see shocks unlike those associated with burns, localized pains, functional disorders, and clinical manifestations related to functional damage and functional disorders of the respiratory, cardiac, circulatory, nervous systems, and other organs.

4.3 Comprehensive Judgment of Burn-­ Blast Combined Injury Condition When both burns and blast injury are minor, or if only one is at moderate level, usually patient conditions would be severe. If both burns and blast injury are moderate or more serious, patient’s overall condition should be one level more serious than the more severe of the two injury types. If there are obvious shocks, multiple injuries, or other composite injuries, add another level of severity to the most severe rating of the overall patient condition.

4.4 Treatment Principles for Burn-Blast Combined Injury Plateau environment could lower the body’s tolerance for blast injury, worsen patient condition, and raise fatality rate. Third-degree burns on 40% of the body were inflicted to dogs under simulated plateau environment with elevation of 4000  m (after 24-h acclimatization in low pressure chamber), and the Parkland formula was used to calculate amount of replacement fluid required, then fluid infusion began 1 h after injury. Outcomes indicate that cardiac output (CO) and left ventricle working index (LCWI) of dogs in both plain group and plateau group exhibited obvious drops after injury, with decrease in the plateau group being bigger. Therefore, it is necessary to pay attention to the dilemma between the need to increase fluid volume and the decline in the body’s tolerance when performing fluid infusion on plateau. It is suggested to carry out fluid infusion under strict and careful monitoring, pay attention to improvements in cardiac functions and oxygenation in tissues, and refrain from simply limiting fluid volume at the cost of affecting recovery. The key to treatment of burn-blast combined injury in the early stage is timely and accurate diagnosis and appropriately handling the treatment dilemmas between the injury forms and injury types of composite injuries and multiple injuries. It is also important to carefully observe pulmonary hemorrhage and edema, prioritize the use of capsules when administering anti-shock fluid infusion, strengthen airway care and support treatment for the respiratory tract, heighten defend against pulmonary cerebral and edema, and endeavor to prevent and cure visceral complications such as ARDS, air embolism, and disseminated intravascular coagulation

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(DIC). Other treatment principles are, respectively, similar to those of pure blast injuries and burns.

5 Features of Plateau Projectile-Blast Composite Injury Conventional weapons of modern day (i.e. missile, cannon shell, mine, grenade) could generate a substantial amount of dangerous fragments and shock wave upon detonation. Hence, blast injury and projectile injury are the main killing and injuring factors of explosive weaponry. In a projectile-­ blast composite injury, injury from projectile worsens the severity of blast injury and is usually more dire than plain blast injury. On plateau at an altitude of 2500 m or higher, due to the lack of oxygen and low-atmospheric pressure, the body’s physiological compensation increases the stress on tissues and organs while lowering the body’s tolerance for external harms, thereby raising damage caused to the body when injured. Due to the low-atmospheric pressure and air resistance on plateaus, projectiles fly faster and create bigger impact upon collision with tissues. Therefore, tissues have to absorb more energy from injuring projectiles and in doing so sustain more damage.

5.1 Injuring Features of Plateau Projectile-­ Blast Injury Research by Lai Xinan et al. proves that a projectile’s terminal velocity on plateau is faster than that at plain, and comparing subjects in the plateau injury group with subjects in the plain injury group, entry and exit wound areas, wound tract volume, wound tract length ratio, excised necrotic ­tissue and ratio of broken muscle tissue were all larger in the former. Extents of wound tract muscle fiber ruptures and changes of subjects in the plateau spherical projectile injury group and plateau triangular projectile injury group were both more severe than those in the plain injury group, with the falling activeness in muscle tissue succinate dehydrogenase and ATPase being only 26.86% and 55.77%, respectively, of the plain group. Cavitation in soap shot at plateau is larger than that at plain. Degree of projectile injury on plateau is more serious than that on the plain, this is because, among other reasons, plateaus have less air density, therefore, projectiles have lower air resistance and could fly faster than on plains, creating bigger temporary cavity upon impact with tissues. The aforementioned study also revealed that a projectile’s terminal velocity on plateau is faster than that at plain, with a 1.03 g steel ball’s velocity on plateau being 112.79% of that on plain, and triangular projectile’s velocity on plateau being 115.25% of that on plain. The difference in projectile veloc-

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ity between plateau and plain is attributed to difference in atmospheric pressure. Under normal circumstances, for every 100 m rise in elevation, atmospheric pressure falls by 7.45 mmHg, and the atmospheric pressure on a plateau at an altitude of 3658 m is only 64.35% that of sea level. At the same time, air density also drops by 37.35%, as it is closely related to atmospheric pressure. The rate at which a projectile slows down in flight hinges on drag. Since the lower air density on plateau gives less resistance, a projectile decelerates at a slower pace, which is why projectiles on plateau fly at higher velocity than those on plain. The drag area of triangular projectile is larger than that of steel ball, resulting in more obvious velocity changes. Not only do fragments from explosions on plateau cause a larger area of damage, but also more severe injuries to tissues compared with those on plain. A projectile on plateau flies faster than that on plain, and when it hits tissue the rate of deceleration is bigger, releasing more energy through the wound tract. On plains, a bullet’s collision velocity against tissue is (660.54 ± 14.22) m/s, while a bullet’s collision velocity against tissue on plateau is (701.43 ± 2.98) m/s.

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peacetime is mainly attributed from ventilation. Prior to firearm injuries on plateau during peacetime, the compensatory reductions in PaCO2 and HCO3- result from acclimatization to the plateau environment. Thirty minutes to two hours after injury, pH edged higher by a small amount, while both PaCO2 and HCO3− dipped slightly compared to pre-injury levels, and respiratory alkalosis was also observed, yet recovery was obvious after 24 h. At the 24-h mark, pH dropped to below 7.35, which is mostly manifested as metabolic acidosis coupled with respiratory alkalosis. This development may possibly be attributed to a state of hyperventilation early after injury, manifested as respiratory alkalosis 24 h later when hyperventilation ameliorated and the body’s acidosis worsened, the result was metabolic acidosis coupled with alkalosis. In wartime on plateau, due to the body’s rapid entry to the plateau, hypoxia, and wartime factors, obvious metabolic acidosis and respiratory alkalosis in animals were existing obviously before injury. Due to decreased respiratory efficiency caused by the low-oxygen and low-atmospheric pressure of plateau environment, respiratory rate early on after injury is higher than that on plain, and hyperventilation is rather serious and sustains longer, which are manifested as respiratory alkalosis and decompen5.2 Pathological and Physiological sation. The acid–base disturbance also coexists with obvious Features of Plateau Projectile-Blast hypoxemia in the animal, which is even more pronounced Injury during wartime on plateau. Research indicates that the respective partial pressure of Under the effects of a low-oxygen, low-pressure, and low-­ oxygen during peacetime and wartime on plateau is only temperature environment, a series of pathological and physi- 63–73% of those on plain. This difference is primarily ological changes would take place in the body. The storage attributed to plateau factors. PaO2 readings 30  min to 6 h functions of key organs decline significantly, and upon this after firearm injuries on both plain and plateau during peacebasis, projectile injury would more easily cause damage to time declined then gradually restored, demonstrating that internal stability, leading to physiological dysfunction in the the body’s compensation capacity for firearm injuries durvarious systems, more post-injury complications, and higher ing peacetime is relatively sound. PaO2 readings before firerate of death from injury. arm injuries on plateau during wartime were significantly lower than that on plateau during peacetime, and the figures 5.2.1 Changes in Respiratory System After ­continued to fall after injury 24 h after injury, the levels Plateau Projectile-Blast Injury were still significantly lower than the plateau peacetime The respiratory rhythm and ventilation volume of the human group and before injury, and hypoxemia was also observed. body is regulated through the respiratory center in the ner- This difference may possibly be attributed to the following vous system. The remote effect, stress response, pain stimuli, reasons: (1) Excessively fast respiratory rate early on after blood loss, and other issues arising from plateau firearm injury resulted in an increase in ineffective cavity in the airinjuries may cause compensatory breathing increase. way; (2) accelerated heart rate after injury resulted in accelResearch by Yin Zuoming indicates that for the majority of erated blood flow in alveolar capillaries, leading to small pigs tested, after being afflicted with plateau projectile ventilation and perfusion ratio imbalance, with some blood wound, they exhibited apnea for several tens of seconds, then flow not fully oxygenated by functional shunt, in turn caustachypnea, eventually stabilizing and gradually turning to ing a rise in respiratory rate as a feedback; (3) after firearm deep breaths with respiratory rate obviously slower than injuries, the lungs were injured by a large quantity of inflamusual. This kind of respiratory change could lead to arterial matory substance, resulting in alveolar gas diffusion dysblood gas changes and acid–base disturbance in the body, function; (4) the low-oxygen and low-atmospheric pressure further intensifying hypoxia and disturbance of internal envi- of plateau environment resulted in lower respiratory effironment of the body. The minor respiratory alkalosis seen ciency; and (5) lung injuries arising from remote effect early on in animals after firearm injuries on plain during could also be one of the reasons.

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5.2.2 Rise in Endothelin After Injury from Hi-Speed Projectile Study by Yan Jiachuan et al. discovered that extremity injury on one side of the body caused by hi-speed projectile aggravates moderate blast injury, with the aggravation primarily seen in the lungs. After blast injury, or blast injury coupled with projectile injury, endothelin (ET) content in plasma and lung tissues would rise, taking effect through endothelin receptors. Pulmonary vasoconstriction results in elevated pulmonary artery pressure while simultaneously worsening any existing pulmonary hemorrhage and pulmonary edema. The extent of pulmonary vasoconstriction is contingent on the volume of endothelin, and since ET contents in subjects in composite injury group were markedly higher than other groups, therefore, their pulmonary artery pressures and lung injuries were also more severe than those in other groups. ET contents in plasma and lung tissues in subjects of pure projectile injury group did not change much. Therefore, changes in their pulmonary artery pressure and lung injury were not obvious. Pulmonary capillary endothelial cells were damaged from blast injury, leading to increased seepage, reduction in the capacity of lung tissues in ridding plasma ET and elevated ET release. At the same time, the powerful pressure wave generated by the injuring hi-speed projectile imparts varying degrees of mechanical force on vascular endothelial cells in different parts of the body, and said pressure wave would further cause damage to the pulmonary vascular endothelial cells that are already injured by blast wave. This in turn leads to additional ET release, a surge in plasma ET concentration and heightened pulmonary artery pressure. The rise in ET contents in plasma and lung tissues may possibly be linked to the following reasons: (1) Severe edema and hemorrhage in lung tissues; (2) effects of cytokines; (3) stimuli from injuring hi-speed projectile’s pressure wave and hemodynamic disorder; and (4) reduction in the capacity of lung tissues in clearing out ET. Outcomes from said research indicate that after injury plasma ET concentration soared, vasoconstriction intensified, and pulmonary artery pressure elevated, exacerbating pulmonary edema and hemorrhage and worsening pulmonary circulation obstruction, while pulmonary edema and hemorrhage could increase ET synthesis and release. This vicious cycle intensifies pulmonary edema and hemorrhage severity and worsens lung injuries. The mechanism behind how high-speed projectiles worsen blast injury is associated with the increased release of endothelin after injury. 5.2.3 Impacts of Plateau Injury from Hi-Speed Projectile on Hemodynamics Outcomes from study by Liu Jiancang et  al. indicate that right ventricular systolic pressure (RVSP) in subjects in the plateau injury group surged significantly above those in plain injury group, demonstrating that other than cardiac function

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damage, the aggravation of lung injuries and elevation in pulmonary artery pressure caused a rise in RVSP, leading to heart failure, reduction in cardiac ejection function, and significant drop in ejection fraction that is much more pronounced than that in the plain injury group. At the same time, obstruction of venous return occurred, blood flow was clogged up in the venous system, exacerbating the ischemia and hypoxia in vital organs and tissues. Consequently, CVP readings of subjects in plateau injury group 6 h after injury were significantly higher than subjects in the plain injury group. In this series of changes, the differences in subjects of the projectile-blast composite injury group were most marked. The mean arterial pressure (MAP) readings in the various plateau injury groups all exhibited a rising trend, which may possibly be attributed to the increase of blood flow through initiating contraction of peripheral arterioles, as a way for the body to compensate for the shortage of oxygen in plateau regions. The outcomes above demonstrate that plateau projectile injury could substantially worsen blast injury. Due to the lack of oxygen and low-atmospheric pressure on plateau, blast injury, projectile injury and composite injury are clearly worse than those that occurred on plains. Degree of hemodynamics injury also intensifies, with the difference being most prominent in composite injuries.

5.2.4 Hypercoagulable State Instigated by Plateau Injury from Hi-Speed Projectile Prostacyclin (PGI2) imparts a profound effect on vessel dilation and platelet depolymerization, and it is primarily synthesized in vascular endothelial cells. Thromboxane A2 (TXA2) is released by platelets, which is not only a potent vasoconstrictor, but also increases platelet aggregation. With ischemia and hypoxia, on the one hand vascular endothelial cells are damaged and PGI2 generation declines, while, on the other hand, platelets release more TXA2, leading to PGI2/ TXA2 imbalance. The outcome is marked rise in vasoconstriction and platelet aggregation, which release ­ more TXA2, causing formation of thrombus and vascular thrombosis, consequently damaging affected tissues. Research by Yin Zuoming et al. demonstrates that in highaltitude wartime environments, there were increases in plasma TXB2 before injury, while PGF1α and PGF1α/TXB2 fell, indicating that wartime factors induced PGF1α/TXB2 imbalance in the body prior to injury. Firearm injuries on plain during peacetime, firearm injuries on plateau during peacetime, and firearm injuries on plateau during wartime all showed significant climb in plasma TXB2, and all peaked at 6 h after injury. This may possibly be associated with ischemia reperfusion damage caused to tissues and organs throughout the animal’s body due to strong stress. Varying patterns of firearm injuries during peacetime on plateau and those on plain are basically identical, but the rises in the former were more obvious, demonstrating that the whole body

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is in a hypercoagulable state after firearm injuries on plateau during peacetime. This is a state in which disseminated intravascular coagulation (DIC) could easily occur alongside other complications, which would affect perfusion in tissues throughout the body. The body-wide hypercoagulable state may possibly be attributed to the hike in inflammatory agents like TNF-α after injury, which causes damage to vascular endothelial cells. The rise in firearm injuries on plateau during wartime is higher than that during peacetime, with the figure sustaining at a high level even 7–10 days after injury, demonstrating that plateau and wartime factors together wreak havoc on the body in a relatively marked manner. The body remains in a hypercoagulable state for a prolonged period after injury, leading to greater risks of thrombus and DIC. This matter is of key importance when treating firearm injuries on plateau during wartime, namely appropriately dealing with the dilemma between hemostasis after injury, and prevention of thrombus and DIC. Research by Yu Xiyong et al. indicates that after large dosages of vitamin C ingested orally (1.0 g each time), 6-keto-PGF1α level in plasma rose dramatically, while TXB2 level remained basically constant, hence, PGF1α/TXB2 ratio climbed. Meanwhile, such changes are not seen when small dosages of vitamin C were ingested orally (placebo control group), demonstrating that vitamin C concentration inside the body must reach a certain level to produce the intended effect. Vitamin C is the most effective water-­soluble antioxidant in plasma and acts as the first line of defense in the extracellular fluid antioxidant defense system by interrupting lipid peroxidation occurring in plasma. Vitamin C gets rid of free radicals and lipid peroxide that suppress prostacyclin (PGI2), thereby increasing synthesis of PGI2. At the same time, vitamin C also stimulates endothelial cells to synthesize PGI2. Worth noting is that during the antioxidation process, vitamin C both clears away radicals and causes damage through radicals. In other words, a low concentration of vitamin C engenders the production of oxygen radicals, and only when concentration is high enough vitamin C would clear away radicals, which is why the effect of vitamin C hinges on its concentration. Therefore, treatment of firearm injuries on plateau needs to pay attention to strengthening vitamin C administration and other full-body support and treatment.

5.2.5 Impacts of Plateau Injury from Hi-Speed Projectile on Inflammatory Response Research by Yin Zuoming et al. discovered obvious declines in expressions of inflammatory agents such as TNF-α, IL-1β, and NO in wound tracts of plateau peacetime injury group, and inflammatory response and tissue edema severity levels were clearly less dire than the plain group, and these also occurred later than subjects in the plain group. Wound tract tissue wet/dry ratio and histology results both prove this point. Expressions of anti-inflammatory agents IL-4 and

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IL-10 in  local tissues of the wound tract were markedly lower than those in the plain peacetime group and were expressed at a later time. This also illustrates that local inflammatory response in wound tract after firearm injuries to the limbs on plateau is less severe than that of firearm injuries to the limbs on plain. Possible reasons for these differences between plateau group and plain group might be: (1) Lack of oxygen in plateau environment means less local production of oxygen radicals in wound tract, thereby inducing smaller inflammatory response. (2) The cold environment of plateau delays the onset of and lessens wound tract infection. Due to the reasons mentioned above, critical time of local immunity changes in wound tract of firearm injuries on plateau during peacetime was delayed to the second or third day, hence, debridement deadline could be delayed to the second day after injury. This is conducive to early-stage surgical treatment of firearm injuries wound tract on plateau and cold alpine regions during peacetime, but is unfavorable to the recovery and healing of wound tract on plateau. (3) The expressions of inflammatory agents such as TNF-α, IL-1β, and NO in wound tracts of plateau wartime injury group were obviously higher than plateau peacetime injury group but less than plain peacetime injury group, and time of appearance of anti-inflammatory agent IL-10 was substantially later than plateau peacetime injury group, at a concentration substantially higher than plateau peacetime injury group. This demonstrates that rapid entry into simulated combat environments characterized by features such as plateau, stress, tiredness, hunger and cold temperature, a series of pathological and physiological changes already took place in animals in the plateau wartime injury group before injury. Upon this basis, projectile injury would cause a sort of accumulated trauma, and wound tract inflammatory response after injury was more severe than that of plateau peacetime injury group but less than that of plain peacetime injury group. Meanwhile, critical time of local immunity changes occurs earlier than plateau peacetime injury group, bringing forward to 24 h after injury. Under this type of special environment, understanding the unique pattern of wound tract inflammatory response produced by firearm injuries during wartime is of great meanings to the design of early-stage surgical treatment options for local wound tract of firearm injuries during wartime in said special environment.

5.2.6 Impacts of Plateau Injury from Hi-Speed Projectile on Metabolism Research by Yin Zuoming indicates that oxygen deficit on plateau itself could affect the body’s material metabolism, increasing the decomposition of sugar, protein, and fat, while protein synthesis weakens and creates water, sodium, and potassium metabolism disorders, among other matters. Upon this basis, projectile injury on plateau leads to a bigger stress response than on plain, leading to a series of neuroendocrine

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reactions in the hypothalamic-pituitary-adrenal axis and sympathetic nervous system, causing raised secretions of cortical hormone, catecholamine, glucagon, TNF, IL-1, IL-6, and lipid mediators. This in turn instigates increases in energy consumption, metabolic rate, protein consumption, and fat decomposition, with sustained period longer on plateaus than on plains. After plateau projectile injury, glycometabolism is mainly manifested as high decomposition and high glycolysis, and lipometabolism is mainly manifested as high decomposition and high consumption, while protein metabolism is mainly manifested as high decomposition and low synthesis. Plateau projectile injury during wartime is often accompanied by serious hypocalcemia and hypomagnesemia in the early stage. Minor hyponatremia in the later stage, while gradual falls in phosphorus, potassium, and chlorine would start in 12 h after injury. Therefore, when treating victims of plateau projectile injury during wartime, pay attention to supplementations of calcium, magnesium, sodium, and other electrolytes in a prompt manner. At the same time, recovery from plateau trauma during wartime necessitates a large amount of nutrients, and the proper metabolism and nutritional support and adjustment can protect organ functions, augment immunity, protect against infection, and promote healing of wound tract.

5.3 Features of Plateau Projectile-Blast Combined Injury Outcomes from research by Yang Zhihuan et  al. show that hi-speed projectile injury to the limbs aggravates the severity of moderate and severe blast injury, with aggravation mostly occurring in the lungs, limited to the region where the primary blast injury took place. In general, patient condition would be one level more dire than the original injury. Mechanism behind how hi-speed projectile intensifies blast lung injury remains unclear, but it may possibly be linked to the forceful disturbance of blood flow instigated by pressure wave from the impact of hi-speed projectile upon hitting the body, and this blood flow disturbance injures the heart and lungs, which are away from the wound tract. Some literature have reported that when animals were injured by hi-speed projectiles, pressure waves were recorded in aorta, aortic arch, and brain tissues, with readings as high as 300 kPa observed in aortic arch. Evidently, this kind of powerful pressure wave can further damage lung tissues that have already been injured, thus worsening existing injury. In addition, after being severely injured by a hi-speed projectile, the body would secrete excessive amounts of inflammatory agents and cytokines such as thrombin, endothelin, IL-1, IL-6, and TNF-α. These could further cause damage to pulmonary vascular endothelial cells and alveolar epithelial cells, to some extent contributing to secondary pulmonary

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injuries. Another study proved that pulmonary index rose significantly in animals afflicted with projectile-blast composite injury, revealing the existence of obvious pulmonary edema. This is also a solid evidence. Therefore, secondary injury could be another major reason why hi-speed projectile worsens blast lung injury. Hi-speed projectile does not seem to exacerbate minor blast lung injury, which could be attributed to very limited area of lung injury, relatively sound integrity of lung tissues and structure, and rather small influence on the lungs imparted by the pressure wave from the hi-speed projectile. Similarly, lowspeed projectile does not appear to significantly worsen moderate blast lung injury. The hypothesis is that the relatively weak pressure wave generated by the projectile is associated with the relatively mild secondary lung injuries, but specific mechanism requires further study. Existing research outcomes reveals that when treating blast injury victims, not only it is necessary to treat projectile injuries on the surface, but it is also required to consider possible existence of visceral blast injury, and aggravation of blast lung injury caused by hi-speed projectile. In case of performing fluid resuscitation, if there is relatively severe blast injury, fluid infusion volume and rate should be adjusted to appropriate degrees. Meanwhile, hemodynamics monitoring should be strengthened to prevent injury condition aggravation and other dire consequences due to inappropriate fluid infusion. All in all, plateau blast injuries could be aggravated when coupled with burns or projectile injuries, giving rise to more severe conditions and higher death rate. Aggravation mostly targets the lungs, while the same aggravation does not seem to appear in blast injury to the gastrointestinal tract when existing as burns-blast composite injury or projectile-­blast composite injury. Therefore, when treating victims of this kind of injury, it is necessary to pay close attention, make correct judgment about injury, and undertake the corresponding treatments and measures.

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Z. Yin et al. 22. Bo Z, Zhihuan Y. Research on the treatment of blast injuries at high altitude. J Traum Surg. 2006;8(4):292. 23. Yuqi G, Zuoming Y, Lei S. War wounds and traumas in special military operational environment. Zhengzhou: Zhengzhou University Press; 2016. 24. Qunyou T, Tianyu S, Ruwen W, et al. Clinical diagnosis and treatment specifications for blast lung injuries (recommendation). Chin J Traumatol. 2014;30(9):865–7. 25. Song Z, Xiaobo L, Weidong T, et al. Clinical diagnosis and treatment specifications for abdominal blast injuries (recommendation). Chin J Traumatol. 2014;30(10):971–5. 26. Zhongdong C, Suzhi L, Hongya W, et  al. Effects of thoracic explosive injury on blood gas and acid base balance in rabbits at high altitude. Med J Natl Defending Forces Southwest China. 2011;21(6):591–2. 27. Youan S, Jianxin J, Zhihuan Y, et  al. Role of hyperbaric oxygen treatment on canine severe lung blast injury. J Traum Surg. 2003;5(5):333–5. 28. Zhilong D, Zhihuan Y, Xiaoyan L, et al. Therapeutic effects of hyperbaric oxygen, anisodaminum and dexamethasone on blast injury in rats exposed to high altitude. J Traum Surg. 2012;14(2):165–8. 29. Zhengguo W. Field surgery. Beijing: People’s Medical Publishing House; 2010. 30. Jihong Z, Zhengguo W, Peifang Z, et al. Clinical guideline to burn-­ blast combined injuries. Chin J Traumatol. 2013;29(9):809–12. 31. Jianxian Z, Bin S, Xinhua Z, et al. Discussion on the clinical treatment of severe burns associated with blast lung injuries. Military Med J Southeast China. 2009;11(5):420–2. 32. Maoxing Y, Zhihuan Y, Ronggui W, et al. Characteristics and emergency treatment experience of explosion-induced burn-poison combined injuries. J Traum Surg. 2003;5(5):344–6. 33. Maoxing Y, Zhihuan Y, Ronggui W, et al. Injury characteristics of “blast-burn-poison” combined injuries and field resuscitation strategies. Med J Traum Disab. 2003;11(3):5–7. 34. Moore LG. Comparative human ventilatory adaptation to high altitude. Respir Physiol. 2000;121(2):257–76. 35. Ishizakia T, Koizumib T, Ruan ZH, et  al. Nitric oxide inhibitor altitude-dependently elevates pulmonary arterial pressure in high-­ altitude adapted yaks. Respir Physiol Neurobiol. 2005;146:225–30. 36. Taniai H, Suematsu M, Suzuki T, et  al. Endothelin B receptor-­ mediated protection against anoxia-reoxygenation jury in perfused rat liver: nitric oxide-dependent and -independent mechanisms. Hepatology. 2001;33(4):894–901. 37. Leon Velarde F, Gamboa A, Chuquizaja, et  al. Hematological parameters in high altitude residents living at 4335, 4660, 5500 meters above sea level. High Alt Med Biol. 2000;1(2):97–104. 38. Antonelli M, Bonten M, Chastre J, et al. Year in review in intensive care medicine 2011: III. ARDS and ECMO, weaning, mechanical ventilation, noninvasive ventilation, pediatrics and miscellanea. Intensive Care Med. 2012;38:542–56.

