b o r d e n i n s t i t u t e m o n o g r a p h s e r i e s

Blast Injury

Translating Research Into

Operational Medicine

James H. Stuhmiller, PhD

e d i t e d b y

William R. Santee, PhD

Karl E. Friedl, PhD, Colonel, US Army 

borden institute
For more than 25 years, the Military Operational Medicine Research Program 

(MOMRP) has been a world leader in the study of blast-related injury. This research 

has produced insights, data, and predictive models that set standards for human 

exposure, guide the design of protective systems, and allow quick responses to the 

questions generated in a rapidly changing battle environment. The work of MOMRP 

continues to address the new blast issues of the 21st century.

This volume was prepared for military medical educational use. The focus of the information is 

to foster discussion that may form the basis of doctrine and policy. The opinions or assertions 

contained herein are the private views of the authors and are not to be construed as official or 

as reflecting the views of the Department of the Army or the Department of Defense.

Dosage Selection: The authors and publisher have made every effort to ensure the accuracy of 

dosages cited herein. However, it is the responsibility of every practitioner to consult appropriate information sources to ascertain correct dosages for each clinical situation, especially for 

new or unfamiliar drugs and procedures. The authors, editors, publisher, and the Department 

of Defense cannot be held responsible for any errors found in this book.

Use of Trade or Brand Names: Use of trade or brand names in this publication is for illustrative 

purposes only and does not imply endorsement by the Department of Defense.

Neutral Language: Unless this publication states otherwise, masculine nouns and pronouns do 

not refer exclusively to men.

Certain parts of this publication pertain to copyright restrictions. 

ALL RIGHTS RESERVED.

No copyrighted parts of this publication may be reproduced or transmitted in any form 

or by any means, electronic or mechanical (including photocopy, recording, or any information storage and retrieval system), without permission in writing from the publisher or 

copyright owner.

Published by the Office of The Surgeon General at TMM Publications 

Borden Institute

Walter Reed Army Medical Center

US Army Medical Department Center & School

This publication is a reformatted version of the April 2008 preprint of the same title. It is made 

available with the understanding that it will not be cited or reproduced without the permission 

of the publisher.

All illustrations and photographs courtesy of L-3/Jaycor, San Diego, California.
contents

Foreword v

Introduction 1

Blast Injury Taxonomy 3

Post-World War II Research 4

Occupational Limits of Blast Exposure 5

Military Operational Medicine Research Program 

(Blast Injury Research) 8

First-Generation Injury Modeling 11

Observed Blast Injuries 11

Exploratory Injury Models 13

Lung Injury 16

INJURY Software, Versions 1.0 to 4.3 18

Simple Waves 19

The Blast Test Device 20

Blast in Enclosures 21

Computational Fluid Dynamics 22

Second-Generation Injury Modeling 23

INJURY Software, Versions 5.0 to 7.1 23

Replacement of the Z-line in Military Standard 1474 27

Secondary Blast Injury Modeling 29
Tertiary Blast Injury Modeling 30

Combined Injury Modeling 31

Closing of the Blast Test Site 31

Third-Generation Injury Modeling 33

Finite Element Modeling 33

Finite Element Modeling in Blast Injury 34

INJURY Software, Version 8 36

Toxic Gas Inhalation 38

Blast Effects Behind Body Armor 42

Fourth-Generation Injury Modeling 43

Performance Endpoints 43

Central Nervous System Injury 44

Blast Traumatic Brain Injury Mechanisms 48

Biomechanical and Physiological Response Models 52

Summary 55

References 57

James H. Stuhmiller is Senior Vice President and General Manager, Simulation, Engineering, 

and Testing, L-3 Communications, 10770 Wateridge Circle, San Diego, California 92121.
Foreword

Blast Injury: Translating Research into Operational Medicine describes 

pioneering biomedical research that forms the basis of our current knowledge of blast injury mechanisms. Much of this knowledge, learned decades 

ago, can be applied directly to solving the blast injury problems of today. 

For example, our understanding of primary blast lung injury, learned from 

nearly two decades of large animal blast injury research, was successfully 

applied to solving the current problem of protecting our warfighters from 

novel explosive weapons. 

The primary goal of the Department of Defense (DoD) Blast Injury 

Research Program is to focus our energies and limited resources on biomedical research that addresses blast injury knowledge gaps. The key to achieving this goal is understanding what has already been learned about blast 

injury. Understanding what we know about blast injury is just as important 

as understanding what we don’t know. As the first comprehensive review 

of the Army’s extensive investment in developing blast injury models, this 

book helps to provide access to the extensive repository of primary blast 

research reports and data. 

 Michael J. Leggieri, Jr.

 DoD Blast Injury Research Program

Introduction

In 1864, during the American Civil War, the 48th Pennsylvania regiment 

was made up primarily of men who had been coal miners in civilian life. As 

the siege of Petersburg, Virginia, dragged on, the idea arose to dig a tunnel 

under the Confederate lines. It was dug, filled with gunpowder, and the fuse 

lit on July 30, 1864. The initial explosion killed 280 Confederate soldiers. 

But, ironically, the subsequent Battle of the Crater led to casualties totaling 

1,500 Confederate and 4,000 Union soldiers, not counting any who were 

wounded or missing.1

In 1968, fuel-air explosives were introduced in the Vietnam War to 

clear densely forested areas, minefields, and enemy soldiers. The tremendous 

blasts from dispersed clouds of kerosene literally crushed everything below. 

The Russians further perfected these thermobaric weapons and used them 

in Afghanistan and the Chechen Republic. 

In 1979, during developmental testing of a new M198 howitzer (Rock 

Island Arsenal, Rock Island, Ill), firing of the most energetic rounds generated 

blast pressures in the crew locations, which slightly exceeded the limits of 

Military Standard 1474 (“Noise Limits for Military Materiel”). By regulation, soldiers could not be exposed to such intense noise, so further testing 

was stopped. Because the capability to fire the energetic rounds was a key 

element in the mission of the howitzer, fielding of a critical weapon system 

was effectively blocked.

On October 23, 1983, the First Battalion, 8th Marines Headquarters 

building in Beirut, Lebanon, was destroyed by a terrorist truck laden with 
2 | Blast Injury: Translating Research into Operational Medicine

compressed gas-enhanced explosives.2 The resulting explosion and the collapse of the building killed 241 marines, sailors, and soldiers. Use of massive 

amounts of low-tech explosives to produce mass casualties has become an 

increasingly common tactic in modern, asymmetric warfare and in civilian 

terrorism.

As of October 2005, improvised explosive devices (IEDs) have accounted 

for one third of all American deaths in Iraq. Roadside bombs were used in 

World War II by Belorussian guerillas to derail Nazi trains as part of the “rail 

war,”3 in Northern Ireland against the British Army, in Afghanistan against 

the Russian Army, in Lebanon against the Israelis, and now against the 

United States throughout the Middle East. In 2005, the US military invested 

$3.3 billion in IED countermeasures, primarily through improved armor and 

other technologies.4

As these examples show, for hundreds of years, blasts from explosions 

have been a threat on the battlefield, a threat to civilians from acts of terrorism, and a threat to soldiers in training. For more than 25 years, the Military 

Operational Medicine Research Program (MOMRP) of the US Army Medical 

Research and Materiel Command (USAMRMC; Fort Detrick, Md) has been 

a leading world research organization in the study of blast-related injury. The 

MOMRP program has

•	 	 conducted extensive animal tests to establish injury patterns, elucidate

injury mechanisms, and provide critical data for establishing injury 

standards; 

•	 	 developedmathematicalmodelsofphysiologicalresponse inbothanimals

and humans to extrapolate test data to situations of military relevance; 

•	 	 developedinjury criteria that areused throughoutthe military and civilian

communities to estimate injury potential and set safe limits of exposure; 

and

•	 	 developed instrumentation to standardize the measurement of blast

environments for injury assessment.

This research covers the traditional blast-effect categories:

•	 	 primary effects—those resulting from the crushing effects of blast overpressure, 

•	 	 secondary effects—those resulting from the impact of debris accelerated 

by the blast wave and following winds, and

•	 	 tertiary effects—those resulting from impacts with walls and the ground 

caused by accelerating the body itself. 
Introduction | 3

In addition, other effects have been studied—for example, incapacitation, 

injury, and lethality from the inhalation of gases generated by explosives and 

effects on sensory systems, including auditory injury. Research findings have 

assisted in human protection in areas other than blast, including the development of better body armor, automobile safety systems, and less injurious 

nonlethal weapons.

Many of the key findings of the MOMRP blast research program have 

been published in peer-reviewed literature. Hardware and software for the 

characterization and analysis of blast pressure have been widely distributed. 

Nonetheless, other results appear only in technical reports and are less accessible. The purpose of this publication is to provide an overview of the 

USAMRMC blast research program, to show how quantitative physiology 

has provided useful solutions to operational medicine, and to indicate future 

directions of research.

Blast Injury Taxonomy

The violent consequences of being near an explosion can produce a wide 

range of injuries that can be organized into a taxonomy (Table 1). The high 

pressures of the blast can crush the body and cause internal injury. These 

injuries are called primary blast injuries. Strong winds behind the blast 

front can hurl fragments and debris against the body and cause the same 

blunt trauma or penetration injuries that would occur if the material were 

propelled by other means. This class of injuries is called secondary injuries. 

The strong winds behind the blast front and the pressure gradient in the 

wave can exert significant forces that can accelerate the body and cause the 

same blunt trauma that would occur in a fall or a car crash. This class of 

injuries is called tertiary injuries. The extreme heat and light released by the 

explosion can cause burning and blindness, whereas inhaling the toxic fire 

gases can lead to immediate incapacitation or delayed lethality. This class of 

injuries is called quaternary injuries. Finally, any of these traumas can lead 

to subsequent effects caused by disruption of the body’s biochemical or neurological system. This class of injuries is called collateral injuries. Although 

blast provides a unique process by which projectiles are propelled, bodies 

are accelerated, and trauma is caused, the resulting injuries and sequelae can 

also result from other traumatic events.

Injuries that result from crushing overpressure, however, are truly unique 

to blast. These primary blast injuries occur because the body is not a solid, 

incompressible mass; it has air-containing organs that will crush under the 
4 | Blast Injury: Translating Research into Operational Medicine

external load. Crushing allows the outer shell of the body in those regions to 

move rapidly inward, thus distorting the air-containing tissue and producing 

local, large stresses. Injuries to the lung, gastrointestinal (GI) tract, and upper respiratory tract (URT) are common manifestations of this effect. Rapid 

distortion of the air-containing organs can transmit stress to neighboring 

solid organs as well. Contusions to the heart, for example, arise in part from 

the strong stress waves that develop in the lung. Large deformations of the 

body can also lead to stresses in solid organs that result in damage (eg, liver 

and spleen lacerations). Finally, rapid volumetric changes outside the normal 

physiological range can disrupt systemic processes. Creation of air emboli 

by forcing gas across the air–blood barrier of the lung and creation of large 

pressure transients in the vascular system may be responsible for brain injury 

and cell death.