Underwater Blast Injury Shengxiong Liu and Zhiyong Yin

Underwater blast injury is a type of injury often seen in combats on and around islands and during landing operations. Detonation of depth charges, naval mines, bombs, cannon shells, and other munitions underwater could generate underwater shock wave, which could inflict underwater blast injury upon personnel in water. To deal with such injuries, scores of scholars both in China and abroad have undertaken active studies and explorations. As early as World War II, several thousand cases of underwater blast injuries occurred, and people noticed that underwater blast injuries could be fatal. During the 1967 Arab–Israeli War, an Egyptian missile struck the Destroyer Eilat of Israel, after which sailors onboard abandoned ship, and another missile detonated nearby when they were in the water. Of the 32 sailors rescued, 27 had been afflicted with blast lung injury, and 24 with blast abdominal injury, of which 22 had been found to have perforated intestines. 19 suffered from both pulmonary and gastrointestinal injuries, and four died. However, experiments pertaining to underwater blast injury were not conducted until the end of the 1960s, after the U.S. military constructed underwater test site at their Kirtland base. Since the “10th Five-Year Plan,” the Chinese military has been performing underwater blast injury studies, and a bevy of on-site experiments have produced numerous revelations about features of underwater blast injury.

1 Injuring Features of Underwater Blast Injury Due to physical properties of water and the difference between pressure in underwater environment and normobaric air, the injuring features of the underwater shock wave S. Liu Chongqing University of Technology, Chongqing, China Z. Yin (*) China Automotive Engineering Research Institute Co., Ltd., Chongqing, China

clearly differ from the air blast induced injuries under normal atmospheric conditions, especially when the source of a shock wave is located underwater.

1.1 Physical Properties of Underwater Shock Wave 1.1.1 Velocity of Propagation A shock wave propagates much faster underwater than when in the air. When the peak pressure of an underwater shock wave is relatively high, its propagation velocity is faster than that of sound in water. In contract, when peak pressure is comparatively low, its propagation velocity roughly equals to the speed of sound in water. The speed of sound in water (1437 m/s at 20 °C) is about four times faster than speed of sound in air (344 m/s at 20 °C). Hence, propagation velocity of underwater shock wave is around three to four times faster than air shock wave of same strength. 1.1.2 Distance of Propagation Since water is denser than air and is relatively incompressible, not only does a shock wave propagate much faster in water, it also propagates much farther. Take explosion of explosive, for example, when 250 g of explosive is detonated on the ground, peak overpressure at a distance of 2 m from the center of explosion is roughly 1.05 kg/cm2. When the same amount of explosive is detonated in water, peak overpressure at the same distance soars to approximately 211.30 kg/cm2. When 100 kg of explosive is detonated on the ground, peak overpressure at a distance of 700 m from the center of explosion is merely 0.0089 kg/cm2, but when the same amount of explosive is detonated in water, peak overpressure at the same distance is about 1.7600 kg/ cm2. Comparing between the two, there is around 200 time difference in pressure at the same distance. The same pattern holds true in nuclear explosion. For instance, when a 100-kiloton nuclear weapon is detonated in water, peak overpressure at a distance of 914.4 m from the

© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 Z. Wang, J. Jiang (eds.), Explosive Blast Injuries, https://doi.org/10.1007/978-981-19-2856-7_30

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center of explosion is around 190 kg/cm2, but when the same nuke is detonated in the air, peak overpressure at the same distance does not even reach 1 kg/cm2.

S. Liu and Z. Yin

0.23–3.60 kg of explosives were detonated 3 m underwater in a pool 9  m in depth, results did not show any obvious effects due to reflection from the bottom of the pool. When an underwater shock wave propagates to the inter1.1.3 Mode and Energy of Propagation face between water and air, it would be reflected and create As stated previously, when a shock wave propagates and tensile wave in water. Consider point A to be any point undermoves in the air, it creates compression zone and rarefaction water. First, the positive pressure of the incident wave imparts zone. At first, air particles advance along the shock wave its effect, then the reflected tensile wave arrives, and since the front, but since their velocity continues to slow, eventually direction of this reflected tensile wave is opposite to the incithey would fall to the back boundary of the compression dent wave, point A would be subjected to negative pressure. zone. At this point, air particles have a velocity of zero. Air The result is a decline in the effect of the incident wave. particles fall into the rarefaction zone after moving with the Effects of the tensile wave differ depending on the depths shock wave front for about 100 m, then start to move toward of the point of explosion and point of effect. Consider point the source of explosion. Finally, air particles would return to A and point B underwater, with point A close to the water their approximate original positions. surface than point B, and the point of explosion has equal This is not the case when a shock wave propagates in distance from both point A and point B. In this setting, tenwater. Due to water’s relative incompressibility and absence sile wave reflected from the surface of the water reaches of clear rarefaction property, the compression zone and rar- point A first, and the incident wave that arrived at point A efaction zone seen in air shock wave are missing, and water would be interrupted at an earlier time by the tensile wave. In particles also do not exhibit obvious forward and backward other words, although both point A and point B are subjected movements because of propagation of a shock wave. A shock to the same peak pressure, still the positive pressure effective wave only transmits the energy of its pressure wave through duration at point A is shorter than that at point B.  Or, we the medium of water, and even water close to the center of could say that the impulse (sum of instantaneous pressure explosion does not exhibit violent movements. during pressure effective duration) at point A is less than that When propagating in water, the features of a shock wave’s at point B. Similarly, points of explosion at different depths physical parameters include high peak pressure but shorter also have different effects on the same point of effect. When effective duration (in the realm of several hundred microsec- underwater explosive 1 (closer to water surface, i.e. shalonds). This duration is much shorter than the range of several lower) and explosive 2 (farther from water surface, i.e. milliseconds to several tens of milliseconds for the air shock deeper) have equal distance away from underwater point A, wave, or about 1/76.0 to 1/32.8 that of an air shock wave’s the tensile wave created from the explosion of the shallower duration. Although an underwater shock wave has a rela- explosive 1 would reach point A sooner, and hence, its incitively short positive effective duration, its high peak pressure dent wave at point A would be interrupted at an earlier time still translates into a much more powerful impulse than that by its tensile wave. Meanwhile, because explosive 2 is of air shock wave. In addition, pressure increase duration at located deeper underwater, the tensile wave created from its the front is extremely short and fast (at the microsecond-­ explosion would reach point A later, and hence, its incident level), much faster than the pressure increase duration at the wave at point A would be interrupted at a later time by its front of the air shock wave. tensile wave, or maybe stay uninterrupted, which is why the Moreover, in terms of energy of a shock wave propagat- impulse generated would be higher. ing in water, when the same mass of TNT is exploded, underBased on the above, it may be understood that in the event water blast wave generates an average peak pressure 227.15 of an underwater explosion and if other conditions remain to 247.86 times bigger than the air blast wave, while impulse constant, persons in shallower locations are safer. Therefore, is 8.48 times to 11.80 times higher. if underwater personnel anticipate an imminent explosion, he or she should swim toward the surface as quickly as pos1.1.4 Reflected Wave and Tensile Wave sible and try to keep one's body (especially the head) above When a shock wave propagates to the bottom of the water or water. the surface of other rigid obstructions, it would be reflected, thereby strengthening the effect of the shock wave. However, 1.1.5 Calculation of Pressure of Underwater since it is rare of the incident wave and reflected wave to Shock Wave reach the same spot at the same time, hence the mutually 1. When calculating the pressure of an underwater shock strengthening effect is not that obvious. For instance, when wave, use the Cole’s equations:

Underwater Blast Injury

453

1.5   W 1/ 3  R  4.41× 107 ×  < 12 6≤  R R    0 P= (30.1) 1/ 3 1.13    R W 7 12 ≤ < 240  5.24 × 10 ×  R0  R  



In the above equation, P is peak pressure (Pa), W symbolizes charge quantity (kg), R represents distance between center of explosion and point of observation (m), and R0 denotes initial radius of explosive charge (m). Simplification of the above equation yields the following equation: P = 13000 3 W / R



(30.2)

In this equation, P is peak pressure and unit is pound/ inch2 (1 pound/inch2 = 1/14.21 kg/cm2 = 6.90 kPa); W symbolizes charge weight and unit is pound (1 pound = 0.454 kg); and R represents distance from point of explosion and unit is foot (1 foot = 0.305 m). 2. When influences from boundaries such as bottom and surface of water are not given considerations, the peak pressure from an underwater explosion of TNT spherical charge may be calculated using the equation below:  3W P = 465   R



1.1

  



(30.3)

In this equation, the meanings of P, W, and R are the same as formula (30.2), but measurement units differ, respectively, being kg/cm2, kg and m. 3. Effects differ depending on the depth at which the explosive is located. If nothing about the underwater explosion could be observed above the surface of water, then the least depth of the explosion may be estimated using:

H ≥ 9.0 3 W

In this equation, H is depth of explosion (m), and W denotes quantity of explosives (kg). Further, for a TNT spherical charge with the density of 1.6, the overpressure from its shock wave underwater may be calculated using R H Cole’s empirical equation:



 3W P = 533   R

1.13

  



(30.4)

In this equation, the meanings of P, W, and R are the same as formula (30.3).

1.2 Relationships Between Injury Severities and Physical Parameters of Underwater Shock Wave As stated previously, under normal atmospheric conditions, the incompressibility and density of water are much greater than that of air. Comparing with an air shock wave, the pressure increase duration and positive pressure effective duration of an underwater shock wave are much shorter. Due to the shorter effective duration, when other conditions remain the same, a person underwater could bear a higher overpressure than when in the air.

1.2.1 Information from Animal Testing Experiments indicate that in the event of an underwater explosion, injury severities of animals directly correlate to the impulse of the shock wave generated. For example, although animals at different locations endure peak pressure and pressure effective duration that differ rather markedly, as long as they are subjected to similar amount of impulse, their injury severities do not vary much. For different types of animals, injury severities differ even subjected to underwater shock wave of the same strength. For example, when 1000 tons of explosives were detonated in water, its shock wave could kill all organisms within a range of one nautical mile (1 nautical mile = 1.853 km), but its lethal range enlarges to four nautical miles for fish with swimming bladders (directly lethal peak pressure is 4.93 kg/ cm2, as in 70 pounds/inch2). This is because although fish with swimming bladders can endure relatively higher peak pressure, they are more susceptible to damage from underpressure (pressure reflected from surface of water). Experiments also proved that birds are more easily injured than mammals. If an animal is floating on water, its injury would be greatly lessened (Table 30.1). Impulses needed to impart different levels of injuries to humans are relatively close to the ones listed for mammals in Table 30.1. 1.2.2 Information of Persons Injured Injury severities of persons are not only dependent on physical parameters such as peak overpressure, but also closely related to quantity of explosives. Generally speaking, the smaller the quantity of explosives, the higher the overpressure the human body could tolerate. Table 30.2 lists selected information about relationships between personnel injury severities and overpressure of underwater explosion In light of all related factors, some have proposed that the standard safe distance for personnel underwater should be 0.3 kg/cm2 or impulse of less than 0.14 kg/cm2 ms. The peak pressure needed to kill a person is roughly 17.6 kg/cm2 (250 pounds/inch2).

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454 Table 30.1  Relationships between injury severities of different types of animals and impulse of underwater shock wave Type of animal Birds (duck)

Mammals (goats, dogs, monkeys)

Quantity of explosive/kg 0.45 0.45 0.45 3.6 3.6 3.6 3.6

Depth of explosive underwater/m 3.0 3.0 3.0 10 10 10 10

Depth of animal underwater/m 0.6 0.6 0.6 Above water Above water Above water Above water

Impulse/kg cm−2 ms 3.17 2.52 0.70 9.15–10.55 7.04–8.45 2.82–4.23 2.11

0.23–3.6 0.23–3.6 0.23–3.6

3.0 3.0 3.0

Head above water, body underwater

2.82 1.41 0.35

Injury severities 50% fatality, severe injury for the rest 1% fatality, mostly moderate injury for the rest Light injury 50% fatality, severe injury for the rest 1% fatality, mostly moderate injury for the rest Light injury No injury Moderate injury Light injury No injury

Table 30.2  Relationships between personnel injury severities and overpressure from shock wave of underwater explosion

Quantity of explosive/kg 1 3 5 50 250 500

Minor brain concussion Injury Overpressure distance/m value/kg·cm−2 100–20 2.93–18.05 300–50 1.28–9.70 350–100 1.30–5.37 – – – – – –

Gastrointestinal hemorrhage and perforation Overpressure Injury distance/m value/kg cm−2 20–8 18.05–50.85 50–10 9.70–59.76 100–25 5.37–25.72 150–75 8.09–17.70 200–100 10.71–23.44 350–50 7.39–10.81

1.3 Injuring Features of Underwater Shock Wave 1.3.1 High Rate of Fatality Due to the differences in properties of the medium, when the same quantity of explosive explodes underwater, the overpressure generated at the same distance from the center of explosion underwater is much higher than an explosion in the air, and the impulse created is also greater than an air shock wave, therefore, underwater blast injury has a relatively higher rate of fatality. Death rate of air shock wave is mostly under 20%, but that for underwater blast injury could range from 40% to 70%. 1.3.2 Large Fatal Range Underwater shock wave can kill in an area nine times that of an air shock wave. 0.5 kg of TNT exploded underwater has the same fatal zone boundary as that of 40  kg of TNT exploded in the air. 1.3.3 Lungs Are the Main Target Organs Lungs are the main target organs in underwater blast injuries. Since the lungs contain a lot of air, a shock wave releases its energy at the interface between tissue and air, thereby causing damage. In addition, when there is severe tearing of lung tissues, air inside alveoli could enter pulmonary veins via

Start to death Injury distance/m 8 10 25 75 100 250

Overpressure value/kg cm−2 50.85 59.76 25.72 17.70 23.44 10.81

tears in the small vessels, creating air embolism, which would move around the whole body through the circulatory system. Death could occur very swiftly if air embolism enters and clogs the main coronary or cerebral artery. Lung injury severity is closely associated with impulse. When impulse is more than 300 kPa ms, extremely severe lung injuries occur in 91.7% of dead animals. When impulse is below 300 kPa ms, the severe lung injury rate is merely 7.7%.

1.3.4 Much More Severe Damage to Abdomen than Air Blast Injury Since the abdomen is directly in contact with water whether the person is underwater or floating on his/her stomach, it is more common for organs in the abdomen (mainly the gastrointestinal tract) to sustain injury during an underwater explosion than an air explosion, and the injury is usually more severe. The frequent colon and small intestine injuries, respectively, occur around 50% and 30%, much higher rates than such injuries caused by air shock wave. Furthermore, when underwater compression wave presses on the abdomen, other injuries could be induced such as diaphragmatic muscle tear, and compression-related ruptures of hollow organs like the intestines and solid organs like the spleen, kidneys, and liver. Compression wave could also propagate inside the anus and cause “explosion” inside the colon.

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Underwater Blast Injury

1.3.5 Severe Injury to Air-filled Organs and Low Rate of Injury to Solid Organs and Liquid-filled Organs A substantial amount of practice and clinical observations prove that hollow organs filled with air after are often severely damaged under the effects of shock wave underwater. Meanwhile, hollow organs containing liquid such as the gall bladder, urinary bladder, and renal pelvis might be spared from injury. The mildness of injury to this type of organs may possibly be associated with the proximity between their densities and water, which means that a shock wave passes through these organs in a short duration, and therefore these organs only absorb a small amount of the shock wave’s energy. Researchers have conducted the following experiment: Fill animal intestinal cavities with normal saline, then place intestines underwater, which remain largely unscathed after explosion, even when intestines were placed near explosives. However, if there were even tiny amount of bubbles in the intestines, then obvious intestinal wall perforations could be observed immediately after explosion. 1.3.6 Extremely Rare Surface Wounds and Multi-injuries One clear characteristic of underwater blast injury is the extreme rarity of wounds on the surface of the body. This is because there usually are not many secondary projectiles generated by an underwater explosion, and therefore, personnel will not or are very unlikely to be injured by secondary projectiles. After an explosion, personnel underwater or on water surface may possibly be tossed because of the waves created, and those on the water surface may even be launched into the air, but usually they will not or are very unlikely to land on any hard object; therefore, external wounds on the surface of body are uncommon. 1.3.7 Rare Craniocerebral Injuries In underwater blast injuries, injuries on the surface of the head are mostly minor, and such injuries might not happen at all. This is because during an underwater explosion, the majority of victims are near the surface and their heads are above water. Animal testing with dogs indicates that if heads are submerged underwater when explosion occurs, eardrum perforation is frequent, and auditory ossicle fracture may even occur in severe cases.

2 Clinical Features of Underwater Blast Injury Clinical documentations on underwater blast injuries indicate features including body surface external wounds that are extremely rare, head injuries that are usually minor, most

injuries inflicted upon organs in the chest and abdominal cavities, severe injuries for organs containing air, mild injuries for organs containing liquid and very minor injuries for solid organs, and more serious injuries on the inside than outside.

2.1 Clinical Pathological Features of Underwater Blast Injury 2.1.1 Lung Injuries are Most Common Pulmonary hemorrhage is the most common type of lung injury. Usually hemorrhage occurs in both sides of the lungs, from dispersed spots of bleeding to widespread bleeding across the whole lobe. Two parts of the lungs are most susceptible to pulmonary hemorrhage: First is located in areas where alveolar tissues connect with the bronchioles and blood vessels; therefore, tube-shaped bleeding could be seen in areas surrounding the bronchus; second is the surface of the lungs adjacent to body parts such as the heart, diaphragm, ribs, and spine, and streaks or patches of bleeding could be observed. For victims of severe pulmonary edema, substantial hemorrhagic infiltration could cause consolidation of lung lobe, which might conceal the minute changes described above. Bloody and foamy fluid or blood clots could be seen inside the bronchus. In addition, pulmonary edema, bullous interstitial emphysema, pneumomediastinum, and blood and gas accumulation in the pleural cavity arising from tearing of the pleura and lung parenchyma may also be found. Under microscopic inspection, ruptured capillaries and internal bleeding in the alveolar walls may be observed in mild cases, and widespread ruptured alveolar septum with large amount of blood in alveolar space could be seen in severe cases. Interstitial or alveolar edema may be seen nearby the bleeding area, but this is more commonly found in those that have already survived for a couple of hours. Microscopic inspection also frequently reveals injuries around the bronchial tree, characterized by the separation of alveolar tissue from airway and blood vessels, causing the gaps surrounding the bronchus and blood vessels to be filled with blood, edema fluid, lymphatic fluid, and/or gas. When the pulmonary vein ruptures, alveolar venous fistula could occur, which may possibly be the main culprit responsible for air embolism that often causes death in early stage of blast injury victims. For underwater blast injury victims with lung injuries, severe cases may exhibit anoxia, breathing difficulty, and problems immediately after injury, but body compensation would initiate in the case of most victims; therefore, clinical symptoms of lung injuries could take some time before appearing. Analyzing clinical information on 27 underwater blast injury victims with lung injuries, the most common symptom is hemoptysis, followed by breathing difficulty, some local or even extensive moist rales and dry rales may

S. Liu and Z. Yin

456 Table 30.3  Clinical features and their occurrence rates among 27 cases of underwater blast injury victims with lung injuries Symptoms and signs Hemoptysis Breathing difficulty Dry rales and moist rales Chest pain Cyanosis

Number of cases 15 11 11 6 5

Occurrence rate 55.6 40.7 40.7 22.2 17.5

be heard on auscultation, and chest pain and cyanosis may be observed in a small number of victims (Table 30.3).

2.1.2 Abdominal Injuries Are Relatively Common and Severe 1. Injuries to the digestive tract: Injury could occur from the lower segment of the esophagus to the rectum, but injuries most often happen in the large and small intestines. Hemorrhage and perforation are common injuries. Hemorrhage conditions differ from cases to cases and could be anything from spots of bleeding behind the peritoneum, under the serous membrane or on the mucous membrane, to extensive bleeding. Based on the form of bleeding, such hemorrhage may be divided into five types: a. Isolated spots of bleeding with the size of a needle, existing independently or in small clusters. b. Thin streaks of bleeding or many spots clumped together, sometimes ring-shaped, having extended to areas around the intestinal cavity. c. Ring-shaped belt of bleeding with clear boundaries, often accompanied by a small volume of effusion of blood in the intestinal cavity. d. Broad bleeding belt comprised of ring-shaped streaks of bleeding, often seen with a substantial amount of blood clots in the intestinal cavity, and found immediately next to the mucous membrane of the area. In some cases, blood clots could be large enough to clog up the intestinal cavity. This type of injury is usually accompanied by perforation. e. Net-like bleeding in ring shape or large swath, but this is rather rare. Bleeding usually occurs on the surface of mucous membrane, often seen on direction opposite to the mesentery. When gas accumulation in the intestinal cavity remains relatively stationary, acute perforation could easily take place, with perforation ranging from 1  cm to 4  cm in diameter and one to several in number, but some cases might suffer from 20 or so perforations. There is usually bleeding around the perforation. Under the effect of shock wave, if the gas moves to another location, the result could be mucous membrane rupture or hemor-

rhage, as in the so-called incomplete perforation. Upon this basis, delayed perforation may possibly occur because of necrosis, secondary infection, or posthemorrhagic ulcer. Upon microscopic inspection, this kind of perforation is characterized by obvious rupture in the intestinal wall, coupled with muscle tear and breakage. Pieces of ripped mucous membrane and blood clots may be seen stuck in perforations, indicating that the rupture occurred from the inside out. 2. Injuries to other organs: Hemorrhage could occur in solid organs such as the liver, kidneys, spleen, pancreas, adrenal gland, and testicles. For some cases, acute tearing in liver, kidneys, and spleen may also be discovered. 3. Symptoms and signs: Victims of underwater blast injury to the abdomen frequently complain about sudden and acute abdominal pain after the explosion, as if he or she has been kicked in the belly. Also common are short-term numbness in the lower limbs, nausea, vomiting (sometimes but not always blood seen in vomit), and tenesmus. Some victims complain about sense of electrocution and testicular pain. For victims rescued relatively late or those with severe injuries, minor to moderate shock may occur. For victims without intestinal tract perforation, different degrees of pressing pain and muscular tension in the abdomen may appear, and sometimes rectum bleeding may be found. For victims with intestinal tract perforation, typical symptoms and signs of acute abdominal disease are common, pressing pain of the abdominal wall, muscular tension in the abdomen, board-like rigidity, followed by abdominal distention, weakening or disappearance of borborygmus, and rectum bleeding, among others. In addition, victims of underwater blast injury to the abdomen are often afflicted with temporary and minor paralysis of the lower limbs, which could be attributed to injury of small blood vessels in the spinal cord. Worth mentioning is that if pain killers are used during the evacuation process, some of the signs and symptoms might not express as obviously. Investigations and survey of 28 cases of survivors of underwater blast injury indicate that signs and symptoms in the abdominal region are very common (Table 30.4).