The study of blast injury can be roughly divided into two objectives: (1) to 

characterize primary blast injuries, processes that are not investigated in other 

trauma research; and (2) to relate blast to projectile impact characteristics, 

whole-body motion, and extreme heat, light, or atmospheric environmental 

conditions that, in turn, lead to nonprimary injuries. The first objective has 

required new research, whereas the second objective has required adaptation of previous research. Together, a complete, quantitative physiological 

understanding of blast injury has emerged.

Post-World War II Research

Following development of nuclear weapons, research into blast injury centered 

on the effects of extremely large blasts—in particular, establishment of lethality criteria for a wide range of conditions. Biological injuries from blast were 

categorized as primary, secondary, and tertiary, but there was little attempt 

to understand the mechanism of these injuries. During this period, empirical 

models of lethality were used.

In the United States, the majority of blast biology research was conducted 

at the Blast Test Site at Kirtland Air Force Base (Albuquerque, NM). The 

Lovelace Foundation for Medical Education and Research (Albuquerque, 

NM) operated this site from the 1950s until 1980, under the sponsorship 

of various defense agencies concerned with nuclear weapon effects or, in the 

1970s, with fuel-air explosions. Animals ranging from mice to steers, as well 

as test dummies, were used to estimate lethality from blast in the open, in 

buildings, in foxholes, and with combinations of blast and thermal effects. 

(See the comprehensive history of the Blast Test Site.5) 
Introduction | 5

Lethality correlations developed during this time have become part of 

nuclear weapons assessment and Army field manuals. The so-called Bowen 

curves relate lethality to the strength of the blast, as measured by peak pressure and duration.6,7 An empirical scaling based on body mass allows the 

same correlations to be used for all large animals and humans.

Occupational Limits of Blast Exposure

Whereas the Bowen curves provide a criterion for lethality, Military Standard 

1474 provides a criterion for hearing protection during occupational exposure 

to blast.8 The standard is based on a 1965 report of the National Research 

Council Committee on Hearing, Bioacoustics, and Biomechanics (CHABA; 

Washington, DC) that sets noise limits for occupational environments.9,10The 

Military Standard, using a relation adopted from CHABA that depends on 

amplitude and duration of the overpressure, limits the number of impulse 

noise (blast) exposures that can be received in a day. If hearing protection 

(plugs or muffs) is worn, a greater number of exposures is allowed. The standard contains a special limit, called the Z-line, corresponding to the auditory 

limit of 5 shots/day when wearing protection. Exposure above the Z-line is 

prohibited, because of the potential for nonauditory injury. Although it is 

unlikely that any data to support this limit existed when the CHABA originally 

met, it is understandable that, at some level—no matter how effective hearing 

protection is—there will be a risk of injuries to other parts of the body from 

blast. In 1965, no occupational noise approached the Z-line limit. 

As noted previously, the M198 howitzer, a critical new weapon system, 

exceeded blast noise limits and could not be fielded. It fell on USAMRMC 

and MOMRP to address this issue. It had always been suspected that the 

Z-line was a conservative limit, but it was not known at what level internal 

injury would first appear or how it would manifest. 

To solve the immediate crisis of the M198 howitzer, a human volunteer 

study was organized.11 Starting from distances known to be safe, the volunteers moved closer to the howitzer until they were at the crew positions. 

Medical examination showed that hearing could be protected and that no 

internal injuries were sustained. The M198 testing proceeded, and the system 

was fielded, although a training restriction on the number of exposures above 

the Z-line was made. Additionally, USAMRMC initiated a research program 

for blast injury to develop a replacement standard for the Z-line. Until a 

new standard was developed, similar human-rated qualification of weapons 

systems would be conducted whenever the Z-line was exceeded.12
6 | Blast Injury: Translating Research into Operational Medicine

Table 1. Taxonomy of Blast Injury 

Characteristics

Unique to high-order 

explosives, results from 

the envelopment of the 

body in the overpressurization wave. 

Body surface and internal organs are rapidly 

distorted because the 

body contains highly 

compressible tissues 

(air-containing organs) 

that undergo rapid 

volume changes.

Impact on the body 

from flying debris and 

bomb fragments. 

.

Category

Primary

Secondary

Body Part Affected

Gas-filled structures are 

most susceptible because 

they suffer the greatest 

distortion—upper airways, 

lungs, gastrointestinal tract, 

and middle ear.

Internal distortions of aircontaining organs cause 

distortion of neighboring 

solid organs—heart, liver, 

spleen, and kidneys.

Differential loadings within 

the body, especially the 

vascular system, can 

cause upset that can be 

transmitted to other parts 

of the body.

Any body part may be 

affected. 

Depends on the speed, 

mass, and shape of the 

impacting object.

Types of Injuries

Blast lung (pulmonary 

barotrauma). 

Tympanic membrane rupture 

and middle ear damage.

Abdominal hemorrhage 

and perforation; globe (eye) 

rupture. 

Concussion (traumatic brain 

injury without physical signs of 

head injury).

Laceration of the liver, spleen, 

and kidneys. 

Contusion to the heart. 

Distortion and rupture of the 

great vessels.

Air emboli introduced across 

the air–blood boundary of 

the lung. 

Surges in blood flow and 

pressure that may lead to tissue 

injury in the brain.

Any injury associated with 

impact of high-speed objects. 

These modes are not unique to 

blast; however, blast provides 

a different way of propelling 

the objects.

Penetrating ballistic (fragmentation) or blunt injuries.

Eye penetration (can be occult), 

skull fracture, etc.
Introduction | 7

Table 1. Taxonomy of Blast Injury (continued)

Characteristics

Whole-body acceleration caused by the blast 

wind.

Uneven forces on 

the body caused by 

the blast winds.

All explosion-mediated 

injuries not associated 

with pressure or wind 

effects.

High temperatures.

Toxic gases.

Secondary 

consequences of 

trauma.

Exacerbation or 

complications of 

existing conditions.

Category

Tertiary

Quaternary 

Collateral

Body Part Affected

Any body part may be 

affected. 

Depends on the surface 

condition that the body 

impacts.

Primarily head/neck and 

extremities that can be 

accelerated relative to 

the torso.

Any body part may be 

affected.

Body surfaces, eyes.

Respiratory system.

Systemic responses from 

massive trauma.

Types of Injuries

Any injury associated with 

whole-body motion and 

impact. These modes are not 

unique to blast; however, 

blast provides a different 

way of accelerating the 

body.

Typical injuries that would 

occur in falls or car crashes. 

Fractures, contusion, and 

closed- and open-head 

injuries, etc.

Traumatic amputation; 

muscle tears.

Burns (flash, partial, and 

full thickness).

Asphyxia.

Injury or incapacitation from 

inhaled toxic fire gases.

Not unique to blast.

Angina, hyperglycemia, 

and hypertension.

Asthma, chronic obstructive 

pulmonary disease, or other 

breathing problems from 

dust, smoke, or toxic fumes.
8 | Blast Injury: Translating Research into Operational Medicine

Military Operational Medicine Research Program 

(Blast Injury Research)

From the beginning, the MOMRP blast research program was model-based. 

The decision to use a model-based system came from a balanced assessment 

of the immediate and long-term benefits of animal, physical surrogate, and 

mathematical model approaches. On one extreme, a test of the actual threat 

against a human under the exact conditions of interest is the least ambiguous way to determine an effect and one that requires no understanding of 

the internal mechanisms. This is ethically not possible for conditions that 

produce injury and is impractical to define the range of conditions. On the 

other extreme, a mathematical model that captured every mechanical, chemical, and biological aspect of the human body can provide a simulation basis 

for studying any situation without risk to an individual. Given the state of 

knowledge and computing, this goal exceeds any reasonable endeavor. In 

between these extremes are combinations of animal, physical surrogate, 

and mathematical models that describe some part or scale of the interaction 

(Figure 1). The goal of the MOMRP effort is to use the appropriate mix of 

tools to derive the best possible immediate answer, while continuing to develop 

incrementally better mathematical models that will expand the generality of 

our understanding. 

The first problem addressed was the interpretation of the pressure signal. 

Unlike the idealized waveforms that had been encountered and characterized in large-scale explosions, the howitzer waveform contained two peaks. 

This form confounded the simple empirical correlates that existed and, 

because they varied in magnitude and time of separation from place to place 

around the howitzer, were suspected to be artifacts of the test geometry or 

the instrumentation. Jaycor, Inc (San Diego, Calif), developed a mathematical model of the propagation of the blast from the muzzle of the weapon, 

accounting for the nonlinear reflection from the ground. The model proved 

conclusively that the waveforms were from those interactions. Furthermore, 

the model was able to provide a complete map of the hazardous areas around 

the gun, for all gun elevations and charge types, without requiring extensive 

physical measurements. With this model, analysis of other weapon systems 

could also be made with data from only a few measurement locations for 

calibration.13

Using the results of the model as a guide, animal studies were formulated 

and conducted at the Blast Test Site. From 1980 until its closure in 1998, the 

focus of the research was injury, not lethality. Studies spanned blast conditions 

that produced no observable effects to serious, life-threatening injury and 
Introduction | 9

death. Great care was taken to document pathologies observed in all organs. 

Primarily sheep were used as test subjects to provide consistency across all 

studies. This 18-year effort produced nearly 2,000 animal exposures that 

represent the most extensive collection of blast-related injury data in the 

world. Subsequently, a comprehensive pathology scoring system for blast 

injuries was developed.

The earliest injury tests were focused on establishing a threshold level of 

blast overpressure, below which injury would not occur. Unfortunately, such a 

level could not be determined definitively, because small probabilities of injury 

required a large number of animals to estimate thresholds with confidence. 

These low-level tests did show, however, that the air-containing organs (ie, 

lungs, GI tract, and trachea/larynx) were the first organs to be injured.14

Next, tests were designed to determine if URT injury occurred before lung 

and GI injuries, with the thought that a harmless precursor injury could be 

used as an indicator of impending, more serious, internal injury. This hypothesis was based on auditory experience in which a temporary threshold shift (a 

minor, transient hearing loss) always preceded permanent hearing loss and, 

therefore, allowed human subjects to be used to establish safe boundaries. 

Unfortunately, blast-caused URT injury occurs at essentially the same levels 

that cause lung and GI injuries.