2.2 Typical Cases Below are three cases of typical underwater blast injuries. Case 1: Male, 20 years old, soldier, injured because of accidental explosion of explosives during underwater ­blasting demonstration. During the explosion, the victim’s body area below the shoulder was submerged in water and was located merely 5 m from the point of explosion. Right

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and drug treatment [immediate use of intravenous therapy to administer deslanoside (lanatoside C), furosemide, phentolNumber of Occurrence amine, hydrocortisone, etc.], the victim's cyanosis lessened, Signs and symptoms cases rate bloody and foamy phlegm disappeared, and moist rales in Right after or soon after explosion both lungs significantly reduced. The victim pretty much  Sensations of the effects of 24 35.7 recovered fully after 2 weeks in the hospital. underwater shock wave 19 67.9 Case 2: Male, 22 years old, soldier, injured at the same  Sudden abdominal pain 11 39.3  Short and sudden numbing of lower 11 39.3 place and same time as case 1. When the explosion occurred, limb 7 25.0 the victim’s body area below the nipples was submerged in  Nausea or vomiting 5 17.9 water. At the instant of the explosion, powerful waves of  Tenesmus 6 21.4 water forcefully struck the side of chest and waist. The vic Testicular pain 2 7.1  Sudden chest pain tim felt sustained and sharp pain in the xiphisternum and  Sensation of electrocution navel area, and the aforesaid symptoms clearly lessened After admission to hospital (8–11 h after explosion) 5  min later. Only sustained, dull pain was felt around the  Symptoms of acute abdominal 24 85.7 navel area afterward. One hour after injury, the victim disease excreted bright red bloody feces a total of three times, totaling around 300 ml in volume. The victim was admitted to the after the explosion, the victim felt a sense of suffocation, fol- emergency room. During inspection, there was mild pressing lowed by sustained and sharp pain in the chest and abdomen. pain around the navel, and digital rectal examination found After being evacuated onshore, the victim passed out and pink, viscous fluid on glove. After hospital admission, the immediately coughed up several coughs of blood. Then chest victim did not consume food for 1 day and was administered pain subsided, but sustained pain around the navel continued with fluid infusion, injected with carbazochrom to stop and even worsened. The victim was admitted into the hospi- bleeding, and orally ingested tetracycline. The victim basital 1 h after injury. After admission to the hospital, the victim cally recovered after 3 days. excreted dark red bloody feces once, around 100 ml in volIn the two cases presented above, even though the victims ume. During inspection, the victim exhibited mental slug- were situated at the same location during the explosion, their gishness, a small amount of moist rales could be heard in the conditions differed drastically. Case 1 suffered from perforamiddle and lower lobe, and left and lower lobe of the right tions in the intestines, but case 2 did not. After analysis, poslung. There were also mild muscle tension around the navel, sible reasons include: (1) body position. During the obvious pain upon contact, rebound tenderness, no dull explosion, case 2 faced the explosion from the side, resulting sounds of movement, and substantial weakening of borbo- in more minor injuries; (2) volume of air contained in intesrygmus. Digital rectal examination only found pink, viscous tines. Perhaps case 1 had more air in the intestines, making fluid on glove. Chest X-ray revealed patches of shadows in them more prone to rupturing. middle and lower lobe, and left and lower lobe of the right Case 3: Male, 21 years old, swimmer, body was sublung, indicating pulmonary hemorrhage. Laboratory exami- merged in water with only head above water, a relatively nation: White blood cells 9 × 109/L, neutrophil granulocyte large firecracker was mistakenly dropped into the water 81%, urine protein ++, WBC 3-4/HP, Hyal-cast +/LP, Gran-­ 1.5 m away from the victim and exploded underwater. After cast 1-3/LP.  Diagnosis determined that the victim was the explosion, the swimmer immediately felt sharp pain, afflicted with injury to the chest and abdomen (blast injury). coupled with breathing difficulty. Before arriving at the hosExploratory laparotomy was carried out after 4 h of treat- pital, the victim was first brought to a nearby clinic where a ment and observation. Laparotomy revealed free gas in the tube was inserted through the mouth. Upon arrival at the hosabdominal cavity and around 300  ml of old blood fluid. pital, the victim suffered from severe breathing difficulty, There were also four perforations 0.2 × 0.2 to 1 × 0.5 cm in with GCS score of 8, blood pressure of 135/91 mmHg, pulse sizes in the lower segment of the ileum. After the laparot- of 116 times/min, breathing rate of 32 times/min, oxygen omy, the victim went into shock, and balanced electrolyte saturation of 95%, and had to use traditional ventilator (FiO2, was quickly administered. This resulted in diffused moist 100%). Upon inspection, breathing sound was obviously rales in both lungs, and the victim expelled a large volume of weaker on the right side, and external wound was found. foamy and bloody secretion through the tracheal catheter. Preliminary CT scan revealed hemorrhagic lung contusion Diagnosis determined that the victim was afflicted with pul- involving multiple lobes, accompanied by bilateral lung volmonary edema. After tracheotomy, and 1 h of oxygen inhala- ume loss and minor hemothorax on the right side. In addition (use oxygen bubbled through a 95% alcohol solution) tion, no abnormalities were discovered in the thoracic and

Table 30.4  Clinical features and their occurrence rates among 28 cases of underwater blast injury victims

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abdominal cavity. Arterial blood gas analysis indicated severe respiratory acidosis, with pH 7.26, PaCO2 value of 54 mmHg, and PaO2/FiO2 value of 222 mmHg. Thereafter, intrathoracic chest tube was inserted on the right side, and victim was transferred to ICU ward. Early treatment objective was to deal with lung contusion, and measures employed included lung debridement, mechanical ventilation, inhaled corticosteroids. On the first morning after hospital admission, X-ray was undertaken, and 4 h later chest X-ray was performed again, and severe opacification was seen in right side of the chest. Neither arterial blood gas analysis nor body check results pointed to any signs of improvement. Bedside bronchoscopy revealed blood and serous secretion. These discoveries, along with worsening clinical process, further confirm the existence of lung contusion. Therefore, in-depth lung debridement and in-depth treatment continued. On the second morning after hospital admission, as in 10 h after signs of worsening clinical process and adoption of corresponding measures, chest X-ray was once again carried out. Results indicated that ventilation of the right lung began to improve, and body check showed that the victim’s mental response had restored, along with better breathing sounds heard from both sides. On the afternoon of the same day, tube was removed from the victim, switching to oxygen mask inhalation of air with 40% oxygen instead. Victim condition maintained its uptrend and was discharged from the hospital on the same afternoon after fully recovering. Telephone follow-up 2 years later, no sequela or chronic effect of injury was found.

3 Treatment Principles for Underwater Blast Injury Underwater blast injury is a common problem in naval battles, but there are not many articles and reports about how to care for and treat underwater blast injuries. We conducted animal testing by inducing injuries through detonation of TNT underwater, then observed pathophysiological changes of underwater blast injuries and related clinical symptoms and signs, and analyzed treatment principles for underwater blast injury, with the aim of providing corresponding theoretical basis for treatment in the early stage.

3.1 Diagnosis of Underwater Blast Injury 3.1.1 Injury Environment Personnel underwater are extremely susceptible to injury to explosions from objects like naval mine, torpedo, or bomb, and first and foremost it is necessary to ask the victim about his or her body position and posture when injured and distance from point of explosion.

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3.1.2 Symptoms and Signs When there are lung injuries, severe cases may exhibit anoxia and breathing difficulty, and respiratory distress, bradycardia, and sustained low temperature are indications of severe condition. Therefore, these indications may also be used as warning indicators for assessing severity of underwater blast injury. If the aforesaid changes occur, that would mean severe patient conditions and further inspection and corresponding first-aid measures should be undertaken. Moreover, hemoptysis often occurs with lung injuries, and blood or bloody and foamy liquid from the nose and mouth are also common. For those afflicted with serious pulmonary hemorrhage and pulmonary edema, signs may appear similar to severe lung contusion, along with dull sounds from percussion, and weakened breathing sounds with widespread dry or moist rales heard through auscultation. B-mode ultrasound, X-ray, CT scan, and MRI may all be used for diagnosis. 3.1.3 Arterial Blood Gas Analysis Arterial blood gas analysis outcome 30  min after injury shows that lung injury severity is closely associated with drop in arterial partial pressure of oxygen (PaO2). For those with extremely severe or severe lung injury, PaO2 figures 30 min and 6 h after injury are both significantly lower than pre-injury level, mostly falling within the range of 8–9.3 kPa (60–70 mmHg). Meanwhile, changes in PaO2 levels are not obvious in those afflicted with moderate or minor lung injury. PCO2 30 min after injury in cases of extremely severe lung injury is substantially higher than that before injury, and PCO2 levels of those with extremely severe or severe lung injury are obviously higher than those afflicted with moderate or minor lung injury. 3.1.4 Exploratory Laparotomy Research indicates that upon the basis of full resuscitation or simultaneously alongside resuscitation, exploratory laparotomy should be conducted promptly. This is because underwater blast injury often occurs simultaneously with injuries to the abdomen involving multiple organs or body parts, such as multiple intestine perforations. Therefore, laparotomy should not be stopped when one injury has been identified, instead thorough and meticulous inspection shall be performed in order to rule out the possibility of missed diagnosis, which could lead to dire consequences.

3.2 General Principles for Treatment of Underwater Blast Injury Based on experiment and research outcomes, we are of the opinion that treatment of underwater blast injury should follow the basic principles listed below:

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1. Keep airway unobstructed: Immediately clean out any bloody and foamy fluid, blood clots, foreign substance, or other obstructions in the oral and nasopharynx cavities, 2. Protect respiratory function and provide sufficient oxygen: For patients suffering from hemothorax or pneumothorax, large-gauge needle should be used to remove air and blood in the thoracic cavity immediately, and if conditions permit closed thoracic drainage should be undertaken. Provide sufficient oxygen for patient, and when condition permits use oxygen bubbled through a 50% alcohol solution to remove bubbles and facilitate breathing. 3. Rapidly restore body temperature: Excessively low body temperature could seriously suppress cardiac, respiratory, and other functions, which would aggravate underwater blast injury. When treating underwater blast injury patients, pay close attention to changes in body temperature, and for critical and serious cases who's body temperature falls and does not restore, use physical methods, drugs, or warming devices to help the patient warm-up, so as to lessen the impacts of low body temperature on the body. 4. Rest in bed: Minimize activities, and for critical and serious cases strict bed rest should be ordered to reduce pressure on cardiac and respiratory functions, so as to prevent secondary hemorrhage. 5. Prevent gastrointestinal tract perforations from worsening infection in the abdominal cavity: When diagnosis is not clear, avoid orally ingested fluids or foods. 6. Use volume resuscitation: For hemorrhagic shock arising from uncontrolled blood loss, treat patient with limited fluid resuscitation to maintain palpable radial pulse and buy time for evacuation. 7. Evacuate with haste: After patient condition stabilizes, evacuate immediately. For severe cases of lung injury, keep the patient in a head down position to prevent air embolism from entering heart and cerebral vessels, and for those not at risk of air embolism, the semi-reclining position may be adopted. If helicopter evacuation is employed, try to keep flight at a low elevation to avoid potential air embolism risks. 8. Use mechanical ventilation: After first-aid treatment, if full-body anoxia has not improved, consider the use of mechanical ventilation for patients meeting any one of the following circumstances: Respiratory rate > 40 times/min; PaO2 < 60 mmHg; PaCO2 > 50 mmHg; pulmonary shunt >15%; or CAT scan shows scope of lung injury exceeding 28% of total area of lungs. Intermittent positive pressure ventilation (IPPV) or high frequency jet ventilation (HFJV) are the ventilation modes most frequently adopted.

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9. Use compressed oxygen: The compressed oxygen treatment method may be employed for patients with air embolism. Quickly place patient within an environment with 6 bar ambient pressure, then decompress based on how symptoms are allaying, and upon reduction to 2.8 bar ambient pressure, immediately switch to using 100% O2. During the subsequent decompression duration, intermittently use 100% O2. 10. Deal with pulmonary edema and protect cardiac function: Treatment principles are identical to treating general pulmonary edema and cardiac insufficiency, including the administration of dehydration, diuretic, and cardiotonic drugs. For patients with bradycardia, administer 0.5mg to 1.0mg of atropine via intramuscular injection. Administer cortical hormone in large dosage early on to prevent pulmonary interstitial edema. 11. Use blood transfusion and other infusions to combat shock: Pulmonary edema is frequently seen in patients with lung injuries, whose tolerance for liquid would decline. Therefore, volume of transfusion and/or infusion should not be too high, and pace not too fast, and prioritize the usage of whole blood, plasma, and other capsules while lowering the administration of crystoloid solution. When condition permits, utilize central vein and pulmonary artery intubation monitoring of hemodynamics, so as to gain information conducive to guiding fluid resuscitation. 12. Prevent bleeding and infection: Administer hemostatic drugs and a suitable amount of antibiotics to prevent bleeding and infection in the lungs and gastrointestinal tract. 13. Prevent diffused intravascular coagulation and hypokalemia: For cases of serious lung injuries, diffused intravascular coagulation and hypokalemia could occur. In such instances, make use of transfusion of fresh plasma, frozen blood cell and platelet, coupled with potassium chloride IV and other corresponding treatments. 14. Beware of anesthetics: Victims of blast injuries usually have a low tolerance for anesthetics 24–48 h after injury, so avoid surgery early on if possible. If surgery is required, opt for local anesthesia or regional anesthesia in lieu of general anesthesia. If general anesthesia cannot be avoided, refrain from utilizing ether as anesthetic. 15. Perform surgery: Treatment principles for liver or spleen rupture, gastrointestinal tract perforations and other internal organ injuries are same as those for general trauma, but endeavor to keep it simple and safe. 16. Monitor clinical developments closely: All underwater blast injury victims with or without gastrointestinal injury need to be hospitalized and remain under observation for more than 1 week in case of any delayed intestinal perforation.

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3.3 Treatment Principles for Underwater Blast Injury to the Chest or Abdomen Experiment and research outcomes indicate that the lungs are still the main target organs in underwater blast injury, as well as the primary reason for death in the early stage. Thus, early stage treatment of underwater blast injury victims should consider caring for the lungs to be the key objective in rescue effort. Further, the effects of large impulse could also result in internal bleeding due to gastrointestinal tract perforation or liver rupture, and these should also be focal points.

3.3.1 Treatment Principles for Underwater Blast Injury to the Chest Since it is very rare to see serious multi-injuries in underwater blast injuries, after ruling out situations such as fractured ribs, pay close attention to injuries to the heart and lungs. Victims afflicted with minor injuries to the heart and lungs can usually recover after adequate rests and symptomatic treatment, provide mask or nasal tube breathing if condition permits, and make sure patients refrain from arduous activities. For cases of moderate or more serious lung injuries, consider adopting the following treatments: 1. Strict bed rest 2. Ensuring airway stays unobstructed 3. Artificial respiration: If the treatments stated above do not yield obvious results, and if arterial partial pressure of oxygen remains below 6.6 kPa (50 mmHg), consider using extracorporeal membrane oxygenation (ECMO) device. 4. Compressed oxygen treatment: Compressed oxygen treatment can prolong time of survival and improve recovery rate, and it is also beneficial to patients with arterial air embolism. 5. Prevention of pulmonary edema and protection of cardiac function: Pulmonary hemorrhage and edema are often seen in cases of severe blast lung injury, and dehydration measures such as mannitol and furosemide may be applied. When shock occurs, use hypertonic solutions such as hypertonic glucose, hypertonic saline, or plasma, and utilize recovered tissue edema fluid to make up for insufficient blood volume. In order to protect cardiac function, drugs such as digitalis, lanatoside C, and strophanthin K may be applied.

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6. Prevention of blood loss and infection: If patient has been afflicted with serious tears in the lungs and when ordinary non-surgical treatments are ineffective, proceed to surgery.

3.3.2 Treatment Principles for Underwater Blast Injury to the Abdomen 1. Drinking and eating shall be strictly prohibited. 2. For those that go into shock due to injury to solid organ or great vessel, carry out exploratory laparotomy as soon as possible, so as to repair injury and stop bleeding. Examination needs to be done in an orderly fashion, particularly beware of overlooking any issues. Ameliorating shock is a prerequisite for any surgery. 3. Simplicity and safety should be considered paramount for surgery. 4. When there is clear abdominal distension or suspected bowel obstruction, apply continuous gastrointestinal decompression and then if necessary perform surgical exploration.

4 Tiered Treatment for Underwater Blast Injury Blast injury refers to a biophysical and physical–chemical phenomenon. Specifically, this refers to clinical symptoms and changes in pathological and anatomical aspects that occur because a living body has been exposed to a powerful explosion or shock wave. At present, blast injury is still a popular and controversial topic of discussion. For medics involved in treating victims of blast injuries in armed conflicts, blast injury is one of their main focal points. In the past, military medical service support and “time-­ effect treatment” both prove that the outcome of military medical care hinges on the time of care and measure of treatment adopted, hence the rule of “time-effect.” Due to the unique characteristics of underwater blast injury (severe patient condition, high injury death rate, and injury disability rate), studies about its first-aid process and tiered treatment model are important to achieving the best “time-effect” outcomes. In general, the treatment methods of underwater blast injury are largely similar to those for dealing with air blast injury. For overall management process of blast injury, please see Fig. 30.1, and its specific tiered treatment methods are outlined below.

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Explosion occurs Suspected blast injury

Transfer to hospital

Otoscopy

Normal tympanic membrane Exclude explosion blast injury

Ruptured tympanic membrane

Laryngoscopy

Normal larynxipsum

Petechia in larynx

Other causes?

Confirm the diagnosis of lung explosion blast injury

Fig. 30.1  Management process of explosion blast injury

5 Protection Against Underwater Blast Injury Blast injury is common in modern armed conflicts and is the main type of injury inflicted in future hi-tech warfare. In the last three decades, blast injury has risen as a key subject matter in military medicine study and has gained the attention of military medicine researchers both in China and elsewhere across the globe. Shock wave is the result of energy released from an explosion, which is formed when local air is compressed and moves outward at an increasing speed. The pressure of shock wave soars immediately after the explosion, then weakens exponentially. In the beginning, a certain degree of overpressure is created in the surrounding air, and then a certain degree of negative pressure is generated, with the peak negative pressure being smaller than its peak positive pressure. An explosion in water also generates shock wave, but since water is much denser than air; therefore, underwater shock wave propagates at a much higher speed and farther distance. When the same mass of substance explodes underwater, its range of injury and fatality is three times larger than the injury range and fatality range when exploded in the air. The damage that shock wave imparts on the human body had already been broadly publicized and reported after World War I. In naval battles, troops crossing the sea and landing on beaches, amphibious recon troops, marine troops in charge of underwater demining, obstruction

removal, and those that fell into the water were highly vulnerable to underwater blast injury. There were several thousand cases of underwater blast injury during World War II.  The injury mechanisms and injury characteristics of underwater blast injury differ from those of air blast injury. Generally speaking, underwater blast injuries are more severe and more difficult to treat. In the 1970s, we once used plaster and plastic products to create protection against shock wave. These had some degree of effect, but were difficult to actually apply in real-world scenarios. In the 1980s, researchers paired artificial leather with foamed plastic to produce protective suit with the aim of weakening the effects of shock wave. Of which, efforts included bulletproof vest researched and developed by Phillips et al., research on shock wave protection using composite layer consisting of copper foil-covered foam and Kevlar-covered foam conducted by Cooper et  al., research on ceramic-Kevlar composite material carried out by Young et al., and research on the performance of foamed plastic in shock wave protection undertaken by Skews. It was discovered that singularly using foamed plastic, Kevlar, copper foil, and bulletproof vest all worsen shock wave injury inflicted on air-filled organs in the human body, while ceramic-Kevlar composite, copper-foamed plastic composite, and Kevlar-­ foamed plastic composite do not intensify the injury effects of shock wave. As studies on high polymer materials and composite materials advance forward, researchers have obtained more insights into protection against shock wave. In the 1990s, outcome from research by Yang Zhihuan et al. indicates that nickel foam offers rather solid protection against blast injury, including reductions in blast injury severity and fatality rate in test animals. Nickel foam can substantially lower peak overpressure of a shock wave, with the performance even more prominent when material thickness is increased, but at the cost of extended shock wave positive pressure effective duration. Outcomes of studies on the performance of polyurethane materials in protecting against shock wave indicate that initial shock wave force in the polyurethane material created by shock wave would significantly decline with the increase in size of initial porosity of material. When initial porosity is equivalent to 0.25 mm, polyurethane foam material possesses rather prominent anti-shock and pressure reduction characteristic against the load of an explosion. Perhaps the underlying mechanism is associated with the large number of pores and gaps inside the polyurethane material. First of all, pores in the porous material are eliminated because of compaction of the material under the effect of the shock wave, elastic deformation occurs in the pores and gaps, with some of the impact energy turning into elastic energy, while air gaps compress adiabatically and absorb a

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part of the energy. Next, plastic collapse or brittle fracture occurs at the walls of the pores, converting some of the energy into plasticity, while the adiabatic compression process of the air gaps ends. This continues until porous material is compressed to a state similar to compacted material. How the propagation of shock wave declines in porous material is contingent on the energy absorbed and consumed during the compaction process. Foamed plastic also offers some buffering effect under the load of shear stress wave, and at the same time, foamed plastic also exhibits obvious stress wave diffusion under the load of shear stress wave, reflecting the viscoelastic property of polyurethane foam material. Yu et al. studied the role of closed-cell aluminum foam material in the cracking of lightweight composite armor back plate and developed corresponding three-dimensional finite element model. Ballistics experiment results indicate that aluminum plate foam material has obvious effects in many regards from shock wave shielding and collision energy absorption, to reduction or prevention of back plate crack. Yang Zhihuan et al. once tested anti-blast injury performance of a composite material comprised of nickel foam, LC4 aluminum alloy, and sponge bars as main components. Outcome from their research indicates that said composite material offers rather ideal protection against blast injury with peak overpressure range of 388.4–399.7 kPa and positive pressure effective duration lasting from 55 to 60 ms. These function as a certain extent of evidence and reference for the research and production of protective equipment. Cfipps et al. used plastic layer and foamed plastic for glass shaping (GRP/PZ) in an experiment with 17 test animals, demonstrating that said material effectively reduced blast lung injury in the test subjects. It offers better protection than foamed plastic covered with shaped lead. Research by Hattihgh et al. shows that after a shock wave acts on a single-layered material, an intensification wave acts on the wall of the protective material again, which may possibly be related to the movement of the material toward its back wall, and also because of the shock wave passing through the material. On the contrary, this intensification wave does not appear in multi-layered composite material. This is due to the scattering effect from the surface and microporous structure of multi-layered composite material, which endows said material with a higher shock wave viscosity coefficient. Experiment outcomes prove that the scattering effect significantly slows down the propagation of shock wave in such multi-layered composite material, and the propagation velocity of shock wave in this kind of structure is also much slower than that in other types of structure. The varying ways in which shock wave propagates through different composite materials have captured the attention of scientists, but the majority of knowledge about shock wave propagation in composite materials come from analysis of

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linear elasticity of ideal composite materials. The applications of composite material layers in protecting against shock wave have made large progress, and such materials offer more advantages than traditional metallic materials in aspects such as resilience, hardness, weight, and convenience. However, there is not a lot of experiment information about the performance of composite materials in terms of defending against impact and collision. Due to its unique properties, polymers have found widespread application in equipment and components that have to bear pulse dynamic load (i.e. collision, explosion, EMP, thermal pulse, etc.), having replaced some metallic materials that have become scarce. Tedesco et al. previously analyzed how layered structures affect the blast wave of conventional weapons, pointing out that a combination of layered materials can weaken blast wave, but stopped short of specifying what kinds of layered material combinations and structures are more effective in attenuating shock waves. Barker and Oved discovered noticeable decline in a shock wave of certain amplitude when it acted on multi-layered composite material, as well as a certain degree of resonance generated because of multi-layered composite material. Multi-layered composite material structure can support a certain degree of shock wave effects. Due to scattering effect of surface, effective impact viscosity increases as surface impedance and mismatch increase and decreases as surface density increases. Research by Mouritz indicates that composite material after resin casting possesses higher tensile strength than composite material without such treatment. Composite materials with resin casting have relatively few disadvantages and are strengthened against the destructiveness of shock wave. If the materials in the various layers remain the same, arranging them in different sequences can directly affect the strength of the shock wave that propagates through and out of them. When a blast wave acts on GRP composite material layer, more layered fracture would be seen, which reduces the compressions, tension, bending, and stress fatigue of the GRP composite material, while adding stitches could lessen the layered fracture of the composite material. Research shows that stitched GRP composite material layer can markedly weaken a blast wave, but conversely offers less protection against bullets. Research by Woodward et al. on GRP composite material indicates that there are two main destruction processes: First is the dynamic compression before the fracturing of the GRP material, and second is the layered fracture destruction on the surface subjected to impact. Both these processes can effectively stop or reduce the effects of shock wave and fragments. Research by Shah Khan et al. asserts that polyurethane-­ resin composite material has higher strength and elastic coefficient than vinyl-resin. Composite material made from

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polyurethane and resin performs better than that consisting of vinyl and resin. MMC or metal matrix composites are comprised of a reinforcing material coupled with a metal basic material. The reinforcer could be continuous fiber or silk made from high-­ strength material such as carbon, boron or carbide, or short fibers or granules like aluminum oxide, silicon carbide or boron carbide. Compared with base metal without reinforcement, MMC offers unique dynamic and physical properties, hence the material has very promising application potentials in hi-tech and military domains. Some studies have shown that Gr/A1 metal composite is a type of material associated with strain rate, as in the higher the strain rate, the higher the material's tensile strength, buckling strain, and residual strength correspondingly. The material is clearly characterized by the strain rate strengthening effect and dynamic fracture toughness. Other studies have reported that poly carbon fiber-reinforced aluminum composite offers a certain degree of protection from underwater blast wave. Aluminum powder crystal (99.0% purity and 100–200 mesh) is the base material for this kind of composite, while PAN is the basic carbon fiber utilized (7 μm diameter and 200 μm length). The components are pressed to form a hard solid. In 2004, Xing Shuxing and Yin Zhiyong tested underwater blast injury protection performance of composite materials on rats, and their research outcome indicates that a composite material consisting of PC polycarbonate porous material layer-poly ester material layer-hard sponge layer-­ fiberglass layer offers clear underwater shock wave reduction effect, with peak positive pressure lowering by 52.55 ± 3.34% and positive impulse decreasing by 46.98 ± 3.38%. This demonstrates that protective measures such as reflecting interfaces created from the conjunction of high-density and low-density media, energy absorption property of porous medium, prestress introduced to and over-expansion restriction applied to the thoracic and abdominal areas of animals, and the utilization of soft, energy-absorbing materials to prolong the pressure increase duration when a shock wave acts on the animal to slow down the acceleration of the underwater shock wave acting on the body are effective. Water is about 800 times denser than air and is characterized by relative incompressibility and sparsity. Therefore, underwater shock wave is characterized by features such as high speed and long distance of propagation. An air shock wave creates a certain negative pressure, but that is not true for underwater shock waves. Compared with air blast injury, underwater blast injury is characterized by features such as severe injury condition, high fatality rate, and large area of injury. In light of these characteristics of underwater shock wave, it is necessary to adopt protective measures different from those for air underwater shock wave. In terms of body parts damaged in underwater blast injury, in addition to the lungs

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being the main target organs, the heart, small intestine, colon, and rectum are all very susceptible to damage. Therefore, other than protecting the chest area to lighten injury on the lungs, underwater blast injury protection should also strengthen defense of the abdominal area to lessen injuries inflicted on organs in the abdomen. Furthermore, underwater blast injury protection has to be practical. The combination of such protective measures into other gears like life vest should be considered or incorporating multiple functions (i.e. impact protection, burns protection, fragment protection, as well as heat preservation and floatation function) into these protective equipment during the research and production process.