Finally, tests were conducted to establish a universal blast exposure dose 

that could predict injury from the blast pressure signal alone, eliminating the 

need to conduct animal or human tests. The logical candidate, based on the 

Response Injury

Human Target

Animal Model

Compliant Physical Target

Rigid Physical Target

Rigid Mathematical Model

Mathematical Model

Complete Mathematical Simulation

Reproducible Operational Biofidelic Validated Statistical

Biomechanical

Correlate

FACTORS FAVORING BIOLOGICAL TESTING

FACTORS FAVORING SIMULATION

Fidelity

Understanding Required

Generality, Knowledge Gained

Risk, Cost

“Compliant” Mathematical Model

Impact

Figure 1. Animals, physical surrogates, and mathematical models. 
10 | Blast Injury: Translating Research into Operational Medicine

trends seen in structural damage from blast, was impulse—the time integral 

of the pressure signal. Impulse, however, did not provide a universal correlate 

with blast injury.

Failure of these attempts to identify simple patterns or markers in blast 

injury was amplified when blasts in enclosures were studied. Results of these 

studies underscored the need to understand actual anatomical dynamics and 

root causes of primary blast injury. Mathematical modeling helped guide 

research and establish criteria.
First-generation Injury 

Modeling

First-generation models correlated injury to mechanical responses of the 

body, rather than to the characteristics of the blast pressure itself. This biomechanically based criteria was driven by failure of pressure-based correlates 

to predict injury for simple waves in the free field or for complex waves in 

enclosures.

The mechanism of injury was hypothesized to consist of three causal 

steps: (1) blast waves create temporal and spatial loading distributions on 

the external body surface; (2) the body deforms under the loading and causes 

internal stresses and strains in the tissues; and (3) when these tissue stresses 

exceed material limits, injury occurs. Computational power, both in terms of 

computer speed and simulation software, was in its infancy in the early 1980s; 

however, mathematical modeling made significant contributions. Four organ 

systems were considered in first-generation injury modeling: (1) the tympanic 

membrane, (2) the trachea, (3) the GI tract, and (4) the lung.

Observed Blast Injuries

Blast can cause a wide range of injuries. As the explosive levels grow, the 

magnitude of the forces acting on the body grows, and the extent of the 

body response increases. Occupational standards, however, focus on iden-
12 | Blast Injury: Translating Research into Operational Medicine

Enclosures

Threshold Severe

Larynx

Trachea

Lung

GI

Liver

Spleen

Kidney

Pancreas

Gallbladder

Death

Normalized Charge Weight (kg/m3

)

0.06

0.05

0.04

0.03

0.02

0.01

0.00

tifying the organs most easily injured and on setting acceptable levels of 

lesser injuries. 

From testing at the Blast Test Site, a clear pattern of blast injuries 

emerged. Over time, as more data have been collected, these patterns 

have been reaffirmed; and, using the animal tests currently available, 

the patterns could be assigned statistical significance. To observe the 

pattern of injury from a range of tests that used different explosive 

weights, ranges, heights of burst, orientations, and number of exposures, 

it is necessary to select a single characteristic of exposure. One such 

parameter is the charge weight per characteristic volume. In the free 

field, this volume is a sphere with a radius equal to the distance to the 

test subject; in enclosures, this volume is the volume of the enclosure. 

Surprisingly, and, perhaps fortuitously, this quantity provides a good 

correlation and similar numerical values for the thresholds in all cases.

The average explosive weight per volume, at which minor and severe 

injuries are seen for each organ group, is shown in Figure 2 for tests in enclosures. A similar trend exists for the free-field tests. Organs can be separated 

into three groups having similar characteristics. The air-containing organs 

(larynx, trachea, lung, and GI tract [forming the first group]) show the first 

signs of injury at approximately the same blast intensity, which is well below 

that seen in other groups. The liver and spleen (Figure 3) fall into a second 

Figure 2. Observed blast injury. GI: gastrointestinal. 
First-Generation Injury Modeling | 13

group, whereas the kidney, pancreas, and gallbladder form the third group. 

Clearly, the air-containing organs are the most vulnerable and, therefore, 

require the greatest consideration for occupational exposure. All organs are 

seriously injured at similar blast intensity. Lethality, which is primarily due 

to a multiple organ failure, is seen at this same level.

Exploratory Injury Models

Mathematical modeling of biological systems is particularly difficult, because 

every aspect of the system (geometry, material properties, and strengths) is 

complex and determined by ever smaller structures, all the way down to the 

Figure 3. Liver injury resulting from blast. 
14 | Blast Injury: Translating Research into Operational Medicine

cells themselves. Therefore, each aspect of the model must be guided and 

validated by experimental data. 

Tympanic Membrane Injury Modeling

Tympanic membrane rupture is a common blast injury and one that occurs at blast levels usually well below any of the internal injuries. Although 

not considered a life-threatening injury, eardrum rupture can be extremely 

painful and may or may not be associated with hearing loss. In the mid1980s, eardrum rupture was a concern of blast exposure in training and 

in combat. Thus, an effort 

to develop a mathematical 

model of the process was 

undertaken. Finite element 

modeling (FEM) was used 

to model the stapes and the 

membrane. The stresses at 

which the membrane tore 

were based on independent 

tissue properties measurements. The model was subsequently validated against 

in vitro data to establish 

biomechanically based injury criterion.15

Tracheal-Laryngeal Injury 

Modeling

The interest in establishing URT injury as a precursor to more serious internal 

injury prompted the need for 

a model that could be used 

to extrapolate URT injuries 

from animal to humans. 

Blast-induced tracheal injury 

is often striated in appearance, corresponding to the 

cartilage between the bony 

rings. In extreme conditions, 

Figure 4. Trachial injury resulting from blast. it can present as a confluence 
First-Generation Injury Modeling | 15

of hemorrhagic tissue (Figure 4). The trachea was selected for modeling because of its geometric simplicity and because material properties were available from the literature. Blast loading on the neck was used as the external 

boundary condition, and injury was correlated with peak stress that developed 

in the tissue. This model predicts the mechanical response of the larynx, and 

the general trends of the injury are correlated with stress in the tissues.16

Gastrointestinal Injury Modeling

 GI injury from blast appears first as small petechia in the gut lining, 

grows in hemorrhagic area as blast intensity increases, and can reach frank 

rupture. In sheep, the injury most commonly appears in the cecum, although 

large blasts produce injury throughout the GI tract (Figure 5). GI injury—

especially rupture of the tract wall—can lead to sepsis and death, and can 

complicate treatment of other injuries, especially those in the lung.

Rabbit experiments confirmed that GI injuries were associated with sections of the tract containing air bubbles. The bubbles collapsed during the 

overpressure phase of the wave and then violently reexpanded. If the bubble 

was close to the tract wall, this rapid volumetric change led to deformation 

Figure 5. Gastrointestinal injury resulting from blast. 
16 | Blast Injury: Translating Research into Operational Medicine

of the wall. The effect varied with bubble size, overpressure, and tract contents. For large overpressure, the stresses became so great that rupture of the 

wall occurred. Once the mechanism was established, surrogate GI models 

were developed that allowed this bubble–wall interaction phenomena to be 

further studied.17–20

With these surrogate observations as a guide, a mathematical model of 

the bubble dynamics and wall response was developed.21The model produces 

the same dynamic response and, when coupled with material properties and 

the strength of the tract wall, can provide a predictive model for GI injury 

from blast.

Because lung injury was eventually selected as the primary injury to set 

blast exposure limits, the GI model was not pursued. The model suggested, 

however, that GI injury may be greater in sheep than in humans because the 

sheep is a ruminant with much more gas in the intestines. A summary of the 

early blast data analysis and model development is found in the publication 

Modeling of the Non-Auditory Response to Blast Overpressure: Characterization and Modeling of Thoraco-Abdominal Response to Blast Waves.

22

Lung Injury

Even though all of the air-containing organs are injured, Walter Reed Army 

Institute of Research (WRAIR) physicians determined that injury to the lung is 

of greatest concern and should be used to set exposure standards. As a result, 

modeling research efforts focused on understanding lung injury mechanisms 

and developing predictive lung models.

Most organs of the body are liquid-filled, some are air-filled, but the lung 

is a complex matrix of more than 500 million small air sacs (or alveoli), with 

tens of millions of connecting airways.23 Under normal physiological motion, 

this structure acts as a simple balloon that fills and empties, with a pressure 

drop from inside to outside that is modest and reflects the resistance of the 

many small airways. Under the rapid motion caused by blast, however, air 

cannot flow fast enough through the airways, and the lung acts as a collection 

of isolated air bubbles—a foam. Foams have the interesting physical property 

that their speed of sound (the speed at which a volumetric disturbance in one 

part of the material can be spread to other parts) is only 30 to 40 m/s—one 

tenth that of air and one fiftieth that of water.24,25 This low speed of sound 

causes the lung parenchyma directly behind the moving chest wall to be 

crushed and severely injured, if the chest wall velocity is great enough. The 

injury produces a characteristic surface hemorrhage pattern predominantly 
First-Generation Injury Modeling | 17

on the blast side in the free field, but can involve the entire lung when the 

blast is enclosed (Figure 6).

In the early 1980s, Jaycor began working with Professor Y C Fung at 

the Bioengineering Department at the University of California, San Diego, 

to collect data that would support the development of a lung injury model. 

Professor Fung had already been studying the material properties of lung tissues.26 Over the subsequent several years, he and his colleagues established the 

key dynamic properties of lung tissue under the rapid motion associated with 

blast.27 They confirmed the low speed of sound and determined its variation 

with transpulmonary pressure. This group also established the correlation of 

internal lung pressure with edema—the breakdown of the alveolar walls.28

They measured the properties of the whole lung and lung tissue for both 

small animals and humans, and they showed that the material properties 

were similar. Experiments were conducted to elucidate the injury process, 

and mechanisms of injury at the tissue level were proposed.28,29 Jaycor, in 

one of the first applications of finite element analysis of biological systems, 

developed a two-dimensional model of the thorax under blast loading to 

quantify these tissue injury processes.30,31 That model reproduced the slow 

speed of the internal pressure waves in the lung, showing that the highest 

values of these pressures were located on the pleural surface of the blast side, 

Figure 6. Lung injury resulting from blast. (left) Complex waves. (right) Freefield waves. 
18 | Blast Injury: Translating Research into Operational Medicine

the heart, and the spinal process. These locations are similar to lung contusion 

observed in animals exposed to blast.

INJURY Software, Versions 1.0 to 4.3

Finite element analysis, although insightful, was too problematic at that time 

to be used as a means to understand the hundreds of animal tests that were 

being collected or to be used as a replacement for the Z-line. Consequently, 

simpler models were used: modeling the inertia of the chest wall and the 

density and speed of sound of the lung to create the so-called pleural surface 

model (Figure 7).22 When blast pressure acts on the chest wall, it accelerates, creating a pressure wave in the lung tissue, which in turn pushes back 

against the chest, thus slowing it down.32 The mechanical model was also 

validated against closely spaced blast loads that produce a double-peaked 

wave within the lung.33 The total work (integral of the product of force and 

velocity) done on the lung represents the magnitude of damage caused by 

crushing the alveoli. This irreversible work was the first biomechanical correlate of lung injury. Normalized work, which is the irreversible work divided 

by the product of the lung volume and ambient pressure, has proven to be a 

reliable predictor of blast lung contusion that can be applied across species, 

body weight, and altitude. The final version of the pleural surface model was 

published in 1996.34

Work also proved to be a correlate of lethality. The Bowen curves, developed decades earlier as empirical correlates of lethality observed in the free field, 

were shown to correspond to a particular work value. This finding not only 

provides a rational basis for the curves, but also provides a way to make lethality estimates in situations other than the free field. The lethality criteria 

based on work also allowed other observations, such as the reduction of lethality for slow-rising blast waves, to be explained with a single theory.34

The first versions of the INJURY software (Jaycor, Inc)—versions 1.0 

through 4.5—were developed to solve the pleural surface model equations and 

provide a prediction of the probability of injury. The input to this analysis is 

Figure 7. Pleural surface model of chest–lung interaction.

Pload Pwave Pbulk dt

dv

m = Pload −Pwave −Pbulk dt

dv

m = ( )
First-Generation Injury Modeling | 19

the so-called free field or side-on pressure measurement, which is converted 

to torso load with formulas for wave reflection. Effects of body orientation 

are accounted for by the angle of the chest to the blast direction. The medical 

staff at WRAIR used these versions of INJURY software to make case-by-case 

health hazard assessments of weapon systems.

Simple Waves

Use of a biomechanical model to describe blast injury requires knowledge of 

torso loading. Loading distributions can be quite complex, even for simple, 

free-field blast waves. A blast wave in the free field has a relatively simple 

description. The explosion produces a high-pressure region that evolves into 

a shock front that moves at a speed greater than the speed of sound. The 

pressure decreases behind the shock and can even drop below the ambient 

pressure. Tables of experimentally determined values and elegant theories 

and correlations capture these data.35 When a blast wave strikes the ground, 

it creates a reflected wave with a second shock front. The incident and reflected waves can interact with one another and, if the blast is strong enough, 

produce a third shock wave, the so-called Mach wave, that moves parallel to 

the ground. Above a certain height, called the triple point, where the three 

shocks intersect, one observes the incident and reflected waves; below the 

triple point, one observes only the Mach wave (Figure 8). As can be seen, 

even free-field explosions produce complicated blast patterns. 

Charge of Weight,W

Incident Wave

Mach Stem

Range,R

Path of

Triple

Point

HOB

Ground Reflection

Figure 8. Mach stem and triple point. HOB: height of burst.
20 | Blast Injury: Translating Research into Operational Medicine

When a shock wave hits a body, another complicated interaction occurs. 

The surface of the body facing the blast source acts as a reflector, producing 

its own reflected wave; but, because it is generally curved, not flat, there can 

be many reflected shock waves. As the wave passes around the body, the 

angle of the incident wave to the surface changes, altering the strength of the 

reflected waves; at the side, there is no reflected wave. Near this location, 

the flow from the blast separates from the body and creates a region behind 

the body that has a pressure lower than the incident wave, but higher than 

ambient. Consequently, the loading pattern on a standing human in a simple 

blast wave is quite complex: (a) the chest, assuming facing the blast, receives 

a loading that can be 2 to 8 times greater than the incident wave; (b) the 

sides receive a loading comparable with the incident wave; and (c) the back 

feels a loading that is a fraction of the incident wave. These interactions can 

be calculated with computational fluid dynamics (CFD) simulations.36–38 If 

the torso is above the triple point, then the distribution is even more complicated because the body is hit by two waves: (1) the incident component and 

(2) the reflected component.

For an animal standing on all fours, there is even more complication. 

One part of the wave passes over the back of the animal in the manner described previously, but the other part of the wave passes under the animal 

and creates additional reflections off the ground. The chest, which is normally 

facing downward, can receive a blast loading that consists of multiple shock 

interactions.

Clearly, even in the “simple” geometry of the free field, the blast loading 

on the body required to determine blast injury can be quite complex. Characterizing the torso loading in terms of a single, free-field pressure measurement 

was not adequate. 

The Blast Test Device

Because the blast loading in the free field was not easily inferred from a freefield pressure gauge, a new instrument was developed. Eventually known as 

the Blast Test Device (BTD), it consists of a metal cylinder, supported from 

the ends, with the approximate diameter of the sheep chest and with four 

surface-mounted pressure gauges evenly spaced around the cylinder. The latest 

BTD has an anthropomorphic shape and provides a host of attachments for 

ease of use in complex testing environments (Figure 9). One pressure gauge is 

oriented facing the oncoming blast wave, with the other gauges corresponding 

to the sides and back. The BTD is oriented in the same direction as the test 
First-Generation Injury Modeling | 21

Figure 9. Blast Test Device. 

subject, vertically for a standing human or 

horizontally for a standing animal.39

Since its inception, the BTD has been 

the preferred instrument for providing 

loading data for blast injury analysis. 

Because it measures the loading directly, there is no need to interpret the 

instrument output, correct for gauge 

orientation, account for being in or out 

of the Mach wave, or other factors that 

are required when free-field gauges are 

used. Over the years, the BTD has been 

placed directly on the ground to simulate 

a soldier firing from a prone position, 

propped up in a seat simulating a passenger in a vehicle, and hung from vertical 

supports to simulate suspended animals 

in an enclosure.

Blast in Enclosures

In the late 1980s, increased importance of Military Operations on Urban Terrain (MOUT) emphasized the need to train on weapons fired from buildings 

or enclosures. Initial animal studies showed that these situations are far more 

dangerous than their free-field counterparts and showed what appeared to be 

nonintuitive trends (eg, that animals farther away from the explosive, but in 

a corner, are much more severely injured than animals closer to the blast, but 

along a wall). These findings meant that the explosive charge weight and the 

distance, which had been mainstays of characterizing free-field blast, were 

no longer sufficient factors to consider.

Blasts in enclosures, often called complex exposures, led to attempts to 

extend previous injury and lethality correlations. Even though the Bowen 

curves provided a correlation of lethality in the free field, it could not be applied to complex waves. Although the peak pressures were about the same as 

would occur at the same distance from the same charge in the free field, the 

durations were much longer because of the wave reflections from the walls. 

If the Bowen curves were used, they would often predict lethality in benign 

conditions. Ad hoc changes were proposed to the definition of duration in 

an attempt to explain the data, but were not satisfactory.
22 | Blast Injury: Translating Research into Operational Medicine

The BTD proved to be the perfect instrument for characterizing the 

effects of blast in an enclosure. BTD measurements in corners showed the 

strong blast loading on the back side of the instrument, the side away from 

the blast and facing the corner. In many pressure traces, clusters of very large 

peaks were observed in the side or back gauges that had never been seen in 

the free field. When the pressure measurements from the back side of the BTD

were used in INJURY software, the large work values calculated explained 

the occurrence of injury in the lung lobes away from the blast. 

Although the BTD measurements offered a plausible explanation for 

the injuries seen in enclosures, the complexity and violence of the pressures 

measured had not been anticipated. It seemed likely that these pressures were 

from a convergence of waves coming to the corner from many reflective paths, 

but there was also concern that some or all of the effects may be artifacts of 

the pressure gauges in such harsh environments. Although simple ray-tracing 

techniques had adequately described the howitzer blast in the open, they 

proved inadequate to capture the complex reflections and interactions of the 

blast waves in an enclosure. 

Computational Fluid Dynamics 

CFD represents the numerical solution of the highly nonlinear, highly coupled, 

fluid dynamics equations. The science and art of CFD were first developed to 

support nuclear weapon design and effects analysis; but, by the late 1980s, 

the technique was used in all areas of engineering. 

This technique was adapted to blasts in enclosures to provide a rational 

understanding of “complex” blast. Simulations using the Equation Independent Transient Analysis Computer Code (EITACC; Jaycor, Inc) were made 

to understand the data from the BTD. Simulations could reproduce, with 

remarkable fidelity, the details of pressure measurements.38 As computer 

power rapidly grew in the early 1990s, CFD was used routinely to analyze 

complex waves (eg, to determine the effects of other objects in an enclosure 

on the blast loading).36

The first-generation models provided a way to predict injuries to the 

tympanic membrane, URT, GI, and, most importantly, the lung. These 

models, although simple, were based on biomechanical principles and had 

parameters that could be rationally determined from anatomy and tissue 

property measurements. The emerging importance of explosions in enclosures 

prompted development of new blast instrumentation, the BTD, and use of 

state-of-the-art CFD tools.
Second-generation Injury 

Modeling

The second generation of injury modeling extended the single-degree-offreedom models of primary blast injury to use the data directly from the 

BTD and to standardize the health hazard assessment process. Also, models 

for secondary and tertiary injuries were developed. The collaborative work 

between MOMRP and the Joint Non-Lethal Weapon Program (JNLWP) 

on projectile impact injury for nonlethal weapons led to the development 

of models to capture modes of impact injury to all parts of the body that 

could be used to assess secondary blast injury. The collaborative work between MOMRP and the National Highway Traffic Safety Administration 

(NHTSA) led to models of injury from whole-body impacts that could be 

used to evaluate tertiary blast injury. Finally, a cooperative project between 

MOMRP and the Defense Nuclear Agency explored the combined overpressure and thermal injuries and the collateral effects of compromised 

immune systems.

INJURY Software, Versions 5.0 to 7.1

Previous versions of INJURY software that considered the loading from a 

single side of the body successfully predicted free-field blast injury. In the free 

field, the injury is primarily in the lobes on the blast side. Complex wave 
24 | Blast Injury: Translating Research into Operational Medicine

exposures, however, showed the importance of loading from all sides of the 

body and, consequently, the pathology showed injury to all lung regions. The 

refinements of the INJURY software benefited from the growing number of 

animal data collected with BTDs at the Blast Test Site.40

Total Work on the Lung

The first change in INJURY software was to compute the normalized 

work from four calculations with the pleural surface model, one for each of 

the BTD measurements. The work was summed and correlated with overall 

observed pathology. This simple approach explained the injury trends, especially the increased hazard in corners of enclosures.

Whole-Body Loading

The importance of simultaneous loading from all sides of the body led 

researchers to consider more complete biomechanical descriptions of thoracic 

motion. The Lobdell model, developed at General Motors Corporation 

(Detroit, Mich), is used in the automotive industry to characterize chest impacts and has been calibrated by cadaver studies.41 The model accounts for 

the entire torso mass and—therefore, can be used to estimate whole-body 

acceleration from blast—replicates the dynamic force–distance relationships 

of large chest deformations with a combination of springs and dampers. The 

Lobdell model, however, is not anatomically based; it characterizes the chest 

with an equivalent mass, but not an equivalent area. For solid-body impacts, 

only the chest mass is needed; but, for blast waves that are described by a 

pressure (force/area), a chest area must be assigned.