Bibliography 1. Zhengguo W.  Advances in battle injury research. Med J Chin People’s Liberat Army. 2004;29(6):465–7. 2. Zhengguo W.  Underwater blast injuries. Foreign Med Sci. 1986;3(6):321. 3. Zhengguo W.  Blast injuries. Beijing: People’s Military Medical Press; 1983. 4. Zhengguo W.  Blast injuries. In: Ao L, Zhiyong S, Zhengguo W, editors. Modern combat wound surgery. Beijing: People’s Military Medical Press; 1998. 5. Peifang Z. The prevention and treatment of underwater blast injuries. People’s Mil Surg. 2006;49(10):560–2. 6. Peifang Z, Jianxin J.  Research on underwater blast injuries to improve China’s military ability to provide security in special environments. Med J Chin People’s Liberat Army. 2004;29(2):93. 7. Zhihuan Y, Peifang Z, Jianxin J, et al. Characteristics of physical parameters of underwater blast wave and morphological changes of blast injuries. Chin J Clin Rehab. 2004;8(5):895. 8. Zhihuan Y, Peifang Z, Jianxin J, et al. A study on the dose-effects relationship of underwater blast injury. Med J Chin People’s Liberat Army. 2004;29(2):95. 9. Zhihuan Y, Xiaoyan L, Xin N, et  al. A comparative study of the effects of underwater shock waves and air shock waves on biological visceral injuries. Chin J Naut Med Hyperbaric Med. 2006;13(2):65–8. 10. Zhihuan Y, Peifang Z, Jianxin J, et al. Preliminary discussion on the management principles of underwater blast injuries. J Traum Surg. 2006;8(3):234–7. 11. Zhihuan Y, Peifang Z, Jianxin J, et  al. Preliminary discussion on the characteristics of underwater blast injuries. J Traum Surg. 2003;19(2):111–4. 12. Zhihuan Y, Huaguang L, Xiaoyan L, et al. Experimental study on the protection effect of composite materials on blast injuries. Med J Natl Defending Forces Southwest China. 1994;4(3):129. 13. Lili L, Shiwei Z, Ran Z, et al. Study on the theory of aging treatment. Med J Natl Defending Forces Southwest China. 2004;14(2):198. 14. Zhiyong Y, Zhihuan Y, Jianxin J, et al. Preliminary discussion on protection against underwater blast injuries. Med J Chin People’s Liberat Army. 2004;29(2):103. 15. Xiuzhu Z, Jihong Z, Jianxin J, et al. The changes and effect of the lungs and blood gas index after underwater blast injuries. Med J Chin People’s Liberat Army. 2004;29(2):100. 16. Xin N, Xiaoyan L, Zhihuan Y, et  al. A comparative study on the propagation speed and physical parameters of underwater blast wave and air blast wave. Med J Chin People’s Liberat Army. 2004;29(2):97.

464 17. Bo Z, Dawei L, Jianxin J, et al. Morphological changes of the main internal organs in dogs with underwater blast injury. J Third Mil Med Univ. 2003;25(11):938. 18. Anjun X, Guoliang C. The development of modern torpedoes and the inspiration for battle wound treatment. Natl Defense Health Forum. 1999;8(8):28. 19. Yaojie L, et  al. Underwater explosion. Beijing: National Defense Industry Press; 1960. 20. Song Z, Xiaobo L, Weidong T, et  al. Clinical treatment standard for abdominal blast injuries (recommendation). Chin J Traumatol. 2014;30(10):971–3. 21. Haifu W, Shunshan F.  Properties of shock pressure caused by explosion loads in polyurethane foam. Explos Shock Waves. 1999;19(1):78–82. 22. Ruoze X, Zixing L. Studies of dynamic shear mechanical properties of PUR foamed plastics. Explos Shock Waves. 1999;19(4):315–21. 23. Yuanxin Z, Xuefeng Z. Effect of strain rate on the mechanical properties of Gr/A1 metal matrix composites. Explos Shock Waves. 1999;19(3):243–9. 24. Shuxing X.  Preliminary study on protection against underwater blast injuries. Chongqing: Third Military Medical University; 2004. 25. Phillips YY, Zaitchuk J. The management of primary blast injury. In: Bellamy RF, Zaitchuk R, editors. Conventional warfare ballistics, blast and burn injuries, vol. 5. Washington: Office of the Surgeon General Dept. of the Army USA; 1991. p. 299–316. 26. Phillips YY, Zaitchuk J. The management of primary blast injury. In: Bellamy RF, Zaitchuk R, editors. Conventional warfare ballistics, blast and burn injuries. Washington: Office of the Surgeon General Dept. of the Army, USA; 1991. p. 231–2. 27. Melzer E, Hersch M, Fischer D, et al. Disseminated intravascular coagulation and hypopotassemia associated with blast lung injury. Chest. 1986;89(5):690–3. 28. Coppel DL. Blast injuries of the lungs. Br J Surg. 1976;63:735–7. 29. Hadden WA, Rutherford WH, Merrett JD.  The injuries of terrorist bombing: a study of 1,532 consecutive patients. Br J Surg. 1978;65:525–31. 30. Hill JF.  Blast injury with particular reference to recent terrorist bombing incidents. Ann R Coll Surg Engl. 1979;61:4–11. 31. Nguyen N, Hunt JP, Lindfors D. Aerial fireworks can turn deadly underwater: magnified blast causes severe pulmonary contusion. Inj Extra. 2014;45:32–4. 32. Saissy JM.  Focus on: Prehospital and emergency trauma care in disaster medicine-blast injuries. Curr Anaesth Crit Care. 1998;9:58–65. 33. Wightman JM, Gladish SL.  Explosions and blast injuries. Ann Emerg Med. 2001;37(6):664–78. 34. Huller T, Bazini Y. Blast injuries of the chest and abdomen. Arch Surg. 1970;100:24–30. 35. Pizov R, Oppenheim-Eden A, Matot I, et al. Blast lung injury from an explosion on a civilian bus. Chest. 1999;115:165–72. 36. Ho AM-H, Ling E.  Systemic air embolism after lung trauma. Anesthesiology. 1999;90:564–75. 37. Yu CJ, Claar TD, Eifery H, et  al. Applications of porous metal foams in hybrid armor systems. Proceedings of international conference on fundamental issues and applications of shock-wave and high-strain-rate phenomena (EXPLOMET2000). 2000, p. 111.

S. Liu and Z. Yin 38. Glemedson S. Air blast loading interaction of blast wave with structure. In: Glasstone S, Dolan PJ, editors. The effects of nuclear weapons. 3rd ed. Washington: United States Department of Defense and United States Department of Energy; 1977. p. 127–53. 39. Yu JH, Ferguson RE, Vasel EJ, et  al. Characterization and modeling of thoraco-abdominal response to blast waves. Blast Load. 1985;2:189–688. 40. Skews BW, Takayana K. Flow through a perforated surface due to shock-wave impact. J Fluid Mech. 1996;314:27. 41. Richmond DR, Yelverton JT, Fletcher ER.  Far-field underwater blast injuries produced by small charges. Washington: Defense Nuclear Agency; 1973. 42. Phillips MD, Mundie TG, Yelverton JT, et  al. Cloth ballistic vest alters response to blast. J Trauma. 1988;28:S149. 43. Cooper CJ, Townend SJ, Cater SR, et al. The role of stress waves in thoracic visceral injury from blast loading: modification of stress transmission by foams and high-density materials. J Biomech. 1991;24:273. 44. Young AJ, Jaeger JJ, Phillips YY, et  al. Intrathoracic pressure in humans exposed to short duration air blast. Mil Med. 1985;150(1):483–6. 45. Cripps NV, Cooper GJ.  The influence of personal blast protection on the distribution and severity of primary blast gut injury. J Trauma. 1996;40(3S):206S–11S. 46. Hattihgh TS, Skews BW. Experimental investigation of the interaction of shock waves with textiles. Shock Waves. 2001;11:115–23. 47. Sun CT, Hermaun AG. Continuum theory for a laminated medium. J Appl Mech. 1968;35:467–75. 48. Tedesco JW, Landis DW.  Wave propagation through layered systems. Comput Struct. 1989;32(3):625–38. 49. Barker LM, Lundergan CD, Chen PJ, et  al. Nonlinear viscoelasticity and the evolution of stress waves in laminated composites: a comparison of theory and experiment. J Appl Mech. 1974;41:1025–30. 50. Oved Y, Luttwak GE, Rosenberg Z. Shock wave propagation in layered composites. J Compos Mater. 1978;12:84–96. 51. Mouritz AP.  The effect of processing on the underwater explosion shock behaviour of GRP laminates. J Compos Mater. 1995;29(18):2488–503. 52. Mouritz AP.  The effect of underwater explosion shock loading on the flexural properties of GRP laminates. Int J Impact Eng. 1996;18:129–39. 53. Egglestone GT, Gellert EP, Woodward RL.  Perforation failure mechanisms in laminated composites. Materials. 1990;1:1–2. 54. Woodward RL, Egglestone GT, Baxter BJ, et al. Resistance to penetration and compression of fibre-reinforced composite materials. Comp Eng. 1994;1994:349–1. 55. Shah MZ, Ben-Amoz M. On wave propagation in laminated composites-­II. Propag Norm Lamin. 1975;13:57–67. 56. Ding XD, Jiang ZH, Lian JS, et al. Dependence of initial stress-strain behavior on matrix plastic inhomogeneity in short fiber-reinforced metal matrix composite. Mater Sci Eng A. 2004;369(1-2):93–100. 57. Minay EJ, Veronesi P, Cannillo V. Control of pore size by metallic fibres in glass matrix composite foams produced by microwave heating. Eur Ceram Soc. 2004;24(10):3203–8.

Cabin Blast Injury Xinan Lai

1 Overview Here, the term “cabin” includes ship, airplane and armoured vehicle cabins, but also generally refers to enclosed or semienclosed spaces where personnel may be located. Hence, “cabin blast injury” refers to direct or indirect injuries inflicted on personnel inside a cabin environment due to explosion that occurred inside or outside the cabin and may also be known as “blast injury in enclosed space environment.” Cabin blast injuries are frequently seen in wartime when tanks, armored vehicles, above-ground or underground fortifications, or vessels are struck by missiles, cannon shells, land mines, or other high-explosive ammunitions. During peacetime, cabin blast injuries could occur in terrorist bombings, such as detonation of improvised explosive devices inside public buses, train coaches or subway coaches, or car bombs outside buildings. In addition, when explosive substances (i.e. fireworks, firecrackers, pyrotechnics items, etc.) explode indoor during production or storage, or accidental explosions involving high-pressure boilers in factories could also cause cabin blast injury. In modern warfare, the frequency of cabin blast injury is much higher than open space blast injury. This is because an increasing number of combatants rely on ground surface cabins (tanks, armored vehicles, field fortifications, permanent above-ground fortifications), underground cabins (tunnels), water surface cabins (naval vessels), and underwater cabins (submarines) during armed conflicts. During the Gulf War in 1991, the U.S. military and Iraqi military fielded some 8500 tanks, and even though ground battles totaled only about 100 h, 4200 Iraqi tanks and 2800 armored vehicles were destroyed, along with nearly 70,000 of fatalities and wounded of Iraqi troops. During the Falklands War in 1983, within a month and a half the Argentinian and British navies, respectively, suffered from 11 and 18 sunk or damX. Lai (*) Army Medical Center of PLA, Chongqing, China

aged vessels. During the War in Afghanistan that began in 2001 and the Iraq War that commenced in 2003, the U.S. military deployed 40% of armored vehicles in service, and 63–70% of American and coalition troop injuries came from armored vehicle cabins being struck by high-explosive antiarmor rounds. During the Afghan War (1984–1987), the Soviet military lost 1461 tanks and armored personnel carriers, and during the Battle of Grozny in the Second Chechen War (1999–2000), 75% tanks and 85% armored vehicles of the Soviet 131st Motorized Rifle Brigade were destroyed. Due to the highly destructive power of weapons used to attack cabins and spatial properties of cabin such as enclosed or semi-enclosed environment, cabin blast injuries are characterized by features such as severe injury, high injury death rate, blast injury, and high rate of combined injuries. For instance, fatality rate for casualties in armored vehicle cabin or vessel cabin could exceed 60%, three times more than regular battle death rate, while composite injury rate is three to five times higher than that of regular infantries, and burns rate is 10–20 times more likely to occur than regular infantries.

2 Types of High-Explosive Ammunitions Used to Strike Cabins There are a plethora of high-explosive ammunitions used against cabins. For instance, based on the type of target, ammunitions may be categorized as anti-armor ammunitions, anti-ship ammunitions, or hard-target penetration bombs; based on the branch of armed forces equipped, ammunitions may be categorized as army, navy, or air force ammunitions; based on the application feature, ammunitions may be categorized as artillery shell, bomb, torpedo, naval mine, missile, rocket, aerial bomb, or demolition device; based on destructiveness, ammunitions may be categorized as explosive ammunitions or kinetic energy penetrator, with the former relying on high-­energy explosive in

© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 Z. Wang, J. Jiang (eds.), Explosive Blast Injuries, https://doi.org/10.1007/978-981-19-2856-7_31

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the warhead to explode and destroy cabin, while the latter uses purely kinetic energy derived from high velocity generated by high-pressure gas of the propellant to penetrate the cabin or penetrates first and then explodes to destroy the target cabin. To better understand the features of cabin blast injuries due to strikes from weapons, the next section provides explanations about military high-explosive ammunitions used to attack chambers based on the injuring characteristics of ammunitions.

2.1 Explosive Ammunitions 2.1.1 High-Explosive Ammunition and HighExplosive Fragmentation Ammunition High-explosive ammunition usually has thin casing, and a sizable quantity of high-energy explosives are packed inside the shell, amounting to some 50–80% of the total weight of the ammunition. The direct effects of explosion or impact of explosion are used to destroy cabin targets. Naval mine, land mine, aerial bomb, missile, among others, belong to this type of ammunition. Naval mines and land mines can hold large charges that yield serious destructive power. They are also cheap to produce and easy to deploy, which are why they are the most common kind of ammunition used to attack cabins. Between 1950 and 2001, among the types of weapons used to attack American naval vessels, naval mines ranked first with 77%, followed by aerial bombs in a distant second with 11%. 70% of U.S. tanks destroyed during the Vietnam War in the 1960s and 1970s came from land mines. High-explosive fragmentation ammunition relies on primary fragments to damage personnel, structures, and material, and charge usually accounts for 20% of the ammunition’s weight. This type of ammunition is chiefly used against personnel. However, if the ammunition explodes near a cabin and when fragments carry enough kinetic energy, the lightly protected cabins like those of light armored vehicles may still be penetrated. 2.1.2 High-Explosive Anti-tank Warhead Also known as shaped charge, these warheads are characterized by a hollow metal liner (often copper or aluminum) which formed in a conical or hemispherical shape, and typically bonded to the explosive fill on the convex side. Upon explosion, the metal liner is rapidly collapsed by the charge, and when the resultant velocity of the metal on the surface of the liner exceeds the rate of collapse, the metal would be turned into a superplastic jet with higher energy density, with the velocity of the jet capable of reaching 7000–14,000 m/s and a temperature of 500 °C.  The jet could generate peak pressure of 100–200 GPa on the armor plate, and after weakening the average pressure ranges around 10–20 GPa. The high pressure resulting from the mutual effects between the

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hot metal jet and target plate causes lateral displacement in the target plate, which would then be penetrated and pierced by the jet. If the resultant velocity of the metal on the surface of the liner does not exceed the rate of collapse, it would create a high-speed projectile also known as self-forging fragment submunition, which would reach a speed of around reaching 1500–3000 m/s and penetrate cabin using its own powerful kinetic energy. Anti-tank rockets, artillery shells, anti-tank missiles, and certain anti-ship missiles use highexplosive anti-tank. The metal jet would create devastating injuries if the jet penetrates the armor and directly strikes personnel inside cabin, causing large losses and damage to tissues and severe burns. Personnel not in the direct path of the jet would be injured mostly by fragments that break off from the cabin.

2.1.3 Enhanced Blast Warheads These warheads, a new sort of enhanced blast weapons, include fuel air explosive and thermobaric ammunition, and are often seen in aerial bombs, artillery shells, and rocket shells. The first generation of enhanced blast warhead is known as fuel air explosive bombs. Such ammunitions are loaded with liquid hydrocarbons, a type of easily gasified fuel. When the payload explodes in the air above the target, the fuel is dispersed and creates a cloud of mixture with oxygen in the air (thermobaric zone), and then this cloud would be ignited. Pressure in the explosion center in the thermobaric zone could reach 2–3 MPa, and sustained explosion duration is several dozen times longer than those from highenergy explosives such as TNT. Remaining fuel would continue to combust, forming a fireball with temperature upward of 1500–2000 °C.  Since overpressure effective duration of the shock wave of the thermobaric zone could last several tens of milliseconds and create high impulse, its explosive power is five to ten times more powerful than TNT of the same mass. This is why fuel air explosive is often considered the current number one explosive when it comes to harm and death to personnel and obliteration of equipment and fortifications. The new generation of fuel air explosive is a thermobaric weapon, which carries solid charge comprised of the explosives with high velocity of detonation and oxidizers such as ammonium nitrate and aluminum nitrate, and powdered flammable metal like aluminum, magnesium, and zirconium. Upon dispersal, the combustion cloud zone consisting of micro solid explosive substance would be detonated, generating higher shock wave overpressure and releasing more heat energy than fuel air weapons of the past. 2.1.4 Improvised Explosive Device IED broadly refers to bombs built from military ammunition or civil explosives and is used in forms such as suicide bomb, car bomb, and roadside bomb. Improvised explosive device could contain a sizable amount of explosives and is often

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detonated with a timer or remote control in close proximity to armored vehicles or buildings; therefore, they can cause serious injury and death for personnel inside these cabins. During the Iraq War and War in Afghanistan, IEDs had become an increasing bane to U.S. soldiers, with troop injury rising from 20% in the beginning to 60% later on.

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2.3 Composite Ammunition

This type of ammunition combines two or more destructive effects of the ammunitions introduced above, such as semi-­ armor piercing high-explosive anti-ship missiles rely on its own kinetic energy to defeat ship armor, then explode inside after penetration, using high-speed projectile, random fragments, and shock wave to damage the target cabin. Artillery 2.2 Kinetic Energy Ammunition shells, rocket bombs, and anti-tank missiles often employ shaped charges that form jets of hot metal to defeat armored 2.2.1 Armor-Piercing Shell targets, while the shrapnels generated from the explosion of the This type of shell features initial velocity exceeding 900 m/s body of the ammunition are effective weapons in wounding and high accuracy, relying on its high kinetic energy to pen- and killing personnel. In addition, to enhance damage, cometrate and damage cabin and to injure and kill personnel posite ammunitions are often loaded with other components inside. These ammunitions are commonly seen in tank guns, such as incendiary, igniting agent, or smoke agent, which anti-tank artillery, naval guns, and coastal artillery, but anti-­ would enter the cabin along the explosion to injure personnel tank missiles and anti-ship missile warheads often adopt this via burns or gas inhalation and cause damage to equipment. structure as well. Structure of armor-piercing shell primarily falls into two categories. The first category features a solid structure with warhead or core made of dense, rigid, and 3 The Influence of Cabin Structure tough material like tungsten or depleted uranium, and the on Blast Injuries parts of the shell remaining after piercing through armor plating and fragments broken off from plating are the main 3.1 Level of Enclosure injury-causing factors. The second category has a charge chamber instead, which would be loaded with a small amount Based on the level of enclosure, a cabin may either be classiof explosives and detonated after penetrating into the cabin, fied as enclosed or semi-enclosed. An enclosed cabin refers causing damage and injury a second time via explosion. to an indoor space that is completely enclosed, like those Depleted uranium and tungsten alloy armor-piercing war- inside vessels, tunnels, tanks, and armored vehicles, and the heads generate heavy metal aerosol particles during the pen- interior air, temperature, and humidity are all controlled by etration process. Depleted uranium aerosol could enter the regulating devices. A semi-enclosed cabin refers to spaces body through the respiratory tract, digestive tract, skin and such as public bus, building, and field fortification, where mucosae, wound, and other pathways, leading to internal indoor environments that are covered but still connected with radiation injury and heavy metal poisoning. In addition, the outside via openings like doors, windows, and observadepleted uranium warheads could easily heat up and ignite tion ports. Air inside and outside the cabin flow naturally, under hi-speed collision and have relatively powerful incen- and temperature and humidity inside are basically the same diary effects. Inhaling substantial amount of aerosol tungsten as those outside. The cabin enclosure level is closely associparticle could trigger damage to kidney functions. ated with blast wave propagation inside, as well as the transmission of heat and dissipation of smoke.

2.2.2 Deep Penetration Warhead This kind of munition is used for attacking defensive fortifications buried underground. Its penetrative warhead is capped with high-­strength steel or heavy metal alloy material, inside of which would be explosives linked to a delayed fuse, giving the warhead time to penetrate deeper underground before detonation. U.S. Air Forces claimed the destructive power of bunker buster aerial bomb, one type of deep penetrating warhead, is 10–30 times bigger than when the same mass of explosive is detonated on the ground. During the Gulf War in 1991, the U.S. Air Force fired two bunker busters at a civilian underground bomb shelter located in capital Baghdad. The body of the ammunition penetrated reinforced concrete 2.15 m thick and the cover layer before exploding, instantly killing more than 400 people hidden inside.

3.1.1 Complex Shock Wave When an explosion occurs inside a cabin, the blast wave acts on the walls of the cabin, leading to reflection and diffraction and creating a complex shock wave comprised of the incident wave and the subsequent series of reflection waves. Unlike the simple shock wave in a free field like that from an explosion in an open space, the peak overpressure of a complex shock wave could be two to eight times more powerful than a free field simple shock wave, while positive pressure effective duration could last anywhere from several milliseconds to more than 10 ms. A simple shock wave surges to its peak pressure at an instant’s notice, then exponentially decays to ambient pressure, with positive pressure effective duration mostly staying within a range of several hundred

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microseconds to 1 or 2 ms. But since a complex shock wave has higher peak overpressure and longer positive pressure effective duration, it causes more damage to the tissues of personnel inside the cabin, resulting in worst fatality rate. For instance, terrorist bombing on public bus could cause death rate up to 49%, while explosion from the same mass of explosives in an open space would only be 8% or so.

3.1.2 Difficulties in Heat and Smoke Dissipation The heat released from the explosion and leftover fuel of the projectile could quickly elevate the temperature inside the cabin. If said temperature reaches the ignition point of some of the more flammable items, additional combustions could occur, and the high-temperature and high-pressure state of the cabin also speeds up the rate of combustion of flammable materials. The occurrence rate of combustion inside cabin and burning personnel is many times higher than open space explosion, with larger areas of and more severe burns. During the Fourth Arab–Israeli War (October War) in 1973  in the Middle East, the occurrence rate of burns in tanks and armored vehicles hit by anti-tank weapon was three times higher than those suffered by infantry, and “anti-tank weapon complex” characterized by blast lung injury, blast injury to eardrums, injury from inhalation, and injury to the eyes appeared. During the Falklands War in 1982, of the injured British navy sailors, 34% suffered burns and serious cases had more than 60% body area burned. Due to the enclosed environment of cabins, smokes generated from explosion and combustion will not dissipate as easily, and carbon monoxide, dust, and particulate matters produced by smokes inhaled by personnel in the cabin will irritate and corrode respiratory tract and lung tissue, with chemical pneumonia or pulmonary edema in serious cases. When a fuel air explosive hits a tunnel or fortification, the combustion of the fireball derived from leftover fuel could consume all oxygen inside, and other than the shock wave and high heat inflicting blast injuries and burns to personnel inside, suffocation is also a main cause of death for those in the cabin.

3.2 Cabin Construction Material Cabins could be built from a wide range of materials from wood and reinforced concrete to steel, aluminum, and soil. The varying physical and chemical properties and differences in ignition point of materials differ drastically, and these variables have a significant impact on the secondary damage deriving from explosion.

3.2.1 Fragments of Cabin Steel has a density of 7.85 g/cm3, elasticity modulus under room temperature of 190–220 GPa, and shear modulus of

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70–80 GPa. Wood meanwhile has a density of 0.54 g/cm3, elasticity modulus under room temperature of 9.8–12 GPa, and shear modulus of 0.5 GPa. Since the aforementioned physical and chemical properties of steel and wood differ by two to three orders of magnitude, cabins made out of the two materials differ markedly in standing up to an explosion. Under the effects of a blast wave and high-speed projectiles, a steel cabin has a much smaller chance of being destroyed compared to a wood cabin, but once the cabin has been damaged, the interior of the steel cabin would be filled with cabin fragments that are high in mass and kinetic energy, which would result in more severe injuries to personnel. Interior of wood cabin meanwhile would be the opposite, cabin fragments are relatively lower in mass and kinetic energy, therefore causing less grievous injuries to personnel struck compared with steel debris.

3.2.2 Combustion Wood has an ignition point of 220–229 °C and therefore could start burning easily. The ignition point of aluminum is merely 550 °C, much lower than steel’s ignition point of approximately 1300 °C. Vessel and armored vehicle cabins made from aluminum alloys inflict more serious burns on personnel inside if combustion occurs after being hit. During the Falklands War in 1982, when a torpedo fired by the Argentine Air Force hit the British destroyer HMS Sheffield, combustion of the bridge’s aluminum alloy materials was a major reason for the severe burns suffered by personnel onboard. 3.2.3 Derivative Shock Waves Blast wave outside could pass through cabin walls, enter the interior of the cabin and form derived air shock wave. In an experiment, 2.2 g of RDX (charge density of 1.34 g/cm3) was attached tightly to an enclosed container with 1.0 cm-thick steel wall. Pressure sensor was used to measure pressure inside the container at the instant of the detonation, and high-­ speed Schlieren photography was used to observe the whole process of shock wave propagation inside the enclosed container. The researchers discovered that the overpressure of the incident wave inside the container could reach 0.030 MPa. The result suggests that when the shock wave from the explosion enters the steel wall, other than the absolute majority being reflected, a small portion of the wave was still projected onto the free surface on the inside wall of the enclosed container. Under the effect of the shock wave, the free surface moved forward, compressed air in front of it and generated derived shock waves. 3.2.4 Impact Shock, and Compressed Wave and Seismic Wave in Soil When the cabin exterior is in contact with an explosion or when an explosion occurs inside a cabin, some of the energy

Cabin Blast Injury

of the explosion would couple with the walls and plates of the cabin and propagate toward the surroundings in the form of stress waves, creating impact shock, and compressed wave and seismic wave in soil. The walls of vessels, tanks, and armored vehicles are mostly constructed from steel plates and other materials that are dense, not very compressible, and do not consume much deformation energy. On the contrary, they can transfer pressure quite well, and when a stress wave propagates along cabin walls and plates, two kinds of impact shock would occur on the walls and plates: First is local acceleration of walls and plates at anywhere from 100 to 1000 g during the instant of the explosion. The acceleration lasts some microseconds, does not cause much displacement, and could increase axial stress on body parts such as limbs and spinal cord in contact with the wall or plate, which might result in bone fracture if stress exceeds fracture threshold. Second is the bending of the wall or plate, as well as the movement of the whole armored vehicle or vessel, and the resulting tossing. At this moment the cabin’s acceleration would be around less than 100 g and could last for seconds, throwing personnel in the air or against the cabin walls and plates and causing collision injury. When underground fortification constructed from soil, rock, and reinforced concrete is hit by an explosive weapon, soil compressed by the shock wave or the contact of the weapon against the ground and exploding would generate compressed wave and seismic wave in soil. When compressed wave and seismic wave in soil act on underground tunnel and fortification, reflections would occur. The overpressure of the incident wave could be several times more powerful than the overpressure of the reflected waves, which would cause serious damage to fortification and injure personnel stationed inside.