To determine the effective area of the chest acted on by a blast wave, a 

finite element model of the thorax based on the National Library of Medicine’s (Bethesda, Md) Visible Human Project data set was developed.42 The 

internal organs were resolved as separate anatomical regions and materials. 

Material properties of the lung were based on earlier, established measurements; the heart treated as a liquid-filled sac; and the ribs and chest wall 

muscles combined into a single material whose elastic properties were selected 

from data in the literature. The model was validated for the same impact 

conditions that had been used to calibrate the Lobdell model, including both 

frontal and side impacts.

The validated finite element model was examined using a series of tests 

for which blast loadings and lung pathology were known in detail. The resulting prediction of internal pressure distribution closely matched the observed 

pathology patterns. The total normalized work was determined from the 

calculated chest wall motion, which also agreed with the simpler INJURY 
Second-Generation Injury Modeling | 25

software estimates. Finally, the fully validated model was used to determine 

the effective area that should be associated with the Lobdell model. The frontal 

area presented to the blast could be divided into the part that is deformed by 

the blast and the part that moves with the entire torso. The resulting modified 

Lobdell model (Figure 10) agrees with the more detailed finite element model 

with respect to chest compression, total normalized work, and whole-body 

motion. The pleural surface model was replaced by the modified Lobdell 

model in the next generations of INJURY software.43

Effects of Multiple Exposures

Based on animal test data available at the development of the first versions 

of INJURY software, it was believed that there was no cumulative injury to 

the lung from blast (ie, the lung was injured on first exposure, or it was never 

injured, no matter how many times the blast was applied). As more data were 

collected, it became clear that there was a cumulative effect in lung injury and 

that this effect was critical to determining the occupational exposure.

The animal data set was analyzed using a model of tissue fatigue to account for cumulative damage. Multiple logistic regressions, incorporating 

the fatigue factor, were used to produce correlations for four levels of lung 

contusion: (1) trivial (small petechia), (2) slight (less than 5% of the lung 

surface area contused), (3) moderate (less than 30% of area contused), and 

(4) severe (more than 50% of area contused).

Ae + Af = Ab

Af

Af

Ae M3

M1

K12

C12

M2

K23i

K23

C23

Kve23 Cve23

Figure 10. Modified Lobdell model.
26 | Blast Injury: Translating Research into Operational Medicine

Probabilistic Prediction

Multioutcome logistic regression was used to generate correlations between normalized work and each level of lung injury severity. This advanced 

mathematical technique brings the greatest statistical power to the development of the correlation and allows INJURY software to predict not only the 

expected injury, but also the most likely distribution within a population 

(Figure 11).

Full Coupling to the Blast Test Device

The interface to INJURY software was changed to allow the software 

to directly use the pressure data files taken from the BTD. Data format standards were established, and standardized reports were generated with each 

analysis.44 A tightly coupled instrument and software analysis procedure was 

established that continues to be used.

Trace Injury: BOP data

Trace Injury: Correlation

No Injury: BOP data

No Injury: Correlation

Moderate Injury: BOP data

Moderate Injury: Correlation

Severe Injury: BOP data

Trace Injury: Correlation

1.0

0.9

0.8

0.7

0.6

0.5

0.4

0.3

0.2

0.1

0.0

–14 –12 –10 –8 –6 –4 –2 0

= 1.8772 In( ) + 0.7752 In(NS)

Probability

Figure 11. Probabilistic prediction of lung injury. BOP: blast overpressure; NS: not significant;

Wsum: sum of normalized work from all sides of the body.
Second-Generation Injury Modeling | 27

Replacement of the Z-line in Military Standard 1474

From the release of the first version of INJURY software, health hazard assessments for nonauditory blast have been made based on its analyses. As 

the BTD gained acceptance, evaluation of occupational exposure conditions 

in which nonauditory blast injury was suspected used the BTD–INJURY 

software combination to estimate the probability of lung injury. Initially, the 

assessments were done by WRAIR physicians, and the upper limit on exposure 

was the occurrence of 1% of the most trivial lung injuries. To transition the 

technology to the US Army Center for Health Promotion and Preventative 

Medicine (CHPPM; Aberdeen Proving Ground, Md), the Executive Agent 

for the Army’s Health Hazard Assessment (HHA) Program, it was necessary 

to standardize the procedure and to interpret the predictions in terms of a 

risk assessment code (RAC). 

The RAC, used by CHPPM to assess the health hazards of military materiel, is a score from 1 to 5 that indicates the potential consequences of the 

hazard. A RAC of 5 represents a hazard that is negligible, whereas a RAC 

of 1 represents a hazard with catastrophic consequences. 

A second form of the blast injury assessment software called BOP-HHA 

(Jaycor, Inc)45 can analyze data from a complex test series in which multiple 

positions, explosive strengths, and repeated shot data are collected. The 

software determines the probability of each of the four levels of primary blast 

injury, from the trivial to the most severe, and incorporating both biological 

and shot-to-shot variabilities. These probabilities are used along with the 

hazard matrix to determine the RAC.

MOMRP sponsored a human volunteer study at the Blast Test Site 

from 1989 through 1997.46–51 The test procedure exposed groups of individuals, each wearing hearing protection, to an increasing sequence of 

blast noise conditions. (See Figure 12 for an example of volunteers being 

exposed to blast from a simulated mortar.) Pretest audiograms established 

baseline hearing profiles for each individual and ensured proper fitting 

of the protective devices. Posttest audiograms established the temporary 

threshold shift at a range of auditory frequencies. Temporary threshold 

shifts of 25 dB were taken as the recoverable failure limit for exposure 

of an individual. Long-term tracking of each individual showed that all 

hearing returned to baseline levels.

The study produced about 2,000 subject-exposure tests designed to 

determine the effects of blast intensity and number of exposures on recoverable failure. As would be expected, the percentage of failures increases 

monotonically with blast intensity and with number of exposures. The design 
28 | Blast Injury: Translating Research into Operational Medicine

of the experiment envisioned groups of 64 subjects progressing through the 

exposure matrix. That number of subjects would allow an estimate of the 

probability of failure at the 95% confidence level. Invariably, some subjects 

dropped out of each group, causing the significance of the results for a particular exposure condition to drop below the target confidence level.52

Figure 12. Volunteers being exposed to simulated mortar blasts.
Second-Generation Injury Modeling | 29

An independent statistical analysis of the volunteer data was conducted 

using logistic regression analyses.53 The subject-exposure tests were pooled 

into a pass-fail outcome with blast intensity, duration, and number of exposures as independent variables. The large number of data gave the analysis 

considerable statistical power and resulted in an estimate of the failure criteria 

with a narrow confidence band. Results showed that the observed threshold 

for failure, a 25-dB temporary threshold shift, is nearly 10 dB higher than 

the current Military Standard limit. In addition, the analysis showed that 

the best correlation of blast injury decreases with duration, but is consistent 

with data on the risk of short duration exposure, such as rifle fire.

Taken together, the estimated human threshold tolerance to both auditory and nonauditory blast injuries are greater than that previously indicated 

in Military Standard 1474. Formal revisions of the Military Standard to 

incorporate model-based criteria for both auditory and nonauditory injuries 

are undergoing consideration for adoption by the HHA Program. 

Secondary Blast Injury Modeling

In occupational settings, primary blast injury is the only concern. In combat, 

where blasts are much larger, debris can be propelled at the soldiers by the 

blast and lead to impact trauma or secondary blast injury. MOMRP has 

developed a biomechanical model of the impact trauma that can be used to 

evaluate this hazard.

In 1996, an interagency collaboration was formed—involving USAMRMC; 

the Armament, Research, Development, and Engineering Center (ARDEC); 

the National Institute of Justice (Washington, DC); and the US Department 

of Transportation (Washington, DC)—to quantify projectile impact injuries 

in terms of the characteristics of the projectile (mass, velocity, shape, and 

composition) and the region of the body impacted. The research collected 

and reviewed all previous studies and mathematical models on impact injury 

and selected the most credible set that would describe the widest range of 

blunt trauma and penetrating injuries. A software program, the Interim 

Total Body Model (ITBM; Jaycor, Inc), was developed and distributed to 

the sponsoring organizations.54

The ITBM software depends on the characterization of the impact 

loads from the projectiles. Specialized instrumentation for measuring the 

magnitude, duration, and extent of the forces delivered by the projectiles 

was developed.55,56 A specialized test apparatus was developed to accelerate 

various projectiles at controlled speeds onto the instrumentation for deter-
30 | Blast Injury: Translating Research into Operational Medicine

mination of dynamic properties and other test protocols for static properties. 

The combination of the testing apparatus, protocol, and model estimation 

became the standard for nonlethal weapon assessment.

WRAIR conducted swine tests to determine internal injuries from nonlethal projectile impacts. Test conditions covered an injury spectrum from 

mild skin bruising to through-and-through thorax penetration. 

Subsequent to this initial work, the Joint Non-Lethal Weapon Directorate (JNLWD; Quantico, Va) was formed, and in 2005, a Memorandum 

of Agreement between USAMRMC and JNLWP was formalized to share 

technology and resources. Under this agreement, joint research continued 

on blunt trauma from projectiles that includes model development, and 

animal and postmortem human subject testing. This research benefits both 

organizations by providing fundamental blunt trauma injury data to support 

USAMRMC soldier protection research programs and JNLWD nonlethal 

weapons assessment programs. 

This partnership has produced new biomechanically based models for 

a wide range of secondary blast (impact) injuries. A finite element model of 

skin response under impact has produced a model for penetration injury 

that takes into account the detailed anatomical structure and clothing.57 This 

model has been validated against animal studies at the Air Force Research 

Laboratory (Brooks City Base, Tex) and historical data collected from the 

literature. Similarly, a biomechanically based correlate for rib fracture has been 

developed that accounts for the detailed anatomical structure and material 

properties of bone.58 Similar cross-applications of head injury, skull fracture, 

and abdominal injury are being pursued. The ITBM, the Advanced Total Body 

Model (ATBM), and derivative applications provide the best estimation of 

injury from secondary blast effects.

Tertiary Blast Injury Modeling

The third mode of injury results from whole-body translation caused by the 

blast pressure differential and blast winds. These forces can hurl the body 

itself into surrounding objects and cause subsequent tertiary injuries. Although 

these injuries can result from blast, they are not unique to blast and have been 

studied in many other circumstances. In 1993, MOMRP began a collaborative effort with NHTSA (Washington, DC) on head and neck injuries—the 

most significant injuries that occur from body impacts. This collaboration 

has produced models of closed-head injury and head-neck injury that can be 

applied to tertiary blast injuries.
Second-Generation Injury Modeling | 31

Combined Injury Modeling

Complications of exposure to nuclear explosions include the following:

•	 physical trauma from the blast wave,

•	 	 burn trauma from thermal radiation, and

•	 	 disturbance to the immune system from the ionizing radiation.

Because of the possibility of sepsis and secondary infection, reduced 

immune function is especially dangerous when it occurs along with injury 

to the gut. In 1990, the Defense Nuclear Agency, now the Defense Threat 

Reduction Agency (Fort Belvoir, Va), approached MOMRP for assistance in defining a relationship between blast and GI injury that could be 

used to assess battlefield consequences. As part of the joint work, Jaycor 

developed mathematical models and a visual assessment of the nuclear 

battlefield showing where combined injury effects could occur. In addition, 

a cellular-based model of the response of the immune system to ionizing 

radiation was developed.59 This model incorporated stem cell dynamics 

and the interaction of white cells with opportunistic infections. The results 

generalized the standard, empirical response curves previously used into a 

form that could study a wider range of exposures and interventions. 

Closing of the Blast Test Site

New residential communities around Kirtland Air Force Base objected to 

the noise from the blasts, making it increasingly difficult to schedule tests at 

the Blast Test Site. Furthermore, the success of biomechanical modeling in 

understanding and predicting blast injury greatly reduced the need for new 

animal studies. Consequently, in 1998, the Blast Test Site in Albuquerque, 

New Mexico, was closed.

Although the original questions about blast injury had been answered, 

data that had been collected for more than four decades of research could 

never be reproduced. With this realization, Colonel Karl Friedl identified 

materials of irreplaceable historical value (eg, the original investigator notes 

from studies conducted at Hiroshima) and sent them to national libraries. 

Other remaining materials were shipped to Jaycor for safekeeping.

Under MOMRP support, these blast data are undergoing sorting, cataloging, and electronic preservation. Figure 13 provides an example of the data 

that can be retrieved from the database with IISYS software (Jaycor, Inc). 
32 | Blast Injury: Translating Research into Operational Medicine

This process continually supports MOMRP’s ongoing blast injury programs, 

including the refinement and extension of INJURY software, the refinement 

of HHA software for occupational exposure, and studies of injury from 

thermobaric explosives.

Figure 13. Example of blast injury data retrieved and displayed using IISYS software.
Third-generation Injury 

Modeling

The third generation of injury modeling expands the anatomical and physiological fidelities of the injury process. These models use finite element analyses 

to capture the mechanical response of the body to blast trauma, and highfidelity, systemic simulations to capture the physiological response to inhaled 

toxic gases. Finite element models allow predictions of regional injury patterns 

and the effects of protective clothing. Physiological models extend the effects 

of blast to include inhalation injury, incapacitation, and delayed lethality.

Finite Element Modeling 

FEM is a mathematical tool developed for analyzing engineering structures 

that is finding increasing application in biomechanics and trauma assessment. 

The approach breaks the object to be studied—in this case the human body—

into small volumes or elements. The elements correspond to parts of different 

tissues or organs, and they can be irregular in shape so that the anatomy is 

accurately represented. Because each element represents part of a single tissue, its mechanical properties are considered uniform. Each of the elements 

interacts with its neighboring elements through the common boundaries. As 

one element moves and changes shape, these forces and motions (stresses and 

strains) are transmitted to neighboring elements. 
34 | Blast Injury: Translating Research into Operational Medicine

A simulation begins with application of an external loading, from the 

blast overpressure or a projectile impact, and the calculation advances in 

time to the motion and distortion of the whole body and all of its internal 

elements. Every part of each tissue experiences stresses and strains as the 

body responds to the external load; when those quantities exceed the 

material strength of the tissue or the organ, damage occurs. The power 

of the FEM approach is that, in principle, if the anatomy is adequately 

resolved by enough elements, if the material properties of each tissue are 

adequately known, and if the limiting stress/strain is known, then injury 

from any trauma can be predicted.

Each of these aspects (geometric features, material properties, and 

failure limits) are only imperfectly known, however, so FEM is still very 

much an art. First, the human body is extremely complicated, with structures on every scale down to the cells; consequently, it is not possible to 

generate a complete anatomical representation. Judgment must be used 

to resolve the anatomical features that are most important for the process 

being studied. Second, almost no biological tissue is truly homogeneous; 

rather, it is made up of finer structural elements that make the apparent 

material properties dependent on the scale of elements being used. Again, 

judgment is needed to select material “constitutive” relations and their 

parameters that will capture the most relevant responses at the scales of 

interest. Finally, most tissues, because of their complex composite nature, 

do not have simple failure stresses and strains. The mechanism of damage 

can be partial, cumulative, and sometimes self-correcting. Furthermore, 

the most important damage is often functional, rather than structural, so 

that simple mechanical failure is not the critical endpoint. For example, 

rupture of a blood vessel can either lead to a small blood loss that is selfcorrecting or it can lead to a fatal hemorrhage, with only a slight difference 

in the extent of the material failure.

Despite the considerable challenges facing the application of these engineering concepts to biological systems, powerful results have been achieved 

and, in time, many of the difficulties noted previously will be overcome by 

the relentless increase in computational power.

Finite Element Modeling in Blast Injury

One of the first applications of FEM to blast injury was the study of 

wave propagation in the lung under blast loading.30,60 This work was 

conducted when FEM software was in its infancy, but was able to dem-
Third-Generation Injury Modeling | 35

onstrate the critical nature played by the lung’s unique material properties on concentrating and distributing loading. The lung, because it has 

the compressibility of air but a density 100 times greater than air, has a 

very low speed of sound—only about 30 to 40 m/s. When the chest wall 

moves at a fraction of that speed (eg, 10 m/s), considerable pressures 

can build up at the inner surface of the thorax wall. When the velocities become greater than 20 m/s, the equivalent of shock waves can be 

produced that are very destructive. These insights helped guide the early 

INJURY software models.

The next application was rupture of the tympanic membrane.61 In this 

case, the geometry of the affected organ is far simpler than other parts of 

the body. The mechanical structure of the outer ear consists of the tympanic 

membrane, a tissue of well-known geometry and material properties; the 

ossicular chain, again with well-known geometry and properties; and the 

cochlea that, although it has complex internal structure, acts only as a flexible base for purposes of determining the load on the ear drum. This model 

was able to provide a biomechanical explanation and a predictive model for 

tympanic membrane rupture. It even explained some of the unique tearing 

patterns seen in this kind of injury.

The first application of FEM to the whole thorax was used to calibrate 

the Lobdell model that was described previously. The Lobdell model is a nonphysiological model of thorax response under impulsive loading. The model 

specifies a mass of the sternum region, but not an area. Because blast waves 

apply a pressure (force/area) to the body, it is necessary to determine the area 

that corresponds to the Lobdell model mass so that the model can be used 

to compute the chest motion. For this purpose, a FEM of the human thorax 

was constructed from the Visible Human Project data set. The anatomical 

detail was quite limited, with the model only resolving the chest wall, lung, 

heart, and diaphragm. Because these are composite tissues, material properties were estimated from composites of the underlying tissue materials. The 

model was calibrated against human cadaver studies using impact masses. 

From these simulations, the Lobdell model could be reinterpreted in terms 

of the true physiological elements and, in particular, the equivalent area of 

loading determined. This model was then used to study blast loading, and a 

correlation was developed to translate pressure loading into forces that could 

be applied to the masses in the Lobdell model. This key correlation forms the 

basis of the INJURY software, versions 5.0 to 7.1.

The joint research program between MOMRP and NHTSA on blast 

and car crash injury produced a series of finite element models of the human 

skull that were used to set skull fracture injury criteria. Here, the geometry 
36 | Blast Injury: Translating Research into Operational Medicine

is relatively simple and can be accurately determined by medical imaging. 

Jaycor developed mathematical transformations to produce FEM models 

of the skull directly from imaging, including the resolution of the composite 

structure of the inner and outer tables and the diploe.62–64 These studies produced biomechanically based head-injury criteria that could be used in the 

automotive field for head impacts against interior vehicle structures and for 

tertiary blast injury. These same biomechanical models are used to predict 

focal skull fractures that arise from the head hitting very small protrusions or 

the secondary blast projectiles.65 These models are also being used to study 

the effects of head protection66 and the creation of a single skull fracture 

criterion for all insults. These models are used in the ITBM.

These four examples of FEM application were developed to improve or 

validate other simpler injury models and correlations. Beginning in 2000, 

MOMRP began a program with Jaycor to model the blunt trauma that 

occurs behind body armor when the armor stops a high-speed bullet with 

FEM as the final product. These models reproduce the anatomy in far greater 

detail than used previously, and required new medical imagery and new 

mathematical treatment to analyze, segment, and build robust elements. The 

models developed have been validated with animal tests in which medical 

imaging is used to produce subject-specific models that are validated against 

instrumented animal tests. 

Starting in 2003, MOMRP and JNLWD formulated a collaborative 

research program to apply these high-fidelity thoracic response models to 

the impact of projectiles. The result is ATBM, which uses finite element 

simulation to determine rib fracture and lung contusion based on projectilespecific, subject-specific, and location-specific conditions. JNLWP uses ATBM 

to provide the most accurate estimate of nonlethal weapon effects. The same 

model increases the fidelity of estimation of secondary blast injury. 

In addition to better biomechanical response, ATBM computes the 

trajectory and impact locations of projectiles, including the determination 

of impact locations on individuals in a crowd. This capability, when applied 

to secondary blast injury, allows for computing the statistics of both injury 

locations and injuries under realistic combat conditions.

INJURY Software, Version 8

The latest version of INJURY software, released in 2005 from the MOMRP 

Web site, introduces further anatomical refinement (Figure 14). Account 

is taken of the fundamental anatomical difference between sheep (narrow 
Third-Generation Injury Modeling | 37

chest, wide sides—for which the majority of the injury data have been 

determined) and humans (broad chest, narrow sides—for which the model 

is applied). In addition, body orientation is accounted for by distinguishing 

the front and back in the Lobdell model. This generation of the model has 

been validated against Blast Test Site data that have been carefully quality 

checked, and the code offers a red-yellow-green characterization of the 

relative hazard of the blast exposure.

Figure 14. INJURY software, version 8.2, used to estimate lung injury from blast exposure.
38 | Blast Injury: Translating Research into Operational Medicine

Toxic Gas Inhalation

In addition to the mechanical blast injuries, explosives produce toxic gases 

that, when inhaled, can lead to disorientation, incapacitation, or death. Both 

health hazard and survivability assessments require a means to estimate the 

probability of these endpoints from exposure to gases generated by blast or 

the resulting fires.

The Live Fire Test Program (LFTP; Director of Operational Test and 

Evaluation) is a US Department of Defense organization responsible for 

overseeing and evaluating the survivability of US systems and vehicles from 

enemy weapon systems. In 1994, the LFTP invited MOMRP to participate 

in the formulation of human effects from enemy weapon fire in the areas of 

blast and toxic gas. MOMRP entered into a series of projects with Jaycor 

to evaluate existing toxic gas exposure standards, identify shortcomings, 

and demonstrate improvements that could be made in the near term to 

assist the LFTP. Small animal tests were conducted that highlighted the 

shortcomings of existing standards.67 These projects resulted in the airway 

blood chemistry model that was used to expand toxic gas survivability assessments. This work identified that the shortcomings of existing standards 

arose from their lack of a physiological basis, both to scale results from 

animals to humans and to account for critical physiological responses.