4 Injuring Mechanisms Mechanisms behind damages caused to cabin and injuries inflicted upon personnel inside when cabin is struck by ammunition may be classified into either primary or secondary. Primary mechanism refers to direct effects of the ammunition, such as penetration, blast, fragment, heat, and other damaging and injuring effects. Secondary mechanism meanwhile refers to secondary damaging and injuring effects resulting from the aforesaid mechanism, such as secondary fragments, craters, additional explosions, and combustions.

4.1 Primary Mechanism 4.1.1 Penetrating Effects Bunker buster and high-explosive anti-tank create hot metal jet flow that penetrates through cabin plate and wall, damag-

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ing the cabin and injuring personnel inside. This is called penetrating effect. Armor-piercing shell, bunker buster, and high-speed projectile can use their high kinetic energy to penetrate into cabin, damaging the cabin and injuring personnel inside. When a warhead collides with cabin plating at high speed, the spot of contact bears immense pressure (30–50 GPa), and when the pressure exceeds the cabin wall material’s yield strength, the spot of cabin wall struck by the ammunition would structurally deform, the cabin plate would be plugged or be broken. When the ammunition enters the cabin, if there is enough kinetic energy in the remaining shell or fragments broken off from the cabin wall, they could kill personnel within and detonate or ignite ammunition contained inside. Cabin wall, under the effects of impact load, would generate compression wave, shear wave, or other types of stress waves with high velocity and big amplitude, which could lead to slight displacement and acceleration in cabin plating within several milliseconds, leading to noticeable macro movements like bending or vibration. Body parts directly in touch of cabin plating near the spot struck by ammunition could be injured in forms such as soft tissue contusion, bone fracture, contusion of thoracic and abdominal organs, and impairment of peripheral nerve conduction. High-explosive anti-tank rounds could generate hot metal jet flow with acceleration of up to or exceeding 7000 m/s at the front, and the mutual effects between the jet flow and cabin wall would create a super high-pressure penetration at the GPa level capable of defeating and piercing cabin walls. The extensiveness of destruction of cabin wall caused by the high-speed jet flow penetration depends on the thickness and strength of the cabin wall material. When a jet flow pierces a reinforced concrete cabin wall, the diameter of the perforation created would be five to seven times the diameter of the jet, and the concrete on the path of the jet flow would burst from the back of the cabin wall (engineering equation for calculating concentrated jet flow penetration of concrete panel). Metal material hit by a jet flow could be damaged in the form of cratering, layered fracture, or perforation. When a metal cabin wall is perforated, the remaining high-­temperature metal jet flow containing metal particles and cabin wall fragments would turn into a high-energy fragment cloud that could hit personnel in high density, causing large areas of damage and loss of tissue and burns to deep tissue.

4.1.2 Blast Effects Static overpressure of shock wave and dynamic pressure of blast wind created by the explosion could damage cabin and injure or kill personnel in what are collectively termed blast effects. Blast effects are most obvious with explosive ammunition, and sometimes kinetic ammunition hitting a cabin at high speed could also produce blast effect.

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When high-energy explosives such as RDX, TNT, or plastic explosives (C4 or Semtex) in the charge of an explosive ammunition explodes, a substantial amount of high-­ temperature and high-pressure gases would be generated at an instant, rapidly compressing gaseous medium surrounding the point of explosion, and drastically and immediately elevating its density, pressure, and temperature. The interface (wave front) between said compressed gas layer and uncompressed gas layer is the shock wave. At the interface, the level of static pressure exceeding atmospheric pressure is the static overpressure, and it decays in the air to the reciprocal of the distance cubed from the explosion center, or put it differently, overpressure at twice the distance would be 1/8 of overpressure at the explosion center. For example, when 1  kg of explosives detonate and create shock wave static overpressure of 500 kPa at the explosion center, static overpressure at a spot three meters from the explosion center would drop to 18.51 kPa. When the shock wave from an explosion inside a cabin, or when shock wave from an explosion outside enters a cabin through channels or cabin wall cracks, due to reflections from cabin walls and concentrations at cabin corners, in addition to the surge in indoor temperature of the cabin caused by the explosion, a shock wave’s peak static overpressure could soar by several to several dozen times, while positive pressure effective duration would also extend. As the shock wave front propagates forward, static overpressure behind the front would gradually decline, eventually turning into negative pressure. Cabin subjected to static overpressure could be crushed, deform, collapse, or suffer other structure destruction, and human organs containing air such as eardrum, lungs, and gastrointestinal tracts could be afflicted with contusion, tear, or other injuries under the effects of static overpressure. Compared with the pressure tolerance of buildings, human organs have relatively strong injury resistance against static overpressure. For instance, static overpressure reaching lung injury threshold is around 210–280 kPa, but the same static overpressure is more than enough to damage reinforced concrete structures and buildings. Due to the pressure difference, air behind the shock front would flow toward explosion center rapidly, creating blast wind or else known as “drag wind,” and its impact on a target is known as dynamic pressure. Peak dynamic pressure is related to cube of wind speed, and effective duration is longer than that of static overpressure. The generation of blast wind depends on static overpressure. For instance, at a static overpressure of 7 kPa, blast wind could reach a maximum velocity of 17 m/s, and 73 m/s when static overpressure is 34.5 kPa. When a blast wind is strong enough, it could displace, toss, and strike the human body, with bone fracture, skull fracture, organ bleeding or rupture, and disfiguring amputation in severe cases. Combat injury investigation indicates that under the effect of blast wind, if movement of

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a 70  kg human body equals to or exceeds 3 m, fatality is likely to occur; when movement is more than 1.5 m but less than 3 m there would be serious injury; and when movement is between 0.3 m and 1.5 m, injury severity hinges on angle of strike against another object and could range from no obvious injury to moderate injury. In addition, blast wind could mobilize sand, rocks, wood splinters, and glass shards nearby, weaponizing them into secondary projectiles that could wound anyone struck. When a shock wave’s static overpressure and blast wind act on the human body, the static overpressure tolerance of the person’s organs and tissues clearly declines. For instance, static overpressure that only causes eardrum rupture in 1% of victims when acting alone could be fatal when combined with a blast wind with maximum velocity of 73 m/s (Table 31.1). During a cabin explosion, the majority of personnel inside would be afflicted with both static overpressure and blast wind, which is why injuries are often severe. For example, when an armored vehicle drives over a land mine, shock wave static overpressure concentrates stress locally on longer bones of the limbs of the passengers, and the subsequent blast wind that tosses the crew around would cause bone fractures at those spots of high-stress concentration.

4.1.3 Fragmentation Effects Fragmentation effects refer to injuries and deaths caused by fragments dispersed from the shell of the ammunition upon explosion. Ammunition fragments could be categorized as random fragments, preformed fragments, semi-preformed fragments, and high-speed projectiles. Random fragments are naturally formed from the bursting of the shell, and fragments could fly at speeds somewhere between 1500 m/s and 2000 m/s. The shape, size, mass, and number of fragments are random. Preformed fragments are those loaded into the shell by design, while semi-preformed fragments come from a piece of slit material in the shell, which would readily break off into fragments upon being shattered by the detonation of Table 31.1  Synergistic injury effect of static overpressure of shock wave and dynamic pressure of blast wind Peak static Maximum wind overpressure (kPa) speed (m/s) Human injury effect 7 17 Flash burns 14 31 Fragment injuries (glass shards) 21 46 Serious injury can result in death 34.5 73 Fatal injury occurs frequently 69 131 Fatal most of the time 138 224 100% death Zipf, K.  R. J., & Cashdollar, K.  L. (n.d.) Explosions and Refuge Chambers. Aug 14, 2016. www.cdc.gov/niosh/docket/archive/pdfs/ NIOSH-125/125-ExplosionsandRefugeChambers.pdf

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explosive. Preformed fragments, semi-preformed fragments have more uniform kinetic energy and penetration power and can cause more damage to cabin and those inside compared with natural fragments. High-speed projectiles are formed from explosion of warheads of armor-piercing shells, and properties such as high mass, high speed, and structural shape are conducive to breaching armors (analysis of damage and destruction caused by warhead of semi-armor-­ piercing explosive anti-ship missile). Fragments driven by explosives can cause a large area of damage and injury, some ten times more than that of shock wave. Weapon research and production organizations usually consider fragments with 80 J of higher kinetic energy to be capable of injuring, including immediately incapacitating or even fatal wounds. However, from blast injury rescue instances it can be observed that effectively injuring fragments depend on not only kinetic energy, but the relationships between anatomical features of the body part struck and injuring effects are also crucial. When a fragment with kinetic energy below 80 J hits the heart or a large vessel, the wound could be lethal. When a fragment with kinetic energy above 80 J strikes soft tissue of the limbs but does not damage large vessel, such injuries are mild and combatant would not be incapacitated right away. When a depleted uranium fragment stays in the body for an extensive period, depleted uranium content in the body would rise significantly. The chemical toxicity of and radiation injury of heavy metal are not to be ignored and could cause cancer or mutations. Depleted uranium in the body could result in chronic injury to the liver and kidney and damage to the reproductive system.

4.1.4 Thermal Effects Damages to cabin and injury or death of personnel caused by heat energy released from the detonation of explosives are called the thermal effects of explosion. When high-energy explosives such as TNT explode, one-­ third of chemical energy converts into shock wave and high temperature (2500–5000 K) at the instant of explosion, and the remaining two-thirds are released slowly in the form of combustion. The fireball resulting from this combustion could reach a temperature of 2000–3000 K and last for milliseconds. Enhanced-shock wave ammunitions like thermobaric bomb and fuel air explosive disperse and detonate energetic heterogeneous mixtures to produce a thermal effect. The fireball resulting from such weapons is several times or several dozen times larger in terms of diameter and duration time than those formed by high-energy explosives such as TNT. When an armor-piercing shell or bunker buster penetrates a target, the powerful impact would rapidly raise the temperature of the core or shell. Depleted uranium or zirconium particles in armor-piercing shells that contain such metals might spontaneously combust during the armor-­

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piercing process. When a high-explosive anti-tank explodes, it creates a metal jet flow comprised of microscopic metal fragments that could reach a temperature of around a thousand degrees. Due to the enclosed environment of a cabin, high temperature from the explosion or leftover fuel of the missile will not dissipate quickly, and this heat inflicts obvious injury upon personnel inside the cabin in the forms of transmission, convection, and radiation. Smoke produced from combustion contains toxic gases such as carbon monoxide, nitrogen monoxide, nitrogen cyanide, hydrogen chloride, and formaldehyde. These toxic gases would stay within the enclosed environment of a cabin for prolonged duration, and personnel inside could easily be poisoned. Moreover, combustion also uses up oxygen and could potentially kill by suffocation.

4.2 Secondary Mechanisms 4.2.1 Secondary Fragmentation Effects When struck by an explosive weapon, damage of the cabin and equipment inside the cabin, scattered parts of cabin, equipment fragments, glass shards, rocks, and other secondary fragments and splinters could further cause damage and injury. These are known as secondary fragmentation effects. Secondary fragments fly at speed much lower than other fragments and metal jet flow fragments, and transfer energy upon hitting the human body through cutting or crushing. Secondary fragments of high mass could cause destructive injuries to personnel, while secondary frags with smaller mass would usually inflict non-fatal, soft tissue injuries to the torso and limbs. 4.2.2 Cratering Effects When an explosive ammunition detonates near the ground, upon contact with the ground or after burrowing a certain depth underground, or when a bunker buster explodes after penetrating deep underground, soil and rocks around the point of explosion would rapidly compress due to the effects of products of explosion and shock wave, leaving an explosion cavity and resulting in the cratering effect. For example, if an explosion occurs relatively deep underground, there might not be a bulge or collapse on the ground surface. If an underground explosion occurs relatively closer to the surface, soil on the ground surface would rapidly move upward due to pressure inside the cavity beneath, bulging or throwing media outward, and leaving a crater. Cratering from explosion and the stress wave generated by drastic compression of media surrounding the point of explosion could cause damage or collapse of cabins in underground or above-­ ground fortifications within a certain area, and personnel inside these cabins would be buried or crushed.

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4.2.3 Secondary Blast or Ignition Effects If a cabin is struck with ammunition that explodes, and such explosion causes ammunitions or flammable items contained inside the cabin to explode or ignite, the resulting cabin damage and personnel injury are called secondary blast or ignition effects. A secondary blast would occur when pressure of the initial blast wave is greater than or equal to the critical initiation pressure of the explosive item. Secondary blasts also happen when explosion product, high-speed projectile or fragment, or hot metal jet flow hits ammunition inside the cabin. Secondary blasts often obliterate a cabin completely, and personnel within usually will not be spared from death or critical injuries. When heat energy released from the ­initial explosion reaches the ignition point temperature of flammable objects, secondary ignition would take place. 70% of British tanks in World War II ignited after being hit.

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lated explosion source would be detonated inside or outside the cabin. These studies reveal insights about local or bodywide pathological and physiological changes induced by single or composite injuring factors of the tested weapon or ammunition and serve to verify theories about cabin blast injury mechanisms and treatment of such injuries. In recent years, the Field Surgery Research Institute (currently Army Medical Center) of the Third Military Medical University of the People’s Liberation Army has carried out relatively systematic animal testing using live rounds to induce destructive effects, and studies based on laboratory simulations, having accumulated a rather comprehensive set of test and experiment data about features and injuring mechanisms of cabin blast injuries, and their treatments. In this chapter, cabin blast injury features not only reference past injury cases in battle and terrorist attacks of enclosed environments, but also cabin blast injury research outcomes produced by said research institute.

5 Features of Cabin Blast Injury There are two main pathways to gain an understanding about the features of cabin blast injuries. The first is to analyze past cabin blast injury cases, such as cases of blast injuries in armored vehicle cabins or naval vessel cabins, or blast injuries in enclosed environments targeted by terrorist attacks. The second is to conduct animal testing using live rounds to induce destructive effects, and studies based on laboratory simulations. Cabin blast injuries are the most realistic, but they are hard to access. At the same time, there are limitations such as form of combat, environment of explosion, type and equivalent mass of explosion ammunition involved, which make it difficult to gain a thorough understanding about related injuries. Animal testing conducted using live rounds to induce destructive effects and studies based on laboratory simulations can supplement the shortcomings of real-world combat data and provide a more comprehensive comprehension about the features of injuries inflicted upon personnel inside a cabin struck by different kinds of explosive ammunition. Animal tests conducted using live rounds to induce destructive effects are based on actual combat exercises designed based on specific forms of battle. Live rounds are used to strike targets such as tanks, armored vehicles, underground or aboveground fortifications, buildings, or 1:1 models of vessels, armored vehicles, and other cabins, then researchers would perform observations of injury conditions of animals placed inside targets, so as to determine the probability and features of injury if people were housed inside such target cabins. Studies based on laboratory simulations rely on simulated armored vehicle or vessel cabins containing small test animals, then a small equivalent mass of simu-

5.1 Severe Injuries and High Death Rate Death rate of cabin blast injuries is much higher than average death rate of ground surface battles. In all ground surface battles since World War II, average fatality rate of combatant fluctuates around 18–20%. Analysis of statistics of 769 injured or killed riders in British tanks and armored vehicles during World War II reveals a death rate of 37%, one-third of burned victims were afflicted with third-degree burns, and 45% of limb injuries were open fractures and disfiguring amputations. The majority of these injured British armor troops were caused by armor-piercing shells (51%), followed by high-explosive anti-tanks (37.5%), anti-tank mines (8%), and other weapons (3.5%). Death rate of Soviet tank troops reached as high as 69% and severe injury rate was 22%, while minor injury rate was only 9%. On May 17, 1987, Dassault Mirage F1 fighter, an Iraqi jet aircraft, fired two Exocet missiles at the American frigate USS Stark, with death rate as high as 69%. In terrorist bombings, the death rate, primary blast injury occurrence rate, and area of body burned in bus bombings are all several times higher than blast injuries in open spaces. Statistics of terrorist bombings with 30 or more persons injured that took place in 27 nations between 1991 and 2000 show that occurrence rates of blast lung injuries, blast lung injury complications and pneumothorax in buildings, subway stations, hotels, and other enclosed environments are three times higher than explosions in open spaces. Similarly, eardrum rupture, bone fracture, and burns occurrence rates are, respectively, six to seven times, three times, and 22 times higher than those in open areas (Table 31.2 and Table 31.3).

Cabin Blast Injury Table 31.2  Comparison between bus bombing and open space blast Open space blast Bus bombing Mortality 8% 49% Occurrence rate of 34% 78% blast injury Burn area 18% 31% Average ISS 4 (minor) 18 (moderate/severe) Leibovici D, Gofrit ON, Stein M, et al. Blast injuries: bus versus openair bombings: a comparative study of injuries in survivors of open-air versus confined-space explosions. J Trauma. 1996;41:1030–1035 Table 31.3  Distribution of injuries caused by terrorist bombings Open space Cabin blast blast injury Injury type injury (%) (%) Notes Blast lung 21 7 Diagnosed as lung injury contusion, pneumothorax, mediastinal emphysema, and blast lung injury Pneumothorax 9 3 Including cases of hemopneumothorax and blast lung injury requiring chest tube insertion Blast lung 16 5 Including cases of injury acute respiratory complications distress syndrome and blast lung injury requiring mechanical assisted ventilation Ruptured 35 5 tympanic membrane Intestinal 3 0 perforation Fractures 20 6 Including cases of open fractures Amputation 3 1 Including phalanx Burns 22 1 Arnold JL, Halpern P, Tsai MC.  Ming-Che, Mass casualty terrorist bombings: a comparison of outcomes by bombing type Ann Emerg Med. 2004;43:263–273

Outcomes of animal testing on destructive effects of weapons show that when an anti-ship missile hits a simulated destroyer, test sheep/goats placed in various cabins around the point of impact all died instantaneously due to destructive injuries caused by shock wave and fragments. When high-explosive ammunitions penetrate tank, armored vehicle, or above-ground fortification, half of the test sheep/ goats inside these cabins died within 3 h. Using the “new injury severity score” (NISS) to evaluate injury severity of test sheep/goats inside above-ground fortification subjected

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to explosive weapon strike, the average score for test sheep/ goats injury is 20.00 ± 15.76 with a median of 17.5 (9.29) when the fortification is penetrated, and the average score is 12.06 ± 10.88 with a median of 10 (2, 19) when the fortification is hit but not penetrated. These results prove that the respective NISS figures of animal injury in the two different fortification damage conditions stated above differ significantly (Z = −2.568, P < 0.05). Instantaneous death rate of test sheep/goats inside cabin is related to the type of combat vehicle/structure cabin tested. Armored vehicle cabin has the highest death rate (75%), followed by penetrated tank (67%) and penetrated above-ground fortification (53%). Outcomes of laboratory simulation studies indicate that when a small equivalent of high-energy explosives detonates in a simulated armored cabin, occurrence rate of abdominal organ injury in test rats inside the cabin was 1.2 times higher than explosion of equivalent explosives in open space, with liver injury occurrence rate 2.13 times higher than explosion in open area (36.7%/11.7%); intestinal endotoxemia occurrence in test rats inside cabin took place 2.5 h earlier than animals subjected to open space explosion, while duration lasted 24 h longer; and positive rate of blood bacteria in mesenteric lymph nodes, liver, portal vein, and periphery in test rats inside cabin was 2.27 times higher than those in open area explosion (35.0%/15.4%). The aforementioned research outcomes reveal that explosions in the enclosed space of a cabin, relative to explosion in open area, result in more severe injuries to solid organ in the abdominal cavity, earlier bacterial translocation from intestine and earlier onset of intestinal endotoxemia.

5.2 Obvious Polarization of Injury Conditions There is obvious polarization in cabin blast injuries. When the American frigate USS Stark was hit by the two Exocet missiles in 1987, of the 17 survivors, other than two that suffered from moderate to severe burns, the other 15 were all afflicted with minor injuries, including three with fragmentation wounds, eight with soft tissue contusion, three with corneal flash burns, and one with dehydration. Outcomes of animal testing on conventional weapon effects indicate that for tank cabins hit and penetrated by armor-piercing shells, 70% of the tanks would ignite, 67% of test animals within would die, and two-thirds of test sheep/goats had open fractures and disfiguring amputations. Of the test sheep/goats that survived for 10  min or more, 25% had severe injuries, while the remaining 75% suffered from mild injuries.

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5.3 Complicated Injuries

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from degeneration of nerve cells and mild cerebral edema as observed under microscope. Abnormal EEG waveforms were Armored cavalry troops and navy troops, which rely on their seen in 50% of the sheep/goats, 12.5% of the animals had left respective cabin spaces in combat, suffer from much higher ventricular subintimal hemorrhage, and ECG T-wave abnorrates of blast injury, burns, blunt trauma, and composite inju- malities were seen in 12.5% of the sheep/goats. When a highries than infantries. Statistics of blast injuries in British explosive weapon strikes an above-­ground fortification, 160 armored vehicle passengers during World War II indicate test sheep/goats placed inside the cabin were injured or killed. that 75% had fragment/shrapnel injuries. Of the tanks hit, Of which, 110 animals or 68.75% had blast injury, 101 ani39.7–70% were ignited, and 25% of riders were burned. mals or 63.13% had primary or secondary fragmentation Blast injury occurrence rate was 1–20%. Of the British tanks injury, 15 animals or 9.38% had collision injury or crushing that carried burn victims, 66% were hit by armor-piercing injury, 12 animals or 10.91% had burns, and 67 animals or shells, 25% by high-explosive anti-tanks, and 9% by anti-­ 41.88% had two or more different types of blast injuries. tank land mines, with an average of 0.3 person burned per tank struck. During battles in the Sino-Vietnamese War in 1979, 58% of struck Chinese tanks were hit by high-­explosive 5.4 High Occurrence Rate of Bone Fracture and Visceral Injury anti-tanks, followed by explosive ammunitions (14.9%), and then anti-tank land mines (11.3%), with a burns occurrence rate of 8.4%. During the Fourth Arab–Israeli War in 1973, According to statistics on body parts injured among the 608 most of the Israeli tanks destroyed were hit by high-­explosive troops injured in U.S. armored vehicles hit by land mines anti-tanks fired by the Egyptian military. The occurrence rate during the Iraq War and War in Afghanistan, of the 152 casuof burns was 9.3%, and an average of 0.9 Israeli troops was alties there were 2912 wounds, of which 53% were bone fractures, with the largest number of bone fractures inflicted burned for every tank struck. Of the 12,067 injured troops of the U.S.  Navy during on the head, followed by ribs/sternum, pelvis, and limbs, etc. World War II, 39.09% were injured from projectiles, 17% in that order. Of the 456 survivors there were 1637 wounds, from burns, and 12% from blast waves. When the American of which 53% were bone fractures, with the largest number destroyer USS Cole was damaged by suicide bombers in an of bone fractures inflicted on the feet and ankles, followed by inflatable boat. 17 sailors near the point of impact were shin bone/fibula, lumbar vertebrae, and upper limbs, in that killed, of which 14 died from blunt trauma and three were order. In 2000, when the American destroyer USS Cole was drowned. In 1987, the American frigate USS Stark was hit by damaged on one side by suicide bombers in an inflatable two Exocet missiles fired by an Iraqi jet. Of the sailors killed boat, 92% of the crew killed in the cabins had fracture in in the incident, 45.9% died from fragmentation injuries, 35.1% from burns, 8.1% from fragmentation-burns compos- long bone, 50% had pelvis fracture, 71% had spine fracite injuries, 5.4% from inhalation injuries, and 2.7% from ture, 86% had skull fracture, and 100% had rib fracture. Of suffocation. During the Falklands War between Great Britain the survivors, 15% had fracture in long bone, none had peland Argentina, the British destroyer HMS Sheffield was hit vis fracture, and the number of skull fracture, collar bone by an Exocet missile. Of those killed onboard, 25% died fracture, and spine fracture were all 3%, while rib fracture from suffocation because of inhalation of smoke and dust, was 8%. According to statistics on body parts injured among the and of the 26 injured sailors, 24 had burns and smoke and troops injured in armored vehicles hit by land mines, head dust inhalation injuries. Outcomes of animal testing on destructive effects of weap- injury occurrence rate was highest in casualties, followed by ons show that when new types of armor-piercing shells hit a chest, abdomen, and spinal cord in that order, while chest tank, if tank armor has been penetrated, the cause of death of injury was most common among survivors, followed by test sheep/goats was all fragmentation-blast composite inju- abdominal and cranial injuries, in that order. Outcomes of animal testing on conventional weapon ries or fragmentation-burns composite injuries, and for anieffects show that in above-ground fortification struck by mals that survived, they suffered from smoke inhalation high-explosive weapon, injury to the thoracic cavity organs injuries, fragmentation injuries, blast injuries, and acceleraof test sheep/goats had the highest occurrence rate (60.44%), tion injuries. If the shell hit but did not defeat the armor, test animals inside would suffer from impact and acceleration followed by head injury (36.26%) and abdominal cavity injuries, with 62.5% sheep/goats afflicted with varying injury (30.8%). 20.9% of injured sheep/goats had chest-­ degrees of dilated meningeal vessels and blood clot resulting abdomen composite injuries (Table 31.4).