Following this initial evaluation, an effort to develop a detailed physiological model of the body’s response to toxic gas inhalation was undertaken. 

This effort produced a series of source books that reviewed and summarized 

existing models and experimental data from which the research effort had 

been planned. The first book of this series reviewed all previous models, 

mechanisms, and assessments of biological effects caused by toxic gas 

inhalation.68 The all-existing test data—from books, reports, and papers—

were collected in a second book.69 These data were digitized and analyzed 

to evaluate current standards and to identify missing data that would be 

needed to construct a physiologically based model. The third book of this 

series reviewed all control-of-breathing models, because ventilation was the 

dominant physiological factor missing from previous models.70

These reviews clearly identified the lack of knowledge of ventilation 

changes that occur during toxic gas inhalation; thus, an extensive series of 

small animal tests have been conducted at WRAIR and at the Lovelace Respiratory Research Institute (Albuquerque, NM). These studies on ventilation 

effects, coupled with a compilation of thousands of previous animal tests on 

incapacitation and lethality, provide the basis for developing physiologically 

based models.
Third-Generation Injury Modeling | 39

The first version of the Toxic Gas Assessment Software (TGAS, Jaycor, 

Inc) provides estimates of immediate incapacitation from any combination of 

seven toxic gases: (1) carbon monoxide, (2) hydrogen cyanide, (3) hydrogen 

chloride, (4) nitrogen dioxide, (5) acrolein, (6) low oxygen, and (7) carbon 

dioxide. The gases can vary in concentration over time, and TGAS accounts 

for animal species, mass, and activity. TGAS estimates ventilation changes 

and tissue absorption to compute a body-weight–normalized internal dose, 

accounting for all of the factors described previously. The normalized internal 

dose is used to determine a dose-response curve that is species and exposure 

independent. The model predicts the probability of immediate incapacitation 

that can provide a toxicological assessment of survivability for both military 

and civilian applications.71

TGAS version 2.0 provides estimates of immediate incapacitation and 

immediate and delayed lethalities from combinations of these same gases.72

Many irritant gases produce lung injury that can lead to death long after 

exposure. Because the exposure levels that can cause these effects might 

be much smaller than those that cause incapacitation, it is necessary to set 

standards based on the most limiting condition.

Explosions often occur in enclosures or vehicles that have fire suppression systems. These systems often contain halide compounds, which 

can break down by pyrolytic processes and introduce acid gases into the 

enclosure atmosphere. These acid gases are toxic themselves and have a 

strong effect on ventilation. Furthermore, the explosion can cause secondary fires that release other complex toxic gases. The combination of 

these primary and secondary effects of explosions leads to an even more 

complex mixture of noxious gases that must be considered to determine 

incapacitation and lethality.

In the past 30 years, physiologically based pharmacokinetic (PBPK) 

models have been developed to describe the physiological effects of the inhalation of harmful organic gases. These models are used to set internal dose 

limits, based primarily on blood concentration levels, for each compound. 

This internal dose approach allows animal data to be scaled to humans and 

allows effects due to time-varying gas concentrations to be estimated from 

data collected under constant conditions. The primary use of PBPK models 

has been in setting short-term environmental exposures, but these results are 

readily assimilated into the TGAS framework.

The first step taken was to survey the current literature on PBPK modeling and the known mechanisms of interaction of halocarbon materials 

with the body. The development of PBPK models involves replicating with 

mathematics the transport, metabolism, and elimination of inhaled chemicals. 
40 | Blast Injury: Translating Research into Operational Medicine

Furthermore, the chemical and physiological parameters used by these models 

must be estimated from in vitro tissue measurements or limited animal testing. 

These quantities generally have large variations in their values and require a 

systematic means to come to a single, accepted value. The mathematical basis 

for PBPK models, their variation in application, the techniques for establishing parameter values, and the methods for interpreting and using the results 

are summarized in a comprehensive source book.73 Although PBPK models 

are used in many aspects of physiology, considerable literature exists just for 

halocarbons. Not only are these substances important to fire-extinguishing 

applications, but also many are ozone depleting and are being eliminated 

from global use for environmental reasons. The sheer number of possible 

compounds that vary in importance—depending on their environmental 

impact, chemical composition, and/or pyrolytic effects— makes this area 

extremely complex. These compounds and the PBPK models that have been 

developed to understand their biological effect are discussed in a second 

source book.74 Finally, not only are the chemical and biological impacts of 

these substances complex, but also so is the regulation that controls their use 

and replacement. Because devising appropriate fire protection schemes is a 

component of blast mitigation, the regulatory landscape of this complex area 

is analyzed and summarized in a third source book.75

PBPK models include a respiratory component that determines the 

amount of chemical inhaled during the exposure. Because these models have 

been developed at different times and by different researchers, there is little 

consistency in the selection of normal physiological parameters, especially 

ventilation. Furthermore, all of the models assume that ventilation is unaffected by the gases inhaled and ignore any interaction in ventilation caused by 

gas mixtures. A PBPK model (which uses common physiological parameters) 

has been developed that has been recalibrated against all halocarbon test data 

available in the literature. Furthermore, this model has been coupled to the 

TGAS version 2.0 model for describing ventilation changes from chemical 

and exercise effects. The combined model can analyze more than 30 gases 

in combination and is designated TGAS version 2.0P.76

TGAS versions 1.0 to 2.0P account for ventilation changes with factors 

that vary with the external concentrations of the gases. The animal studies, 

however, show that these ventilation changes vary with time in a complex 

way. Many of the changes do not occur for several minutes in small animals, 

corresponding to the time required for critical blood chemistry changes to 

occur. Because of large differences in the ventilation-to-body mass ratio between small animals and humans, these effects might take longer to occur. 

Because some toxic gases suppress ventilation, whereas others enhance it, 
Third-Generation Injury Modeling | 41

ventilation is critical to properly account for the temporal and species effects 

in extrapolating small animal results.

To account for these complex ventilation changes, a Dynamic Physiological Model (DPM) was developed.77 The DPM includes models of ventilation, 

circulation, and metabolism and, most importantly, models of the neural 

control systems that govern these processes. The neural controls are driven, 

in turn, by blood chemistry changes sensed by chemoreceptors in the carotid 

arteries and the medulla oblongata of the brain. Consequently, the DPM 

contains extensive blood chemistry models and models for the metabolism in 

the brain. This model reproduces most of the significant ventilatory changes 

seen in animal tests and provides a physiologically based means to extrapolate 

these critical changes to humans (Figure 15). 

Experimental Data

Upper Range

Lower Range

Dynamic Physiology Model

1.5

1.4

1.3

1.2

1.1

1.0

0.9

0.8

0.7

0.6

0.5

0.4

0.3

0.2

0.1

0.0

Minute Ventilation/Body Mass (L/min/kg)

Time (min)

–5 –4 –3 –2 –1 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15

Figure 15. Ventilation response to acute carbon monoxide exposure.
42 | Blast Injury: Translating Research into Operational Medicine

Blast Effects Behind Body Armor

As the US military is engaged in urban and asymmetric warfare, soldiers are 

increasingly exposed to blasts from nonmilitary explosives. In the Afghanistan and Iraq conflicts, nearly 65% of all casualties are from blast injury. 

Because of the concern that ballistic body armor may have some unexpected 

amplifying effect on blast injury, the Natick Soldier Center (Natick, Mass) 

has teamed with MOMRP to make a scientific determination of the effects 

of body armor on blast injury.

MOMRP is assisting this effort in two key areas. First, the considerable 

experience of WRAIR in animal tests has been applied to assisting the Natick 

Soldier Center to conduct animal tests that will provide hard evidence of the 

effect of blast on armor and the resulting injury. The experience of Jaycor 

is being used to analyze test data, utilize mathematical models to interpret 

animal results, and extrapolate the findings in humans. This effort is providing further validation of the INJURY software model, especially in extreme 

environments where lethality occurs.

To support armor evaluation, a specialized BTD to measure the force 

under clothing and armor is being developed. This new device, coupled with 

a new series of INJURY software models, will provide the assessments needed 

to determine the vulnerability of current protection systems.
Fourth-generation Injury 

Modeling

The fourth generation of injury modeling integrates mathematical models of 

the mechanical response of the body with those describing the physiological 

and systemic responses. These integrated models will predict physical and 

cognitive performance consequences, not just pathological outcomes, and will 

address neurocognitive injury that occurs through secondary processes. These 

models are important steps toward a complete, quantitative understanding 

of biological response to all traumas.

Performance Endpoints

Previous modeling of blast effects has focused on predicting injury and 

lethality. Although these are important endpoints, they do not characterize 

the complete hazard caused by blast nor the full operational impact. At exposures far less than required to produce immediate incapacitation and death, 

blast can degrade the physical and mental performances of the warfighter, 

with the consequence that he may be unable to accomplish the mission or 

to protect and defend himself against other lethal threats. 

The goal of the Physical and Cognitive Performance Modeling Project 

is to develop and validate mathematical models that predict these performance endpoints. The work will combine the finite element models used 
44 | Blast Injury: Translating Research into Operational Medicine

to characterize the physical 

damage of blast trauma with 

the DPM used to characterize the physiological consequences. The integrated 

finite element model consists 

of models that describe the 

head, neck, thorax, and 

abdominal regions (Figure 

16). The DPM is used to 

estimate oxygen delivery and 

incapacitation in hypoxic 

and toxic gas exposures78–82

(Figure 17). Integration of 

these two modeling systems 

will produce a complete 

description of the physical 

and physiological responses 

to blast trauma.

Central Nervous System Injury

The possibility that blast is responsible for the traumatic brain injury (TBI) 

observed in returning war-fighters has become an issue of national importance. Similar concerns exist in sports and automotive safety. Blast-induced 

TBI involves a complex and not fully understood mechanical pathway that 

is different from that encountered in civilian settings. The ability to assess the 

magnitude of this risk, prevent its occurrence, and detect and diagnose it may 

be enhanced by a predictive methodology that can link traumatic events to 

meaningful neurocognitive measures and clinical outcomes. The Predictive 

Model of the TBI project will use focused laboratory and clinical tests to 

strengthen the links in the causal path and mathematical modeling to tie the 

links together into a usable predictive methodology.

Figure 16. Integrated finite 

element model of the head, neck, 

thorax, and abdominal regions.
Fourth-Generation Injury Modeling | 45

Epidemiological data from Operation Enduring Freedom/Operation 

Iraqi Freedom (OEF/OIF) are correlating mild TBI to blast. A recent study 

indicated that 59% of blast-injured patients from OEF/OIF admitted to Walter 

Reed Army Medical Center had at least mild TBI.83 In that study, data were 

provided by Dr Deborah Warden, Director of the Defense and Veterans Brain 

Injury Center, based on patients seen at Walter Reed Army Medical Center. 