Cabin Blast Injury Table 31.4  The test of injured site of sheep/goats inside aboveground fortification subjected to explosive weapon strike Frequency of The occurrence frequency of various types of various injuries in the Injured site animal injury corresponding injured site Head injury 36.26% – Open brain 1.10% 3.03% injury Closed brain 35.16% 96.97% injury Chest trauma 60.44% – Open chest 5.49% 9.09% injury Closed chest 54.95% 90.91% injury Abdominal 30.77% – injuries Open 8.79% 28.57% abdominal injury Closed 21.98% 71.43% abdominal injury Note: Since two or more injuries may occur in the same animal simultaneously, the cumulative value of injury frequency of each part is greater than 100%

5.5 Prominent Closed Injuries and High Rate of Traumatic Brain Injury During the Soviet–Afghan War (1979–1989), of the Soviet armored vehicles hit by land mines, occurrence rate of closed pulmonary contusion in personnel inside vehicle cabins was three times that of explosions in open space. During the Iraq War, of the American military vehicles hit by improvised explosive devices, occurrence rate of blunt impact injury was as high as 96%. Outcomes of animal testing on destructive effects of weapons show that in above-ground fortification struck by high-explosive weapon, test sheep/goats had obvious closed injuries, with occurrence rate three to 32 times more than that in open space injuries. Traumatic brain injury (TBI) occurred frequently in victims injured during cabin explosions. During the War in Afghanistan, TBI existed in 50% of British military casualties from cabin explosions between November 2007 and August 2010, ranking first in terms of cause of death. During the Iraq War and War in Afghanistan, more than 60% of blast injury troops evacuated back to the U.S. had TBI, with around 80% being minor TBI (mTBI). In order to understand mTBI injury features in personnel inside cabin due to explosion inside cabin, experiments were carried out by detonating small equivalent of high-energy explosives either inside simulated armored cabin or stuck to the exterior of bottom plate of cabin, then influences of explosion on physiology and cognitive behaviors of test rats inside the cabins were observed. Research results indicate

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that peak pressure, effective duration, peak impulse, and positive pressure effective duration in explosion inside cabin were all substantially higher than those in an open air explosion, with significant difference (P < 0.01). After an in-cabin explosion, cerebral blood flow to the parietal cortex in rats rapidly decreased compared to pre-explosion levels, reaching lowest point 1 h after injury, with a drop of roughly three times more than test rats in the open space explosion group (58.8% vs 18.9%). The levels recovered gradually, but still below pre-injury threshold 24 h after injury. Administering S-Nitrosoglutathione (GSNO) early on after injury could increase cerebral blood flow. Using triphenyltetrazolium chloride (TTC) rapid dyeing to evaluate brain injury, it was discovered that for the rats in the in-cabin explosion group, cerebral ischemia occurred earliest in the part of the brain facing the source of explosion, and cerebral ischemia onset was about 4 h earlier than rats in the open space explosion group. Also, area of cerebral ischemia gradually spread to surrounding tissues, with cerebral ischemia area expanding to largest 8 h after injury, which then gradually decreased but was still obviously larger than open space explosion group 72 h after injury. Water maze and shuttle box were used to observe the impacts of explosions on the cognitive behaviors of test rats. Experiments show that water maze escape latency and average shuttle box reaction time in rats in the in-cabin explosion group were significantly longer than those in the open space explosion group (P < 0.05), with the difference most significant 24 h after explosion (P < 0.01). The aforementioned results indicate that overpressure from in-cabin explosion is the injuring factor behind the mTBI suffered by personnel inside cabin, with the pathological injury features being impaired cerebral blood perfusion and progressive cerebral ischemia. Compared with explosion in an open environment, cerebral ischemia would occur earlier, last longer, and recover slower. Reversible learning and memory cognitive disorder might exist in injured personnel, being most obvious 24 h after injury. To understand features of the process of how TBI is inflicted on cabin passengers by the process of high-­ acceleration changes of the cabin plate when an explosion occurs outside the cabin, a small equivalent of high-energy explosives is placed tightly against the bottom of simulated armored cabin plating, and detonated, then acceleration changes of steel seats in direct contact with cabin bottom and rats positioned in sitting posture on those seats were observed. Experimenters saw that after the explosion there was no obvious deformation of the cabin bottom plating, but acceleration upward of 1000 g was recorded in steel seats in direct contact with cabin bottom that sustained for several milliseconds. After the explosion, rats positioned in sitting posture on those seats had no anatomical damage as far as the eyes can see, but 6 h after injury, some neurons in the spinal cord anterior horn, cerebral cortex, pyramidal cells in

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hippocampus, and Purkinje cells in cerebellum exhibited pathological changes of degeneration and necrosis when viewed under optical and electron microscopes. Rats inside the cabin after the explosion were subjected to water maze test, and results indicate that the rats’ learning and cognitive abilities declined, most obviously 24 h after the explosion. If the seats were suspended in mid-air to interrupt the effects of the acceleration of cabin plating on the rats, optical microscopy and electron microscopy reveal that cerebral and spinal cord neuron pathological changes, spatial learning and memory dysfunctions and other issues obviously lessened compared with rats positioned in seats in direct contact with cabin plating. The research outcomes stated above demonstrate that when an explosion occurs outside the cabin, physical contact with high-acceleration deformation of cabin plating could induce minor TBI in passengers and transient cognitive dysfunction.

6 Treatment Principles and Techniques for Cabin Blast Injury To improve the cabin blast injury treatment levels of the Chinese military and standardize cabin blast injury treatment procedures and techniques, in 2017 the Logistics Support Department of the Central Military Commission authorized the issuance of the People’s Republic of China national military standard Cabin Blast Injury Mechanism Standard (GJB9012-2017). Said standard was compiled by this chapter’s author as lead author, with contributions and participations from more than 20 experts and professors with the Field Surgery Research Institute (currently Army Unique Medical Center) of the third Army Medical University Hospital of the People’s Liberation Army. During the formulation of said standard, members of the “standard formulation group” carried out in-depth studies on cabin blast injury features. In accordance with the Chinese military wartime treatment system and mission requirements, proven cabin blast injury treatment techniques from both Chinese and foreign militaries were consolidated, and after evaluation by the Chinese Military Trauma Special Commission and application by the military, said technical standard was formed. Said standard is applicable to organizations and personnel at various levels involved with the battlefield/on-site first-­ aid, emergency treatment, and early treatment of combat cabin blast injuries in cabins like armored vehicle, vessel, tunnel, and fortification during wartime. The standard also serves as a reference for treatment of blast injuries in enclosed environments such as building, bus, subway, and civilian vessel before and after arrival in hospital during peacetime. Said standard is not applicable for treatment of

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bodily harms caused by chemical, biological, or radioactive agents or substances released in cabin explosion. The following section outlines the main cabin blast injury treatment principles and techniques stipulated in said standard.

6.1 In-cabin Emergency Treatment This is a part of the emergency treatment segment in the battlefield/on-site combat injury treatment system of the Chinese military. The interior environment of cabin after explosion is a dangerous place, and victims should be evacuated from the hazardous space as soon as possible. In-cabin emergency treatment focuses on controlling fatal bleeding of limbs using tourniquet.

6.1.1 Searching Rescuers should gain knowledge about type of in-cabin explosion, cabin structure, and victim distribution before entering the cabin, then assess the damage extent and safety level of cabin, and choose and confirm the appropriate time, method for cabin search and rescue, and personal protection measures. Stay low when entering a smoke-filled cabin for search and rescue. When extinguishing fire on clothes of victims, do not use plastic cloth or chemical fiber and blended fabric to cover the fire. Rescuers should assess victim’s vital signs immediately upon discovery, identify life threats rapidly such as major bleeding of the limbs, or suffocation, and adopt protective measures to prevent victims from suffering further injury. 6.1.2 Emergency Treatment The interior environment of cabin after explosion is a dangerous place, and victims should be evacuated from the hazardous space as soon as possible, so as to avoid emergency treatment procedures that require spending extensive period in the cabin. If the post-explosion cabin environment is ­relatively safe, early-stage emergency treatment may be performed inside. Rescuers should use tourniquet to control ruptured large vessel, traumatic amputation, large area of soft tissue avulsion, and other fatal bleeding of the limbs. Tourniquet should be applied at the part of the wound closer to the heart (5–8 cm), and in exigent situations the tourniquet may be applied on the surface of clothing near the wound. When using belt, cloth strap, gauze strap of other items as temporary tourniquet, width of item should be no less than 5 cm. Rescuers should swiftly clean out any blood clot, foreign substance, or secretion blocking the oral and nasal cavities and upper respiratory tract of the victim, and position victim on his or her side, or with his or her head tilted to one side. Rescuers should relocate victim to a safe area outside the cabin by sup-

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porting, propping up, carrying on back, carrying on arms, dragging, lifting or carrying on stretcher. When moving victims with head, neck, or back blunt trauma injury, rescuers should stabilize the person’s head and neck, keep the his or her head in a straight line with the long axis of the spine so as to minimize movement of the spine.

6.2 Emergency Treatment Outside of Cabin This is a part of the emergency treatment segment in the battlefield/on-site combat injury treatment system of the Chinese military. Rescuers should perform emergency treatment procedures in a safe area outside of cabin, quickly assess injury level, categorize injuries, prioritize treatment of life-threatening injuries, and pay attention to special treatment requirements for different injuries.

6.2.1 Injury Level Assessment Rescuers should assess the victim’s ventilation, respiration, and circulation statuses, ascertain the victim’s cognitive level through yelling, check eye movement and fixation, and responses to pain and stimulation, and quickly identify life-­ threatening injuries. Rescuers should use sphygmomanometer or blood pressure gauge to measure central arterial blood pressure. When unable to use sphygmomanometer or blood pressure gauge, make an approximate judgment by touching peripheral artery pulses with hand. If carotid artery, femoral artery, or radial artery pulse can be accessed, systolic blood pressure (SBP) should, respectively, be more than 60–70 mmHg, 70–80 mmHg, and 80–90 mmHg. Determine the injuring factors in the cabin explosion, and categorize the injuries. 6.2.2 Open Up Airways For unconscious victims, or those already suffering or could suffer from airway obstruction, tilt the person’s head up or lift the person’s chin to open up his or her airway. Thereafter, if a mouth or nose breathing tube is inserted to help an unconscious victim breathe, lie the person on his or her side (recovery position). For a conscious victim using nose breathing tube, position the person in any position favorable to keeping the airway unobstructed. Do not tilt head and lift chin of victim if he or she is suspected to have neck injury or serious head injury, and do not use nasal breathing tube if victim has maxillofacial trauma or exhibits symptoms of skull fracture such as cerebrospinal fluid rhinorrhea or cerebrospinal fluid otorrhea. After the treatment procedures outlined above, if airway obstruction symptoms still did not ameliorate, consider the options of cricothyrotomy or tracheostomy, and if conditions permit, use laryngeal mask, trachea and esophagus dual pipe, or trachea pipe.

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6.2.3 Maintain Respiration Rescuers should use airtight wraps to seal any open or sucking wound on the chest, apply pressure with bandage, pectoral girdle, and cotton pad to stabilize thoracic wall of victims with chest injury, so as to mitigate abnormal breathing movement. If victim with unobstructed airway exhibits progressive respiratory distress, perform needle decompression immediately if tension pneumothorax is suspected. Needle decompression puncture site should be at the space of the second rib at the midclavicular line on the side of injury, or in between the fourth rib and fifth rib at the anterior axillary line. If there is still no improvement after needle decompression, or if hospital evacuation is expected to take a rather long time, insert breathing catheter or set up closed thoracic drainage. When conditions permit, oxygen inhalation should be provided to patients with saturation of pulse oximetry (SpO2) < 90%, unconsciousness, shock, chest injury, serious head injury, or inhalation injury. 6.2.4 Control Bleeding Rescuers should check the tourniquet in use, and switch to pressure dressing for non-lethal bleeding. If distal pulse of limb with tourniquet is still accessible, reapply the tourniquet, or add another tourniquet near the existing tourniquet on the end near the heart until the distal pulse disappears. If tourniquet applied to forearm or calf could not control bleeding, switch tourniquet to upper arm or thigh, and remember to record time of tourniquet application. Use of tourniquet should not exceed 2 h, and during the span of application the tourniquet must remain tight. If tourniquet is used for more than 2 h, it may be loosened cautiously to facilitate inspection of blood loss control. If major bleeding occurs again, reapply the tourniquet immediately. Loosening tourniquet on patients with shock should only be undertaken after ascertaining efficacy of fluid resuscitation. Tourniquet that has been applied for 6 h or more should be removed at medical care organization with amputation surgery capability. Rescuers should use hemostatic agent, hemostatic wound dressing, or pressure bandaging to bandage or fill up and control bleeding in areas like the torso, neck, groin, and armpit, or apply pressure with hand or finger. If the aforesaid methods are futile, try inserting balloon catheter into wound and expanding balloon to apply pressure and stop bleeding. Dress and stabilize fractured pelvis to reduce bleeding. Using hemostat forceps or ligature to stop bleeding should only be utilized if other measures are ineffective and do not use hemostat forceps without proper consideration. Medical anti-shock trousers may be used to control large soft tissue injury of lower limb bleeding or the pelvis.

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6.2.5 Dressing Rescuers should use sterile dressing to dress wounds. For exposed brain tissue and intestine protruding from the abdominal bowel, do not put them back in the cavity, instead use protective dressing. Airtight dressing should be applied to seal any open or sucking wound on the chest, and breathing status should be closely observed. Rescuers should perform needle decompression immediately if signs of tension pneumothorax are observed. When dressing limbs, keep fingers and toes exposed to facilitate observation, and beware of excessively tight dressing that overly restrict blood flow to limbs. For foreign substances lodged relatively deeply in the body, do not remove them without full consideration, instead keep and stabilize them in their place and then dress the wound. 6.2.6 Fixation Rescuers may use standard plywood boards, expedient devices, or other materials for over-articular fixation of fractured long bones, injury to major joints, limb crushing injury, and large-area soft tissues injury. Prior to fixation, inspect limb circulation and nervous function status, and fixation should be fastened to a tightness level just enough to feel distal pulse. For those with spine or spinal cord injury, the victim’s spine should be stabilized. When applying fixation to a patient in supine position, ensure that his or her cervical spine and lumbar spine remain at natural physiological curvatures. Use objects like triangular bandage or pelvic fixation band for fixation of fractured pelvis. 6.2.7 Cardiopulmonary Resuscitation For patients with respiratory or cardiac arrest due to suffocation, electric shock, low temperature, poisoning, or other factors, carry out cardiopulmonary resuscitation right away. For patients with blast injury or penetration wound no vital sign, it is not necessary to perform cardiopulmonary resuscitation. 6.2.8 Hemorrhagic Shock Fluid Resuscitation Fluid replenishment by oral means may be administered for conscious patients that are able to swallow. For patients with the following conditions, it would be advisable to administer intravenous infusion 1 h after injury: 1. No noticeable head wound but exhibits mental status changes and/or weakened or absent pulsation of the radial artery. 2. Systolic blood pressure (SBP) < (80–90) mmHg. Use 18 G intravenous infusion needle or detaining needle to establish venous access. If venipuncture is difficult, use bone marrow infusion needle to puncture sternum, shin bone, near end of humerus, and other cancellous bone locations to

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establish intraosseous infusion access. Intraosseous needle should not remain inside body for more than 24 h, and efforts should be made to switch to intravenous infusion as soon as possible. Other than hypertonic fluids, all fluids and medications delivered through intravenous infusion may also be administered via intraosseous infusion. Delivered fluid should be any crystalline fluid or colloidal fluid available on-site. Colloidal fluids are preferable, such as hydroxyethyl starch, dextran, and gelatin, followed by crystalline fluids like Ringer’s lactate solution and other balanced salt compound solution. Intravenous infusion rate should be 500 ml/(15–20 min). If conditions permit, use whole blood or other blood products. Adopt a low-pressure fluid resuscitation strategy, check patient after every 500  ml of delivered fluid, and stop the infusion process when patient reaches one or more of the following conditions: 1. Patient’s consciousness improves (can be awaken or/and lift his or her own head); 2. Apical-radial pulse can be felt; 3. Systolic blood pressure (SBP) 80–90 mmHg; 4. Mean arterial pressure (MAP) 50–60 mmHg. Low-pressure fluid resuscitation should not be over 90 min, and blood loss should be stopped within this duration. Norepinephrine, dopamine, and other vasoactive drugs, as well as inotropic agents, should only be used when low blood pressure persists under the premise of controlled blood loss and sufficient fluid replenishment.

6.2.9 Analgesia For victims who have not lost combat capacity, provide orally ingested non-steroidal anti-inflammatory drugs such as meloxicam (mobic) tablets, acetaminophen (paracetamol), etc. For victims who could no longer reengage in combat and suffer from serious pain but do not exhibit shock or ­respiratory distress, use opioid analgesics, preferably morphine administered via intravenous or intraosseous infusion, and administer again after 10 min if necessary. Promethazine is synergistic with opioids in terms of pain relief, nausea, and vomit alleviation. For victims that could no longer reengage in combat and already showed or might suffer from shock or respiratory distress, administer 50 mg of ketamine via intramuscular injection, and administer again after 30  min if necessary. Or administer 50 mg of ketamine via intravenous or intraosseous infusion, and administer again after 20  min if necessary, until pain subsides or when victim exhibits nystagmus. When applying opioid analgesics or ketamine, pay close attention to victim’s mental state and circulatory and respira-

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tory conditions, and apply symptomatic treatments should the need arises. Naloxone administered via intravenous or intramuscular infusion can antagonize the side effect of suppressed breathing caused by opioid painkillers.

6.2.10 Application of Prophylactic Antibiotics For victims that are expected to be delivered to brigade/ division-­level or equivalent medical care institution within 3 h after injury, antibiotics may be applied. For victims that are not expected to arrive at medical care institution within 3 h after injury, or if evacuation might be delayed, the following antibiotics are recommended: Oral ingestion of 500 mg of levofloxacin or 400 mg of moxifloxacin for patients with shock or those that cannot ingest orally, administer 1–2 g of ceftriaxone every 24 h or 1–2 g of cefazolin every 6–8 h by way of intravenous therapy or intramuscular injection. 6.2.11 Maintain Body Temperature It is necessary to minimize exposure of the victim’s body, remove any wet clothing, cover victim with thermal reflective blanket, or other insulation material. When conditions permit, heat up IV fluid to 40–42 °C. 6.2.12 Outside Cabin First-Aid for Several Types of Cabin Blast Injuries Blast Injuries Victims with the following signs and symptoms may possibly have blast injury: ruptured eardrum, bleeding fluid from the external auditory canal, or bloody foam discharge from the mouth or nose; in shock but without obvious external wound; chest pain, breathing difficulty, hemoptysis, abdominal pain, bloody urine, etc. Rescuers should keep victim’s airways unobstructed; decompression measures should be performed promptly for those showing symptoms of tension pneumothorax; after being provided with hyperbaric oxygen therapy, saturation of pulse oximetry (SpO2) still below 90% after oxygen inhalation is an indication of severe injury and unfavorable prognosis. When victim exhibits signs or symptoms of arterial air embolism, position the person in a left decubitus position with head low posture, then provide pure oxygen for inhalation via face mask or airway breathing tube. When conditions permit, swiftly send victim to hyperbaric oxygen chamber for treatment. For victims with abdominal blast injury indicated by signs or symptoms such as abdominal pain, nausea, vomiting, or peritoneal irritation, do not replenish fluids or foods by oral ingestion. When paralytic ileus occurs, use nasogastric tube to relieve pressure in the gastrointestinal tract. Beware of excessive fluid delivery, which

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could worsen pathological progression of cardiac and pulmonary blast injuries. Burns and Inhalation Injuries Use clean and cool water to wash surface of burn wounds, and after rinsing apply burn dressing or dry and clean cloth to cover and protect surface of wounds. Take measures to maintain victim body temperature. For victims with burns covering less than 20% of body surface area, oral ingestion of fluid is acceptable, and burn formula fluid (100 ml containing 0.3 g of sodium chloride, 0.15 g of sodium bicarbonate, 0.005 g of phenobarbital, and a suitable quantity of sugar) is recommended. For victims with burns covering 20% or more of body surface area, administer crystalloid solution (Ringer’s lactate solution or normal saline). For an adult weighing between 40–80 kg, fluid input rate should be (percentage of body surface area burned) × 10 ml/h. For victims with burns around the face and neck area, sputum containing carbon particles, scratchy or loss of voice, respiratory distress, or wheezing, dry rales, twirls, or other inhalation injury signs and symptoms heard from auscultation of the lungs, pay close attention to his or her ventilation status. If signs and symptoms of airway obstruction appear, quickly undertake cricothyrotomy or endotracheal intubation, and provide hyperbaric oxygen therapy to maintain saturation of pulse oximetry (SpO2) >92%. Carry out pain relieve measures. Crush Injuries Before relieving victim from crush situation, at least 1000 ml of normal saline should be administered via intravenous therapy at rate of 1000–1500 ml/h. If IV is not possible, before relieving victim from crush situation, wrap tourniquet around the crushed limb on the section closer to the heart, not to be removed until completion of fluid resuscitation. Continue intravenous therapy after removing victim from crush situation, and beware not to administer liquid containing potassium or lactate. Alkalized urine; administer sodium bicarbonate via intravenous infusion, with total volume of 200–300 mmol, equating to 300–500  ml of 5% sodium bicarbonate solution, on day one. Ensure stabilization and fixation of crushed and injured limb and/or pelvis, and avoid using anti-shock trousers for fixation or dressing using elastic bandage with pressure. Administer antibiotics to prevent infection, but refrain from using drugs that are detrimental to kidney functions. Apply pain relieve medications and sedatives. Combined Injuries Prioritize the treatment of combined injuries. Choose the appropriate fluid resuscitation strategy in accordance with

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the main injuring factors. When hemorrhagic shock coexists with other types of shock, prioritize fluid resuscitation for hemorrhagic shock.

body temperature. As a preventative measure, use antibiotics to avoid infections.

Impact Injuries Stabilize and fix head and spine when moving victims with head, neck, or back injuries. For fluid resuscitation of victims with impact injuries to the torso, avoid excessive fluid delivery to prevent worsening injuries to internal organs. For fluid resuscitation of victims with neurogenic shock of spinal cord injury, use crystalloid solution. Resuscitation should achieve systolic blood pressure (SBP) ≥110 mmHg or mean arterial pressure (MAP) ≥80 mmHg. When necessary, after delivery of 2000–3000 ml of fluid, apply norepinephrine, dopamine, or other vasoactive agents to adjust vascular tension.

6.3 Initial Surgical Resuscitation

Eye Injuries Check victim’s eyesight, and for those with impaired vision, evacuate to specialized medical institution for treatment as soon as possible. Use hard goggles to protect open wounds of eyeballs, and refrain from applying any pressure on injured eyes. For foreign objects in conjunctiva or cornea, rinse them out or undertake surface anesthesia and then use sterile wet cotton swabs to remove foreign objects. Traumatic Brain Injury (TBI) Assess vital signs and cognitive level of victims with head injury, observe the size of his or her pupils, and monitor the person’s arterial blood pressure (AP) and saturation of pulse oximetry (SpO2). For victims suffering from hemorrhagic shock, it would be ideal to quickly administer 3% or 5% hypertonic saline at a rate of 250 ml/15 min using intravenous therapy, with total volume not to exceed 500 ml. Then use isotonic crystalline or colloid solution. Resuscitation targets are systolic blood pressure (SBP) >90 mmHg and mean arterial pressure (MAP) >60 mmHg. Keep airway unobstructed, and provide hyperbaric oxygen therapy until saturation of pulse oximetry (SpO2) >92%. For victims exhibiting uncoordinated movement, fixed or dilated pupil(s) on one side or both sides, accompanied by aggravated cognitive dysfunction and other symptoms of high cranial pressure, it would be advisable to quickly administer hypertonic saline at a rate of 250 ml/15 min using intravenous therapy, and maintain continuous IV at a rate of 50–100 ml/h during the course of evacuation, but total volume should not surpass 500  ml. If hypertonic saline is unavailable, mannitol may also be delivered via intravenous therapy for victims with urine. Tilt victim head at a 30° angle, and adopt measures to sedate victim and lower his/her

This is considered an early-stage treatment technique and process in the military medicine system of the Chinese military. Complete life-saving and limb-preserving damage control surgery or emergency surgery at the division- or brigade-level medical institution, carry out resuscitation and rewarming, stabilize the patient’s physiological state and prevent the onset of infection to facilitate the safe and smooth evacuation of the victim.

6.3.1 Injury Condition Evaluation Conduct physical examination and any necessary supplemental testing, evaluate the injury levels and scopes of the victim’s heart and circulatory system, chest and respiratory system, abdomen, spine, head, pelvis, limbs, arteries and nerves, monitor his or her physiological functions, identify life-threatening main injuries and those that affect limb functions, and determine the treatment measures needed and application sequence. 6.3.2 Damage Control Surgery 1. For the following types of severely injured victims, employ damage control surgery to control internal organ bleeding, bleeding from injury to large vessels and infections from substances flowing out of ruptured stomach or intestine, rectify low body temperature, acidosis, and coagulopathy, then relocate victim or conduct definitive surgery after his or her condition stabilizes. a. Victims with injuries involving multiple body parts, multiple organs, or large vessels, such as those with injuries to multiple organs in the abdomen coupled with large vessel injury; retroperitoneal vascular injury; pancreas and duodenum injury; open pelvic fracture or rupture of pelvic hematoma; major vessel injury to the chest or severe laceration to the lung; multiple traumatic amputations, etc. b. Victims whose systolic blood pressure (SBP) remains below 90 mmHg after fluid resuscitation and with unstable hemodynamic status. c. Victims with severe injuries at or near one or two of the following indicators: core temperature 1.9 and/or activated partial thromboplastin time (APTT) >60 s. d. When there are many victims.

Cabin Blast Injury

2. Abdominal damage control surgery: After entering the abdomen, control abdominal bleeding by directly applying pressure with hand or dressing. If there is obvious abdominal arterial bleeding, press down on the abdominal aorta at the diaphragmatic foramen with hand, and after temporarily restricting blood flow, control bleeding from ruptured vessel using methods such as ligation, abdominal wall repair, temporary vascular bypass, extravascular balloon compression, etc. Stuffing dressing into abdominal cavity can effectively control bleeding in areas like the liver, pelvis, and retroperitoneum, and stuffed dressing should be removed within 24–48 h. If blood pressure does not clearly restore after stuffing dressing, adopt measures such as suture, excision, and repair to control bleeding from ruptured solid organs. Use techniques and devices like clipping together, ligation, u-shaped staples, repairing, and excision to control contents flowing out from openings in stomach or intestine. For extraperitoneal rectal injury, administer external colon treatment or colostomy. For injuries to bile duct or pancreatic duct, external drainage may be performed. For injuries to distal superior mesenteric artery pancreas, carry out pancreatectomy or drainage. For proximal superior mesenteric artery injury, debridement and closed drainage are feasible. Temporarily closing abdominal cavity with negative pressure dressing is recommended or close wound using materials like polypropylene mesh, pieces of IV bag, or artificial patch, but do not use towel forceps to clamp the wound close, stitching instrument, or continuous stitching technique to close the abdominal cavity. 3. Thoracic damage control surgery: To control major bleeding from lung injury, utilize cutting stapler to perform wedge pneumonectomy, or use long clamps to fasten the two ends of a lung wound and then open up the wound passageway to gain a direct sight for ligation to stop bleeding and control air leakage. For severely injured pulmonary lobe, pulmonary lobectomy may be performed. To control bleeding from ruptured large vessel, utilize temporary vasculature, or Fogarty balloon catheter insertion to block blood flow. If situation is particularly dire, use temporary hilar ligation technique. When the airway is injured, inserting tracheal catheter through the wound is a viable option. For victims with severe bronchus rupture or injury, it would be advisable to conduct pulmonary lobectomy of the involved lobe or pneumonectomy of entire lung on the affected side. For injuries of the esophagus, it would be feasible to perform diversion and drainage, while definitive repair is not suggested. Use continuous stitching to close thoracic wall, do not use towel forceps to clamp the wound close.

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4. Other damage control surgeries: For repairable large vessel wound on limb, it would be wise to conduct temporary vessel bypass 3 h after injury, including vascular wound exploration, thrombus resection, restoration of distal blood supply, and limb fasciotomy decompression, among other steps, and damaged vessel repair should be completed within 12 h of injury. If conditions do not permit such a method, temporary ligation may also be employed, and finish damaged vessel repair within 4 h of injury. To control bleeding of fractured pelvis, ideal procedures are extraperitoneal pelvic packing conducted with external fixation or suprapubic incision and utilize vessel embolization when the option is viable. Internal iliac artery ligation should be carried out only when other methods have failed. For victims suffering from traumatic brain injury with continually worsening symptoms of cerebral hernia, it would be advisable to perform cranial decompression or cranial decompression.

6.3.3 Resuscitation and Rewarming Fluid Resuscitation When bleeding is still uncontrolled, low-pressure fluid resuscitation should be adopted. After bleeding is controlled, resuscitation should achieve all the following objectives: (1) systolic blood pressure (SBP) >110–120 mmHg, and mean arterial pressure (MAP) >65–70 mmHg; (2) urine volume larger than 0.5 ml/(kg h); and (3) base excess (BE) > −2 mmol/or lactic acid 6.5. If the patient’s urine volume does not reach 300 ml/h, administer mannitol solution via intravenous infusion at a volume of 1–2 g/(kg day) and at a rate slower than 5 g/h. Maintain water and electrolyte balance, and if serum potassium exceeds 5.5 mmol/L coupled with obvious electrocardiographic abnormality, it would be advisable to take the following steps to reduce serum potassium while maintaining continual serum potassium and ECG monitoring: (1) intravenous therapy of calcium gluconate or calcium chloride; (2) sustained intravenous infusion of sodium bicarbonate and glucose-regular insulin; (3) oral ingestion of cation exchange resin (sodium polystyrene sulfonate); and (4) intravenous therapy of furosemide for patients with urine. Surgery should remove inactivated muscle tissue, then dissect deep fascia longitudinally for decompression. Amputate limbs that have no chance of survival. Administer antibiotics to defend against infection.

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Composite Injuries When treating burns and perforation wounds, first and foremost ascertain that there are no concurrent blast injuries or collision injuries. If there are concurrent blast injuries, during treatment keep airway unobstructed, maintain victim respiration, avoid excessive fluid delivery, and be circumspect with the use of anti-shock trousers. If there are concurrent collision injuries, during treatment pay attention to the possibilities of closed thoracic and abdominal organ injury or fractured spine and long bone. It would be advisable to utilize external fixator for fixation of open limb fracture with burns. Collision Injuries For victims suspected of suffering from traumatic brain injury (TBI), injuries to organs in the chest or abdomen, injuries to spinal cord or spine, and bone fractures, conduct X-ray scan of injured area, focused assessment with sonography in trauma (FAST), regular ultrasound examination, electrocardiogram (ECG), and other supplementary examinations. Also, monitor arterial blood pressure (AP) and saturation of pulse oximetry (SpO2), as well as arterial blood gases if the option is available. Victims with contusion myocardiaque should lie in bed and inhale oxygen, while fluid input should be limited. Also, positive inotropic drugs (dopamine or dobutamine) should be administered to augment myocardial contractility. Perform pericardial puncture decompression to deal with cardiac tamponade caused by hemopericardium. Eye Injuries For victims with perforation wound to the face or serious loss of vision, eyeball structural damage, ocular proptosis, dyscoria and ocular movement disorder, evacuate to specialized medical institution for treatment as soon as possible, and it would be ideal to complete debridement and other surgical treatments within 6 h after injury. Administer antibiotics to defend against infection. Traumatic Brain Injury For head injury victims with perforation wound to the head, open skull fracture and Glasgow Coma Scale (GCS) score of ≤13, evacuate to specialized medical institution for treatment as soon as possible. For victims with Glasgow Coma Scale (GCS) score of 14–15, evacuate depending on the situation. For the physiological parameters of a victim being evacuated, maintain his or her systolic blood pressure (SBP) >90 mmHg, mean arterial pressure (MAP) >60 mmHg, saturation of pulse oximetry (SpO2) >92%, and arterial partial pressure of oxygen (PaO2) >80 mmHg. For

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victims showing symptoms of cerebral hernia such as dilated pupil, elevated blood pressure, or bradycardia, it would be advisable to administer mannitol via intravenous infusion at a volume of 1 g/kg and a high input rate, and when necessary administer mannitol again after 4 h via intravenous infusion at a volume of 0.25 g/kg and a high input rate. However, do not administer mannitol to victims with hypovolemia, no urine or cardiac failure. For a patient that has unimproved or worsened symptoms of cerebral hernia even after undergoing dehydration treatment, carry out decompressive craniectomy if the option is viable. Keep the patient under monitoring and only relocate after his or her condition has stabilized. Administer antibiotics to protect again infection, and use drugs in the benzodiazepine or barbital category to prevent the onset of epilepsy in victims with cerebral perforation injuries.

Bibliography 1. Standardized Emergency Management of Blast Injuries in confined Spaces (GJB9012-2017). Logistics Support Department of the Central Military Commission, 2017-04-17. 2. Zhengguo W. Surgery and field surgery. Beijing: People’s Military Medical Press; 2007. p. 579–822. 3. Leibovici D, Gofrit ON, Stein M, et  al. Blast injuries: bus versus open-air bombings  – a comparative study of injuries in survivors of open-air versus confined-space explosions. J Trauma. 1996;41:1030–5. 4. Explosive weapon effects – final report, GICHD, Geneva, 2017. 5. Langworthy MJ, Delong WJ, Gould M. Terrorism and blast phenomena: lessons learned from the attack on the USS Cole (DDG67). Clin Orthop Relat Res. 2004;422:82–7. 6. Weapons effects and war wounds. Emergency War Surgery: Fourth United States Revision. Published by the Office of The Surgeon General, Borden Institute, Fort Sam Houston, Texas 78234-6100. 7. Zipf KRJ, Cashdollar KL.  Explosions and refuge chambers. 2016. www.cdc.gov/niosh/docket/archive/pdfs/NIOSH-­125/125-­ ExplosionsandRefugeChambers.pdf. 8. Cross K, Dullum O, et al. Explosive weapons in populated areas: technical considerations relevant to their use and effects. Armament Research Services (ARES). www.icrc.org/en/download/file/23603/ aresweb-­generic.pdf.

X. Lai 9. Champion HR, Holcomb JB, Young LA. Injuries from explosions: physics, biophysics pathology, and required research focus. J Trauma. 2009;66(5):1468–147. 10. Dougherty CJ.  Armored vehicle crew casualties. Mil Med. 1990;155(9):417–21. 11. Alvarez CJ.  Epidemiology of blast injuries in current operation. https://www.sto.nato.int/publications/pages/results.aspx?k= epidemiology%20of%20blast%20injuries%20in%20current%20 operation&s=Search%20All%20STO%20Report. 12. Tank crew casualties. http://forum.shrapnelgames.com/archive/ index.php/t-­38329.html. 13. Champion HR, Bellamy RF, Roberts CP, et al. A profile of combat injury. J Trauma. 2003;54:13–8. 14. Arnold JL, Halpern P, Tsai MC. Mass casualty terrorist bombings: a comparison of outcomes by bombing type. Ann Emerg Med. 2004;43:263–73. 15. Humphrey A, See J. A Methodology to assess lethality and collateral damage for nonfragmenting precision-guided weapons. ITEA J. 2008;29:411–41. 16. Lieutenant-Colonel MS, Owen-Smith MS.  Armoured fighting vehicle casualties. JR Army Med Corps. 2007;153(3):210–5. 17. Haoyang S, Tingyu D, Xinan L. Analysis of casualties in ground firm works based on animal experiments. J Third Military Med Univ. 2018;40(1):7–13. 18. Xinan L. Study on the characteristics and treatment of injuries from combat cabin explosions. Field Surg Newsl. 2014;39(1):38–40. 19. Haoyang S, Xinan L, Ran Z.  Characteristics and implications of anti-ship missile combat injuries. Military Med Sci Press. 2017;42(3):218–21. 20. Jie G, Jianyi K, Lili W, et al. Study on the neurophysiological mechanism of disabling brain injuries to rats from explosion of airtight cabins. Med J Chin People’s Liberat Army. 2015;40(8):666–70. 21. Hongye Z, Zhengzhi F, Xinan L, et al. Effects of intra-­compartmental explosion on the learning, memory and behavior of rats. J Traum Surg. 2008;10(4):341–3. 22. Xu Mingwei X, Minhui LX, et al. Changes in cerebral blood flow and significance in rats after blast brain injury in enclosed space. J Third Military Med Univ. 2010;32(18):1962–6. 23. Zihuan Z, Xinan L, Minhui X, et  al. Transient, high acceleration induces early deficits in spatial memory of rats in airtight cabin. J Traumat Surg. 2010;12(6):487–90. 24. Xinling L, Yue S, Xinan L, et  al. Characteristics of brain injury induced by shock wave propagation in solids after underwater explosion in rats. Med J Chin People’s Liberat Army. 2016;41(8):689–93. 25. Hai N, Xiankai H, Xinan L, et al. Analysis of abdominal injuries to rats caused by cabin explosion. J Traumat Surg. 2008;10(2):145–8. 26. Song Bo H, Shisheng ZH, et al. Experimental research on shock wave overpressure in an airtight container. J Ballist. 2001;13(3):68–71.

Part VI Different Types of Blast Injuries

Nuclear Blast Injury Yang Xu, Cheng Wang, Chunmeng Shi, Binghui Lu, and Zhou Jihong

1 Section One: Nuclear Weapons 1.1 Overview of Nuclear Weapons The appearance of nuclear weapon completely changed the course and history of development of weaponry in the twentieth century and realized the leap of weapon development from hot weapons to nuclear weapons. The world has never seen any weapon as destructive as nuclear weapon. The course of the research and development of nuclear weapon was filled with twists and turns, interspersed with many tales of intrigue. During the turn of the twentieth century, progress in natural science advanced by leaps and bounds. The discovery of radiation and proposal of theory of relativity in the realm of physics formed the theoretical bedrock for the research and development of the atom bomb. At the same time, various scientists of eminence such as the Curies, Ernest Rutherford, and Enrico Fermi carried out their respective experiments, gradually fleshing out the theories behind atomic reaction. The theory of chain reaction meanwhile was the key that opened the doors to the atom bomb. It would not be long before the first atom bomb was forged. Starting from the 1930s, nuclear weapon research and production picked up steam in nations such as Germany, Japan, the USA, the UK, the Soviet Union, and France. Germany was the first country to conduct nuclear weapon research and experiment. In December 1938, German scientists Otto Hahn and Friedrich Wilhelm Strassmann identified the phenomenon of nuclear fission in uranium after 6 years of study and grasped the basic method to induce fission of nucleus. In 1938, Otto Hahn succeeded in splitting the nucleus of uranium atom and shocked the global scientific community. In August 1938, Albert Einstein personally wrote to U.S. President Franklin Roosevelt and expounded Y. Xu · C. Wang · C. Shi (*) · B. Lu Army Medical University, PLA, Chongqing, China Z. Jihong Army Medical Center of PLA, Chongqing, China

the importance of the research and development of the atom bomb in details. In 1942, President Roosevelt decided to establish an atomic bomb research institution, codenamed the “Manhattan Project” and headquartered in New  York City. This project involved an investment of some USD 2.2 billion and more than 500,000 personnel. The project was under the command of Major General Leslie Groves, University of Chicago, professor Arthur H. Compton was put in charge of preparation for fissile materials, Italy-born American scientist Enrico Fermi was responsible for manufacturing of nuclear reactor, and physicist J.  Robert Oppenheimer was appointed the chief designer of the atomic bomb. Under the directions of Enrico Fermi, the world’s first nuclear reactor was completed at the University of Chicago in December 1942. However, it was a challenge to obtain uranium. After countless experiments, Fermi eventually discovered that plutonium is actually a better fissile material than uranium. That’s why the Americans built three graphite-­ moderated, water-cooled reactors, and a reprocessing plant to produce plutonium. By 1945, the Americans had spent more than 2 billion US dollars and produced three atom bombs, respectively, codenamed, “Gadget,” “Little Boy,” and “Fat Man.” At 5:24 a.m. on July 16th, 1945, the first ever nuclear bomb experiment in human history was carried out with a bomb placed on a 30 m-high tower located inside the “Trinity” test site in Alamogordo, New Mexico. “Gadget” was outfitted with a charge of 6.1 kg of plutonium or 22,000 TNT equivalents. During the experiment, the nuclear explosion created temperatures as high as tens of million degrees and pressure in the range of several tens of billion of atmospheres. The 30 m-high tower that held the bomb was melted into gas, and the explosion left a massive crater on the ground. The nuclear explosion created a mushroom cloud that towered over the land like a beacon of terror. Within a radius of 400  m, the desert sand melted into a yellow-greenish glass-like substance, and all animals within a radius of 1600 m were killed. The force of this atom bomb was nearly 20 times more powerful than scientists originally thought. In August 1945, the

© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023 Z. Wang, J. Jiang (eds.), Explosive Blast Injuries, https://doi.org/10.1007/978-981-19-2856-7_32

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USA deployed two nuclear weapons against Japan at Hiroshima and Nagasaki, which accelerated World War II toward its conclusion. These two instances showcased the tremendous power of nuclear weapon and made nuclear weapon regarded as frightening monsters of terror. A nuclear weapon uses its own sustainable nuclear fission or fusion–fission reaction to release immense energy instantaneously to generate an explosion powerful enough to cause serious and widespread annihilation. Common nuclear weapons include atom bomb, hydrogen bomb, and other specialized types of nuclear weapons such as neutron bomb, electromagnetic pulse bomb, and reduced residual radioactivity weapon. Nuclear weapon usually refers to the warhead and the shell holding it, sometimes also includes the attitude control system and penetration system. These are together colloquially called nuclear bomb. The nuclear warhead is the main explosive device and may simply be called nuclear device. The nuclear device is comprised of nuclear components, explosive components, fission reaction trigger (neutron generator), and other parts. The nuclear device and detonation control system comprise the nuclear warhead. The deployment or launch system of nuclear weapon is made up of the carrier, launch device, and other auxiliary equipment. Nuclear weapon development is currently in its third generation, with the first being atomic bomb, second is the hydrogen bomb, and the current third generation includes nuclear weapons with special purposes. Special purpose nuclear weapons either enhance or weaken one or some of the destructive elements of traditional nuclear weapon to satisfy different needs based on varying battlefield scenarios or objectives. Some examples include neutron bomb, reduced residual radioactivity weapon, salted bomb, etc. A neutron bomb is also called enhanced radiation weapon (ERW). A tactical nuclear weapon that utilizes nuclear fusion reaction to generate large amount of lethal neutron, but physical power of the blast itself is limited to it does not cause much damage to equipment and facilities. The neutron bomb produces less radioactive contamination than atom bomb, which is why it is regarded as a “clean” nuclear weapon. The neutron bomb is a major type of tactical nuclear weapon. Nuclear weapons may come in various forms such as nuclear missiles (missiles with nuclear warheads), nuclear bombs, nuclear depth charges, nuclear bunker busters, nuclear torpedoes, nuclear artillery shells, and nuclear land mines, among others. Delivery system for nuclear weapons includes missile, electric motor, artillery, etc. Nuclear land mines do not require a delivery system. Nuclear weapons may be launched from aircraft, land-based vehicle, or vessels on or below the water surface. Nuclear weapons are increasingly miniaturized in order to meet demands in launch site mobility and striking multiple targets at longer distances. Based on combat usage, nuclear weapons may be sub-­ divided into strategic nuclear weapon or tactical nuclear weapon. Strategic nuclear weapons include ballis-

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tic missiles launched from land-based missile silos or nuclear submarines, long-distance airborne missiles, cruise missiles, and nuclear-powered cruise missiles. Tactical nuclear weapons include mid- and short-range missiles, cruise missiles, and nuclear-powered cruise missiles launched from land, sea, or air, as well as nuclear artillery, nuclear land mines, nuclear naval mines, and nuclear torpedoes, among others. The development trends in nuclear weapon include improving flexibility in usage through miniaturization, ammunition diversification, and adjustable yield, increasing destructiveness, raising accuracy, enhancing penetration capacity, development of multi-warhead technologies, and speeding up rapid response. Nuclear weapon, even when not directly deployed in actual warfare, still plays a crucial role as a significant threat in hi-tech and localized armed conflicts.

1.2 Principles of Nuclear Weapons 1.2.1 Nucleus and Changes Within Nucleus Nucleus A nucleus is comprised of proton, which has electric charge, and neutron, which does not have electric charge. Proton and neutron are collectively termed nucleon. In a neutral atom, the number of protons in its nucleus is equal to the number of electrons outside the nucleus. This is represented as nuclear charge number or atomic number, denoted by Z. The sum of protons and neutrons inside the nucleus is called the mass number, denoted by A. Thus, the number of neutrons inside the nucleus equals to A minus Z. If X is used to denote a certain element, then ZA X shows the nucleus composition of the element. 1. Element: Atoms with the same charge number in their nuclei are classified into an element. 2. Nuclide: Atoms with the exact same number of protons and neutrons are classified into a nuclide. Radioactive nuclides such as 32P and 60Co are called radionuclides. 3. Isotope: One element could include various nuclides, and they have the same number of protons in their nuclei but different numbers of neutrons. Since the different nuclides of the same element occupy the same position on the periodic table, they are called isotopes. For instance, 1H, 2H, and 3H are different nuclides, but they all belong to the element hydrogen, thus they are isotopes. In addition, there is another important concept related to isotope: Isotope abundance refers to the percentage of atoms in the different isotopes naturally found in an element. 4. Isomer: If two nuclides have the same number of neutrons and same number of protons but different energy states, they are called isomers. For example, 99Tcm and 99 Tc are isomers.

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5. Mirror nuclei: A pair of nuclei is classified as mirror nuclei if they have the same mass number, nuclear spin, and parity, but opposite numbers of protons and neutrons. Mass, Conservation of Energy, and Nuclear Binding Energy Mass Effect

A nucleus is comprised of neutrons and protons, but the mass of a nucleus is not the same as the sum of the mass of protons and mass of neutrons inside. Take 42 He for example:

Mass of a helium atom M ( 42 He )  =  4.002603  u (unit for atomic mass) Mass of a hydrogen M ( 11 H ) = 1.007825 u Mass of neutron M (n) = 1.008665 u The nucleus of helium ( 42 He ) is comprised of two protons and two neutrons, and when the masses of the two protons and two neutrons are added together:

2 × M ( 11 H ) + 2 × M ( n ) = 2 × 1.007825 u + 2 × 1.008665 u = 4.032980 u

This does not equal to the atomic weight of helium ( 42 He ), and the difference is: ∆M =  2 M ( 11 H ) + 2 M ( n )  − M ( 42 He ) = 4.032980 u − 4.002603u = 0.030377 u

The calculation above illustrates that when two neutrons and two protons form a helium nucleus, ΔM would be lost, as in 0.030377 u of mass. For all other nuclei, the above calculation can also be used to prove that the mass of a nucleus does not equal the sum of the mass of neutrons and mass of protons contained within. ΔM is defined as “mass defect.” Nuclear Potential

A nucleus is made up of nucleons (neutrons and protons), and between the nucleons inside a nucleus exists a special type of mutual power called “nuclear potential.” Nuclear potential is characterized as a “short-distance” force, whether a nucleus is charged or not does not influence the effect of its nuclear potential, and nuclear potential may be saturated, as a nucleon only mutually affect neighboring nucleons and not all nucleons. A nucleus is formed by nucleons that are mutually bonded together via nuclear potential. When nucleons form a nucleus, they must exert externally, as in release energy. Nuclear potential is more powerful than Coulomb force, and precisely because it is mostly an attractive force, that’s why nuclear potential enables nucleons to overcome Coulomb force to combine into nucleus. Nuclear potential has a very short effective distance, approximately 10−15  m. We know that Coulomb force conversely is a long-range force, with its magnitude inversely proportional to the square of distance,

while nuclear potential is a short-range force. When the distance between nucleons exceeds a certain very short distance, the force of nuclear potential disappears (effective range less than 3 fm). In layman’s terms, nuclear potential is a short-range but powerful mutual effect, and its main mechanism is attractive force. Law of Mass and Energy Connection

Mass and energy are properties that simultaneously exist in a substance. Any substance with a certain mass must have a certain association with energy. Assuming that E denotes energy (J), M denotes mass (kg), and C denotes the speed of light (3 × 108 m/s), then:

E = MC 2

In any situation when there is a change in energy, there would always be a change in mass as well. Similarly, if there is any change in mass of the substance, correspondingly its energy would also change. Binding Energy of Nucleus

The energy released when several nucleons bind together to form a nucleus is called binding energy of that nucleus. The higher the binding energy, the larger the energy released when nucleons bind together to form that nucleus, and the

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tighter the bond that holds that nucleus together. The ratio between binding energy of a nucleus and its mass (as in the number of nucleons) is known as “average binding energy of nucleus.” For those nuclei with a mass in the middle range, each constituting nucleon has a higher average nuclear binding energy. Conversely, those nuclei with a heavier mass or those with a lighter mass, their constituting nucleons have relatively smaller average nuclear binding energy. Therefore, when nuclei with heavy mass split into nuclei with medium mass, their nucleons would bind together more tightly in the relatively lighter nuclei, and in doing so could release a substantial amount of energy. When fusion occurs between two relatively light nuclei, the energy released would be even greater. Changes in the Nucleus Nuclear Decay

In 1896, while studying phosphorescence of uranium ore, Antoine Henri Becquerel discovered the uranium ore emits invisible rays that can penetrate deeply and sensitize photographic negatives. After conducting further research in magnetic fields to study on this kind of ray property, Becquerel proved that the ray is comprised of three components: Of which, the deflection of one component in a magnetic field is the same as that of a positively charged ion stream; the deflection of another component in a magnetic field is the same as that of a negatively charged ion stream; and deflection does not occur with the last component in a magnetic field. The rays are, respectively, called alpha ray (α), beta ray (β), and gamma ray (γ). Nuclear decay occurs when the nuclei of some nuclides naturally emit alpha and beta particles and transform into the nuclei of other types of nuclide, or when a nucleus emits photons (gamma rays) while transitioning from its excited state to its ground state. Types of nuclear decay include: 1. Alpha decay: When the nucleus of a radioactive nuclide (radionuclide) emits alpha particles and changes into the nucleus of another nuclide, this process is called alpha decay. Alpha particles are helium nuclei moving at great speeds. An alpha particle consists of two protons and two neutrons, and so it has a charge of 2e, and its mass is the same as the mass of a helium nucleus. Usually the nucleus before decay is called parent nucleus, and that after decay is termed daughter nucleus. When the nucleus of a radioactive nuclide undergoes alpha decay, the resulting daughter nucleus has an atomic number or nuclear charge number that is two smaller than its parent nucleus. In other words, it would move two spots forward (to the left) on the periodic table. Mass of the

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daughter nucleus meanwhile would be four less than its parent nucleus. These are expressed in the following equation: A Z



A 4 Z 2

Y   (1)

X

For example :

226 88

Ra 

222 86

Rn  42 He

Alpha decay is a feature of the nucleus of heavy elements. The absolute majority of naturally radioactive nuclides that undergo alpha decay are nuclides with atomic numbers Z > 82. The half-life of alpha decay varies drastically depending on the nuclide, with some as short as 10−7 s, while others extend to 1015 a. The distribution of energy of alpha particles usually falls within the (4–9) MeV range. Alpha ray is comprised of helium nuclei (alpha particles) moving at great speeds, and hence, their deflection in a magnetic field is the same as that of a positively charged ion stream. The alpha ray has high ionization and low penetration. 2. Beta decay: When the nuclear charge number of a nucleus changes by ±1 while mass stays the same, this kind of decay is called beta decay. Beta decay refers to the process in which a negative electron e− is emitted from inside a nucleus. Here, the mass of daughter nucleus and the mass of parent nucleus are the same, except that the resulting daughter nucleus has an additional proton. Therefore, 1 is added to its atomic number and it is moved one spot backward (to the right) on the periodic table. Electrons emitted from this kind of nuclei are called beta particles. This may be expressed in the following equation:

A Z

X

Y       neutrino 

A Z 1

For example :

32 15

(2)

 P  32 16 S  e  

Beta decay may be regarded as the conversion of a neutron into a proton in the parent nucleus while simultaneously emitting beta particles and neutrinos.

n  p      (3)

The half-life of beta decay is chiefly distributed within the range of 10−2 s and 1018 a. The energy of emitted particles could reach a maximum of several MeV. Beta decay differs from alpha decay in that not only does it occur in heavy nuclei, but nuclides with beta radiation exist throughout the entire periodic table. Beta ray is a stream of fast-moving electron flow. The beta ray has relatively low ionization and high penetration.

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3. Gamma decay: Different kinds of radioactive decays always result in daughter nuclei in excited state, and bombardment by hi-speed particles or absorption of photons could also activate a nucleus into an excited state. Nucleus in an excited state is unstable and may be deactivated directly to its ground state. The light-emitting process of when a nucleus transitions from an excited state into a low-energy state or ground state is called gamma decay. For example :

203 82

203 83

.8 hours m  Bi 11  203 82 Pb  

.1 seconds (4) Pb m 6  203 82 Pb  

During the process of gamma decay, both the mass and the atomic number of the nucleus remain unchanged, and only the energy state of the nucleus changes. This is why this kind of change is called isomeric transition. Gamma ray is an electromagnetic wave with very short wavelength. The gamma ray has low ionization and high penetration. Law of Radioactive Decay

Temperature, pressure, and humidity of the surrounding environment have no impact on the decay of a radioactive nuclide, which simply follows the law of exponential decay. In other words, the number of atoms decaying every second is proportional to the number of existing radioactive atoms. For example, if a certain radioactive nuclide has N0 atoms at the beginning, after a time period t, only N atoms would remain, then the relationship between N and N0 is

N  N 0 e  t (5)

Of which, λ is decay constant and represents the relative rate at which the different nuclides decay, as in the number of nuclides the decay every second is a certain fraction of the original number of radioactive nuclides. Its unit of measurement is reciprocal of units of time (1/s, 1/min, etc.). Half-Life Time

Half-life time (T1/2) is defined as the time it takes for atoms of radioactive nuclide to decay by half. Half-life is associated with decay constant λ in the following manner:

T1/ 2 

0.693 

(6)

T1/2 for different nuclides varies substantially. For instance, the half-life of 232Th is 1.39 × 1010 years, but that of 212Po is only 3.0  ×  10−7  s. The half-life time of several radioactive nuclides with common medical applications is:

Na has T1/2  =  15.6  h; 131I has T1/2  =  8.1  days; 32P has T1/2  =  14.3  days; 59Fe has T1/2  =  47.1  days; 60Co has T1/2  =  5.3  years; 3H has T1/2  =  12.4  years; and 14C has T1/2 = 5720 years. 24

Nuclear Reaction

The nuclear decay explained earlier is a change that occurs in the nucleus, and the nucleus always changes toward stability, ultimately resulting in a more stable nucleus. If a nucleus undergoes structural change due to external reasons such as bombardment by charged particles, absorption of neutrons or illuminated by high-energy photons, such a change is called nuclear reaction. Nuclear Fission

This may be divided into either spontaneous fission or induced fission. Spontaneous fission is akin to radioactive decay in that the nucleus undergoes spontaneous fission on its own without external factors such as particle bombardment. This occurs because a relatively heavy atom has smaller specific binding energy than that of a nucleus with medium mass, and its nuclear fission process emits energy. Heavy atoms also undergo fission when bombarded by foreign particles, and this kind of fission is known as induced fission. In an induced fission, fission induced by neutron is the most common. Since there is no Coulomb barrier between neutron and target nucleus, neutrons of very low energy can enter and excite the nucleus, resulting in fission. Neutrons are emitted during the fission process and could lead to chain reaction. This is also why neutron-induced fission has gained so much interest. The atoms of some heavy elements such as 233U, 235U, and 239 Pu would split into two new atoms with lighter mass when bombarded by neutrons while at the same time release two to three neutrons and photons. Newly divided nuclei are also called fission fragments, they could be different kinds of isotopes of any elements with atomic number from 30 to 64 and are usually radioactive. The fission process releases an immense amount of energy. Nuclear Fusion

The reaction when two light atoms combine to form relatively heavier atoms under certain conditions is known as light nuclear fusion reaction. This process also emits neutrons and a massive amount of energy. Since fusion reaction could only occur under extremely high temperature, this kind of reaction is also called “thermal nuclear reaction.” For example: Under extremely high temperatures, deuterium and tritium fuse to form helium nuclei and release neutrons and tremendous

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amount of energy. Much more energy is released from thermal nuclear reaction than from heavy nuclear fission reactions.

1.2.2 Explosion Principle and Basic Composition of Nuclear Weapons

may be lowered further. To decrease critical mass, fissile materials are often configured into spheres because spheres have the smallest surface area compared with other shapes of the same size, and thus a ball of fissile material minimizes neutrons loss.

Atomic Bomb

Basic Structure

Explosion Principle

Chain reaction of heavy nuclear fission is the chief principle behind the explosion of an atomic bomb. Upon bombardment by neutrons, atoms of some heavy elements (i.e. 235U and 239Pu) would split into two new atoms (a.k.a. fission fragments) of similar mass and release two to three neutrons along with around 200 MeV of energy. This process is known as heavy nuclear fission. Take, for example, the reaction equation for 235U is: 235



U  01 n  X  Y   2 ~ 3 01 n  200 MeV

(7)

In this equation, X and Y are new atoms (fission fragments). This energy does not look like much, just about enough force to make the smallest grain of sand visible to the naked eye to jump. Yet, this only represents the energy released by the fission of a single atom. One mole of 235U contains 6.02 × 1023 atoms, which weigh a total of no more than 235 g. If all these atoms were to undergo fission, the energy would be shocking, roughly equal to energy released from complete combustion of 600 tons of coal. When 1 kg of 235U undergoes complete fission, it would release energy equivalent to approximately 20,000 tons of TNT. Every fission would release two to three neutrons. If one of these neutrons hits another heavy nucleus and instigates its fission, the same reaction would occur after fission. This would enable heavy nuclear fission to sustain on its own, and this is known as the chain reaction of heavy nuclear fission. However, not all emitted neutrons might initiate a new fission. For example, some atoms are very small and neutrons might not be able to make contact with uranium atoms. If the uranium core is not big enough, some neutrons would miss and fly pass the uranium without triggering new fission. In addition, other substances in the uranium core would also absorb neutrons, preventing the start of new fission reactions. The chain reaction of heavy nuclear fission could only occur within a body of or beyond a certain mass. The smallest mass of fissile material capable of sustaining nuclear chain reaction is called critical mass. The size of the material corresponding to critical mass is called critical size. Critical mass is closely associated with the type, purity, density, and geometrical shape of the fissile material chosen. If the wrapping material is neutron-reflective substance, critical mass

An atomic bomb primarily consists of the nuclear fuel (235U or 239Pu), detonation device, neutron initiator, neutron-­ reflective layer, and the bomb shell, among other components. Detonation Process

After the detonation device is triggered, the various explosive modules would detonate simultaneously. The tremendous pressure generated from the explosion would press toward the center, forcing the separate and small pieces of sub-critical fissile materials to instantaneously combine into a sphere. Reaching a supercritical state. Under bombardment of neutrons produced by neutron initiator, heavy fission chain reaction starts and develops increasingly more intense by geometric order, resulting in heavy nuclear fission of a certain amount within an extremely short period, releasing tremendous energy and creating a powerful nuclear explosion. One kilogram of 235U or 239Pu only needs a few millionths of a second to undergo complete fission. The energy released equates to energy from the explosion of 20,000 tons of TNT explosives. Hydrogen Bomb Explosion Principle

Hydrogen bomb’s explosion principle is light nuclear fusion reaction. The atoms of some lighter nuclides (such as 21 H and 31 H ) would undergo fusion under extremely high temperatures of tens of millions of degrees, and in the process release neutrons and large amount of energy. For example: 6 3



2 1

Li  01 n  31 H  42 He

H  31 H  42 He  01 n  17.6 MeV (8)

Since fusion can only happen under extremely high temperature, fusion reaction is also known as thermonuclear reaction, and hydrogen bombs are also called thermonuclear weapons. Basic Structure

A hydrogen bomb is chiefly comprised of a thermonuclear fuel (usually lithium deuteride), detonation device (a small equivalent atomic bomb), and the bomb shell (usually containing 238U), among other components.

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Nuclear Blast Injury

Detonation Process

The atomic bomb is first detonated, lithium deuteride is subjected to the resulting high temperature, high pressure, and neutron bombardment, and the lithium would produce deuterium. Next, the deuterium–tritium would quickly fuse while emitting high-energy neutrons and tremendous energy, resulting in an explosion even more powerful than that of an atomic bomb. Complete fusion of 1 kg of deuterium–tritium mixture would generate three to four times more energy than that released by the complete fission of 1  kg of 235U or 239Pu. Hydrogen bomb is a fission–fusion double-phase bomb. If the shell of hydrogen bomb contains 238U, the high-energy neutrons produced from deuterium–tritium fusion could instigate fission in the 238U, adding to the yield of fission fragments and boosting the force of the explosion. This kind of hydrogen bomb is a fission–fusion–fission triple-phase bomb. Neutron Bomb A neutron bomb is a tactical nuclear weapon that utilizes fusion reaction from deuterium–tritium to produce ­high-­energy neutrons for lethal effects. Its structure is similar to that of a hydrogen bomb. The neutron bomb is characterized by the following features:

of nuclear weapon detonated in different media and at different heights would create different levels of damage. Nuclear explosions may be classified as air burst (air explosion), ground (water) surface burst (surface explosion), or underground (underwater) burst. Air bursts and ground bursts are differentiated based on ratio relationship between actual height of explosion and equivalent. This ratio is called scale height of burst, or SHOB for short. An explosion with SHOB less than 60 is considered a ground burst, and one with SHOB above 60 is deemed an air burst. SHOB =

Height of burst 3

Equivalent

(9)

During an air burst or ground burst of a nuke, the three classic visual effects of flash, fireball, and mushroom cloud would appear in that sequence, and the sound of the explosion may be heard within a certain area.

Air Nuclear Burst During an air burst, the first sight is a brilliant flash, quickly followed by a bright fireball that suspends in mid-air at the site of the air blast. The fireball fiercely bulges outward, compressing the air around it, and rapidly expands outward, forming a shock wave. The fireball swiftly elevates upward 1. Large yield of powerful neutrons; neutron bomb relies on while at the same time generating a powerful suction on the the fusion between deuterium and tritium, between deute- ground surface, sucking up a considerable amount of dust rium and deuterium, and between tritium and tritium, and and debris, which turn into a column of smoke that rises with 80% of energy released from the fusion comes in the the ascending fireball. This smoke column eventually conform of neutrons. Compared with an atomic bomb with nects with the smoke and vapor around the fireball, forming the same explosive power, a neutron bomb could produce a mushroom cloud. A nuclear explosion causes a great bang, ten times more neutrons, with the average neutron energy which could be heard several tens of km or even hundreds of km away from the center of the blast. reaching 14 Mev or even as high as 17 MeV. Air burst may be categorized as low-altitude air burst 2. Effects of light radiation and shock wave are merely one-­ tenth of an equivalent atomic bomb, and radioactive con- (60 20 cm and extending to subcutaneous area Eardrum perforation area 75%, ossicular chain dislocated Individual foreign object in the conjunctiva sac, or irritation from smoke, fire or light Foreign objects on corneal surface or in conjunctival sac, but quantity limited and countable Laceration of eyelid and lacrimal tubule, or epithelia corneal erosion Eyeball penetrating injury, ocular rupture Minor superficial laceration, no internal organ damage Deep laceration, mild injury of oral tissues and organs Deep laceration, serious injury of oral tissues and organs Mandible fracture, maxilla fracture Contusion, hematoma Laceration, no perforation, incomplete layer Perforation, whole layer Transection, extensive damage Contusion, hematoma Laceration, no perforation, incomplete layer Perforation, whole layer Rupture, transection, extensive damage Facial soft tissue contusion, laceration Severe facial soft tissue laceration, length >20 cm and extending to subcutaneous area Nasal mucosa rupture Nasal bone fracture Cheekbone fracture Nuchal soft tissue contusion, laceration Severe nuchal soft tissue laceration, length >20 cm and extending to subcutaneous area Phrenic nerve injury Bilateral phrenic nerve injury Spinal cord contusion with transient neurological signs (abnormal sensation) Spinal cord contusion with incomplete spinal cord injury syndrome (with partial sensory or motor functions remaining) Spinal cord contusion with complete spinal cord injury syndrome at C4 or below vertebrae (quadriplegia or paraplegia, and with no sense of function) Spinal cord contusion with complete spinal cord injury syndrome at C3 or above vertebrae (quadriplegia or paraplegia, and with no sense of function) Esophagus laceration, no perforation, incomplete layer Esophagus perforation, whole layer Esophagus rupture, transection, extensive damage

1.0 0.3 0.4 0.5 0.7 0.8 1.0 0.4 0.6 0.8 0.9 0.3 0.5 0.3 0.5 0.7 0.9 0.2 0.3 0.4 0.7 0.2 0.3 0.5 0.7 0.3 0.5 0.7 0.9 0.3 0.5 0.7 0.9 0.2 0.5 0.3 0.5 0.4 0.2 0.4 0.5 0.7 0.3 0.5 0.6 0.7 0.3 0.5 0.8

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Table 2 (continued) Body part

Tissue or organ

Description of grade of injury

Injury severity rating

Chest

Diaphragm

Contusion, hematoma

0.3 0.5

Pleural space

Lungs

Ribs

Heart

Pericardium

Aortic arch/thoracic aorta/ abdominal aorta Pulmonary artery/ pulmonary vein

Subclavian artery/ brachiocephalic artery Thoracic vertebra

Brachiocephalic vein/ subclavian vein/superior vena cava/inferior vena cava

Laceration, ≤10 cm Laceration, >10 cm, with obvious tissue loss Rupture, with diaphragmatic hernia formed Pleural laceration Hemothorax/pneumothorax/hemopneumothorax Open (sucking) chest wound, hemothorax/pneumothorax/hemopneumothorax at least on one side >1000 mL Tension pneumothorax Contusion, punctate pulmonary hemorrhage seen on lung surface, diameter 60 >60 >60 >60 21–30 >60 Middle ear damage ≥50%

5 >30

>30

Note: (1) external injury; (2) bone fracture; (3) burn; (4) throat; (5) windpipe; (6) lungs; (7) heart; (8) hollow organ in abdominal cavity; (9) solid organ in abdominal cavity; (10) right ear; (11) left ear

Table 5  Injury score rating details—scoring for severity type (ST) Item 1 2 3 4 5 6 7 8

9

1 Abrasion Incomplete Minor burn One to five petechiae One to five petechiae Petechiae Petechiae Serous membrane or mucous membrane Intracapsular contusion

2 Contusion Complete Moderate/browned More than six petechiae

3 Avulsion or penetration Composite Severe/carbonized Ecchymosis

More than six petechiae

Ecchymosis

Ecchymosis or bulla Ecchymosis or bulla Two layers

Isolated bleeding Isolated bleeding Whole layer

4

5

Diffuse contusion Diffuse contusion Diffuse bleeding Diffuse bleeding

Penetration/rupture Penetration/rupture

Intracapsular hematoma

Note: (1) external injury; (2) bone fracture; (3) burn; (4) throat; (5) windpipe; (6) lungs; (7) heart; (8) hollow organ in abdominal cavity; (9) solid organ in abdominal cavity; (10) right ear; (11) left ear

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522 Table 6  Injury score rating details—scoring for severity degree (SD) Item 1 2 3 4

1 Superficial Close wound Singeing One layer

2 Depth Open wound First degree Two layers

3 Penetration of body wall

4 Perforating injury

Second degree Whole layer

5

One layer

Two layers

Whole layer

6 7 8

Pleura One layer Mucous membrane intact Bladder intact Auditory ossicles intact

Solid organ Two layers Mucosal ulcer

Scattered hepatization Whole layer Rupture/avulsion

Third degree Reduced diameter of hematoma Reduced diameter of hematoma Diffuse hepatization Rupture/avulsion

Avulsion of surface Malleus fracture/ loss

Rupture/avulsion Ossicular chain fracture

9 10 and 11

5

Rupture/avulsion Rupture/avulsion

Round/oval window fracture

Note: (1) external injury; (2) bone fracture; (3) burn; (4) throat; (5) windpipe; (6) lungs; (7) heart; (8) hollow organ in abdominal cavity; (9) solid organ in abdominal cavity; (10) right ear; (11) left ear Table 7  Injury scoring method Injury parameter

Item 1 2 3 4 5 6 7 8 9 10 11

Content External wound Fracture Burn Throat Windpipe Lungs Heart Abdominal cavity hollow organ Abdominal cavity solid organ Right ear Left ear

Extent (E) 0–6 0–5 0–6 0–4 0–3 0–7 0–4 0–8

Grade (G) 0–3 0–4 0–4 0–4 0–4 0–4 0–4 0–5

Severity Severity type (ST) 0–3 0–3 0–3 0–4 0–4 0–5 0–4 0–3

0–5

0–4

0–2

0–6 0–6

0–4 0–4

Severity degree (SD) 1–3 1–2 1–4 1–5 1–5 1–4 1–4 1–3

Injury formula (E + G + ST)(SD)= (E + G + ST)(SD)= (E + G + ST)(SD)= (E + G + ST)(SD)= (E + G + ST)(SD)= (E + G + ST)(SD)= (E + G + ST)(SD)= (E + G + ST)(SD)=

Max score 36 24 52 60 55 64 48 48

1–4

(E + G + ST)(SD)=

44

1–4 1–4

(E + G)(SD)= (E + G)(SD)=

40 40

Table 8  SII scoring method

Injury External Fracture Burn Throat Windpipe Lungs Heart Abdominal cavity hollow organ Abdominal cavity solid organ Right ear

Value range 0–56 0–24 0–52 0–60 0–55 0–64 0–48 0–48

Max value 56 24 52 60 55 64 48 48

Probability 0–1.0 0–1.0 0–1.0 0–1.0 0–1.0 0–1.0 0–1.0 0–1.0

0–44

44

0–1.0

0–40

40

0–1.0

Incidence factors Pneumothorax, hemothorax, hemoperitoneum, coronary air embolism and cerebrovascular air embolism

Score Incidence factor variation probability Score calculation formula range 0, 1, 2 Score = total 0–10.00 probability + total incidence factors × incidence multiplier (1 for survival, 2 for death)

Injuries from Conventional Explosive Weapons

523

Table 9  Relationships between the injury score and injury level of different organs Injury score Injury level Negative Slight injury Minor injury Moderate injury Severe injury

Lungs 0–0.03 0.04–0.06 0.07–0.30 0.31–0.56 0.57–1.0

Throat 0–0.04 0.05–0.067 0.068–0.267 0.268–0.367 0.368–1.0

Windpipe 0–0.04 0.05–0.07 0.08–0.33 0.34–0.51 0.52–1.0

Moderate injury: Petechiae, ecchymosis, or diffuse contusions, with depth of two layers and area less than 60% Severe injury: Diffuse contusions with depth exceeding two layers and area more than 60% For certain cases of upper respiratory tract injury, bleeding or edema may shrink the diameter of the airway and cause breathing difficulty. In certain cases of severe pulmonary hemorrhage, diffuse parenchymal hepatoid lesion with hemorrhagic fluid flowing into bronchus may occur. Abdominal Cavity Hollow Organ Injury Grades 1. Negative: No injury 2. Slight injury: Small intramucosal contusions with depth less than two layers, coupled with contusions to two organs but affecting an area less than 10 cm2. 3. Minor injury: Diffuse contusions with depth between one layer and two layers and affecting an area less than 30 cm2, or coupled with mucosal ulcer. 4. Moderate injury: Full-layer contusions or mucosal ulcer affecting an area between 21 and 30 cm2. 5. Severe injury: Full-layer contusions with mucosal ulcer, or one or more perforations, affecting an area larger than 30 cm2. Abdominal Cavity Solid Organ Injury Grades Negative: No injury Slight injury: Small cysts or hematomas in one or two organs, but with area less than 10% of organ Minor injury: Cysts or hematomas with area less than 30% of organ, and coupled with parenchymal maceration of slightly lacerated organs Moderate injury: Deep lacerations or parenchymal maceration with area more than 60% of organ Severe injury: Deep lacerations or parenchymal maceration with area more than 60% of two or more organs

4.2.4 Assessment for Composite and Overall Injury Severity When an injury involves multiple body parts and multiple systems and organs, it is necessary to make correct assessment of the victim’s overall injury status. Refrain from simple evaluation by adding or averaging the individual

Abdominal cavity hollow organ 0–0.05 0.06–0.08 0.09–0.38 0.39–0.58 0.59–1.0

Abdominal cavity solid organ 0–0.05 0.06–0.09 0.10–0.41 0.42–0.64 0.65–1.0

assessment scores of the different injured body parts, because the relationships between the assessment scores of the different body parts and the IS scores of the various systems and organs are not linear. Since injury severity and death rate are related to the quadratic sum of IS, which remains valid even in patients with multiple injuries, the quadratic sum of IS may be used to estimate overall injury status. Said evaluation method is called injury severity score (ISS). Take the higher IS values of the three most seriously injured areas of the body to calculate the quadratic sum as evaluation value.

ISS =

max

IS2 +

2 nd

IS2 + 3rd IS2 (5)

For the evaluation of composite injuries, use the following formula.

P ( I / H )total = 1 − (1 − P1 ) (1 − P2 ) (1 − P3 ) (1 − Pn )

(6)

Note: In the formula, Pn is injury score for a single body part. Overall ISS evaluation method uses the IS values for a single body part as basis. In evaluation of overall injury status, injury scores for individual single body parts are also used as basis.

4.3 Computer Simulation Evaluation of Injuries from Explosive Weapons Evaluation of injuries from explosive weapons through computer simulation relies on theories and techniques in disciplines such as medicine, ballistics, biomechanics, mathematics, and computer science to develop models for weapon’s injuring and lethal elements, target, and the mutual effects between the two. In other words, mathematical formulas are used to express their physical properties, then computation is utilized to solve models, and obtain mechanical response and damage effect of anatomical structure of target under the action of a weapon’s injuring and lethal elements, so as to analyze, predict, and evaluate damage sustained by the target.

524

J. Wang et al.

4.3.1 Status Quo and Development Weapon damage effect evaluation in the 1950s and 1960s primarily relied on animal testing, whereby researchers observed features of injuries inflicted on organisms by different weapons and munitions, after which damage determination basis of a weapon’s injuring and lethal elements would be developed. Starting from the 1970s, dummy targets were used to examine dynamic mechanical response of a target under the actions of a weapon’s injuring and lethal elements. Physical parameters related to injury were obtained, based upon which injuring effects were determined. With advancements in computer technology, computer models and simulation analysis rose to become main pathways for weapon damage effect evaluation in many countries. ComputerMan In the 1970s, the Ballistic Research Laboratory (BRL) of the USA developed the ComputerMan, which was the first human body computer model used for weapons research. Since injury determinations on humans were predominantly based on anatomic injury assessments of test animals, there were many conflicts and arguments about how to accurately convert animal-based injury effects for human application. Researchers attempted to use computer modeling and simulation of human bodies and injury processes to solve this problem. The form and structure of the ComputerMan were based on the male body, and raw data were sourced from a set of images of the horizontal transverse plane of the human body. The 108 images were divided into five groups based on human body composition: head and neck (1–18); chest, abdomen, and pelvis (19–44); left arm (50–75); left leg and foot (76–113). Layers 45–49 are cross-sectional images of the female pelvic organs. Distance between anatomical layers of the head and neck is 1.2  cm, and that of the chest, abdomen, and pelvis is 2.6 cm. The 108 horizontal transverse plane images were registered based on reference points, then stacked layer upon layer and converted into a 3D model (Fig. 2). ComputerMan included 181 human anatomical tissues, and each group of tissue has a corresponding tissue code. Therefore, the ComputerMan was essentially the aggregation of a series of tissue codes for the human body when it is penetrated and perforated by projectiles that flew along ballistic tracks. Since incapacitation and casualty are the most basic injury types on a battlefield, the ComputerMan was mostly used to predict the probability of incapacitation and fatal effects caused by bullets, fragments, and other projectiles. Incapacitation evaluation mainly focused on two kinds of combat roles and three combat times, as follows. 1. Immediate combat, immediate defense 2. Combat