Of the 450 patients with brain injuries treated between January 2003 and 

February 2005, most brain injuries were caused by IEDs, and closed-brain 

injuries outnumber penetrating ones. It is believed that cases are likely underreported because of lack of prompt diagnosis. Mild TBI adds a significant, 

long-term challenge to patient recovery and rehabilitation, especially when 

other permanent disabilities are involved, such as loss of extremities that 

require the patient to learn new skills. It has also been observed that mild 

External Temp

Clothing

Wind Velocity

External 

O2, CO2

Altitude Activity

Body

Temp

Blood

Chemistry

O2, CO2 Conservation

Heat Conservation

Stroke Vol

Heart Rate

Arterial

Resistance

Cardiac Control

Arterial

Resistance Control

Frequency

Drive

Breathing Control

Shivering

Sweating

Thermal Control

Blood Flow

Distribution

Circulation

Air Flow

Distribution

Ventilation

Figure 17. Schematic diagram of circulatory and respiratory systems in the Dynamic 

Physiology Model. Temp: temperature; Vol: volume.
46 | Blast Injury: Translating Research into Operational Medicine

TBI from the current conflict accounts for a larger proportion of casualties 

than in other recent US wars. 

Extreme head trauma from blunt impact leads to massive damage and 

hemorrhaging that have been studied extensively. Thresholds for high-mass, 

low-speed impact head injury have been based on tissue pathological observations in primates and postmortem human subjects. Although these thresholds 

are not based on biomechanics and neurological modeling, they have served 

the automotive safety needs. Mild TBI is now being seen in returning soldiers, 

as well as in sports, and has a far more subtle injury mechanism, a more 

subtle clinical outcome, and a much lower threshold. Thresholds for these 

lower level injuries will not be developed readily from epidemiological data 

alone and are not easily studied in animal models. A greater understanding 

of the underlying mechanical processes will be required. Furthermore, blast 

presents additional challenges because the primary mechanism of action is 

not blunt impact to the head, may involve other mechanical pathways, and 

is far more rapid than almost all previous head injury causes.

Causal Links of Trauma-Caused Brain Injury

It is generally accepted that TBI is caused by local mechanical stresses in 

the brain that disrupt neural cells and tissues (primary injury), which, in turn, 

leads to functional disruption through metabolic and biochemical processes 

(secondary cascade), resulting in the clinically observed neuropsychological 

consequences. Although the physical, chemical, and neurological processes 

are not rigorously quantified, there is ample evidence that the primary injuries 

lead to the neurological consequences that are seen in patients with TBI.

Mechanically caused primary injury has been observed in animal models for both impact and blast trauma. In blast animal models, astrocyte and 

micro- glial responses have been seen,84,85 as well as changes in apoptotic 

mechanisms.86 Histological studies have detected degenerating neurons in 

the cerebral cortex and hippocampus of rats 1 and 5 days after blast 

exposure.87,88 Evidence of ultrastructural and functional changes following 

blast neurotrauma has also been observed.88,89 Chemical alterations leading 

to motor and cognitive dysfunction follow diffuse TBI in rats.90,91 In isolated 

tissue tests, injury to cells resulting from the application of rapid mechanical 

forces has been observed in endothelial cells,92 in axons,93–96 and in cortical 

astrocytes and neurons.97 Evidence of tension as a regulator of axonal activity 

has also been observed.98 In addition to tension and shear-induced cellular 

injury, there is also evidence of cellular damage from direct pressure effects. 

Cavitation, which has been shown to occur at moderate head acceleration, 

leads to large local pressures (thousands of atmospheres) upon vapor bubble 
Fourth-Generation Injury Modeling | 47

collapse.99 This mechanism has been confirmed in lithotripsy studies.100 Depolymerization of spindle microtubules has been observed at very high static 

pressures (680 atm) and in ultrasound exposures (low-pressure amplitudes, 

but rapid fluctuations). 

The blast-induced primary mechanical damage to cellular structures starts 

a secondary cascade of effects, including ion channel disruption, apoptosis, 

and necrosis. These secondary processes lead to functional and metabolic 

dysfunctions that are observable in advanced magnetic resonance imaging 

(MRI). Quantification of the link between observable microscopic damage 

and MRI parameters is the fourth link in the predictive chain. Observation 

of secondary brain injury, in the form of biochemical alterations, has been 

observed in blast injury.101–104 More importantly, however, it is well known 

that secondary injury is a complex cascade of physiological events caused by 

the residual metabolic, biochemical, endocrinological, and immunological 

alterations initiated by primary injuries.105,106

These secondary effects are readily observable with magnetic resonance 

spectroscopy (MRS). MRS is a powerful in vivo method to detect neurochemicals within the brain that are relevant to brain processes. The most widely used 

methods are 1H-MRS and 31P-MRS that detect compounds with hydrogen 

and phosphorus. Recent studies have shown that the absolute concentrations 

or ratios of concentrations, particularly N-acetyl aspartate (NAA), correlate 

with neuropsychological tests, cognitive dysfunction, and early detection and 

longitudinal change.107 MRS has provided correlates with the following:

•	 	 cognitive decline in the aging brain;108

•	 	 cognitive outcomes in children;109

•	 	 the Wechsler Memory Scale;110,111

•	 	 genetically based Williams syndrome;112,113 and 

•	 	 diseases such as bipolar disorder,114,115 Alzheimer’s,116,117 and 

schizophrenia.118

MRS has correlated with posttraumatic stress disorder (PTSD) in combat veterans,119–121 combat veterans with evidence of biochemical change,122

prisoners of war,123 and nonprisoners of war.124 In some studies, however, 

patients with PTSD did not score differently on attention, memory, or learning tests,125 nor did they show lower levels of NAA.126 Proton MRS also 

has mood disorders.127–133 MRS imaging has correlated with functional 

independence measure,134 Glasgow Outcome Scale, and neuropsychological 

performance.135
48 | Blast Injury: Translating Research into Operational Medicine

Blast Traumatic Brain Injury Mechanisms

Once mechanical stresses have created primary cellular injury in the brain 

tissue, subsequent biochemical, metabolic, and neurological processes will 

lead to neurocognitive dysfunctions and adverse clinical outcomes. The unique 

challenge of blast TBI is to determine how the external stressors (mechanical, 

chemical, and electrical) created by exposure to explosions create and amplify 

those of primary cellular injury. The Predictive Model of the TBI project will 

build on the 25 years of blast model experience and tools to determine a quantitative connection. The following sections frame the nature and magnitude 

of the blast stressors that are likely to be involved in blast TBI.

Characterization of Blast Exposure

 Blast injury is initiated by the mechanical loading of the blast wave on 

the body, with secondary effects of the toxic gas and electromagnetic pulse 

released by the explosive. The strongest blast waves for which there is a high 

probability of survival have a peak pressure of ~20 atm and a duration of a 

few milliseconds. Using CFD and data compiled in the Blast Overpressure 

Database, there is adequate information to characterize blast threats faced by Probability of Lethality

1.0

0.9

0.8

0.7

0.6

0.5

0.4

0.3

0.2

0.1

0.0

Logistic regression for lethality

95% confidence bands

BOP data with 10 sample bin size

0.001 0.010 0.100 1.000

Figure 18. INJURY correlation of lethality. BOP: blast overpressure; Wtot: Wsum corrected 

for the number of exposures.
Fourth-Generation Injury Modeling | 49

US warfighters and to select conditions that will be meaningful for laboratory 

investigation. Characterizing the blast effects is the first step in developing an 

end-to-end predictive model.

IEDs can span an explosive energy range from the equivalent of a few 

pounds of TNT (trinitrotoluene) in pipe bombs to thousands of pounds in 

truck bombs. Distances from these explosions to the warfighter can also vary, 

and the blast loading can be amplified by reflections inside enclosures. The 

ranges of interest for studying TBI, however, are those exposures that will 

not otherwise produce severe injury or death. The biomechanically based 

INJURY software, used throughout the military to estimate blast injury for 

all levels from occupational exposure limits to survivability estimates,136–138 is 

used to select exposure conditions that are in a meaningful range (Figure 18). 

Based on INJURY analyses and confirmed by the extensive blast overpressure 

data repository, it is concluded that the strongest blast waves for which there 

is a high probability of survival have a peak pressure of about 20 atm and a 

duration of a few milliseconds.

Pathway of Internal Disturbances 

Acceleration of the brain from direct blast loading to the head or a surge 

of blood into the brain from blast loads to the torso can produce pressure 

excursions, flow pulses, and mechanical stress far outside the normal physiological range that can cause tissue and cellular damage. Furthermore, temporary disruption of oxygen delivery from immediate neurological response 

and electrical disruption of cellular processes from the explosion-generated 

electromagnetic pulse may further compound these primary injuries. Modeling these pathways is a critical part of building a Predictive Model and 

designing protective solutions.

Acceleration Effects. A blast wave travels at ~300 m/s, so one side of 

the head/body is affected a fraction of a millisecond before the other. This 

differential pressure can accelerate the head, and simulations show that, at 

the maximum survivable peak values, the head can be accelerated up to 300 

g’s. Jaycor has determined that the threshold for mild TBI, based on sports 

injury reconstruction,139 is 50 g’s, so that head acceleration from blast is 

certainly a potential injury pathway. Acceleration also introduces a hydrostatic pressure gradient in the brain, with a pressure difference equal to the 

acceleration × density of the brain × half the width of the brain. For a 300 g 

acceleration, the brain could experience regions of compression as great as 3 

atm on the impact (coup) side. Accelerations greater than 80 g’s are capable 

of lowering pressure in the brain to a point wherein cavitation occurs on the 

opposite (contrecoup) side. Collapse of the vapor bubbles can lead to large 
50 | Blast Injury: Translating Research into Operational Medicine

pressures in excess of 1,000 atm,116 which can cause considerable local damage. This phenomenon has been demonstrated in surrogate models and in 

mathematical simulations,140,141 and is one of the primary injury mechanism 

candidates in head impact.140–146 Simulations further show that small flexure 

of the skull can extend the cavitation to large areas of the brain.141 The biomechanical FEM of the head provides a way of translating external loading 

into stress in the brain tissue (Figure 19). 

Vascular Surge.Distortion of the thorax and abdomen is observed under 

blast loading, arising from the presence of air-containing organs in the torso. 

In the thorax, the inward moving chest wall produces a compression wave in 

the lung that not only does damage to the lung tissue, but can also exert a compressive force on the heart. The application of blast loading to the abdomen 

produces a direct coupling, through the abdominal contents, to the diaphragm, 

leading to an upward motion that also exerts a force on the heart—a “blast 

punch to the gut.” Both of these processes can lead to a surge in blood flow. 

Figure 19. Deformations of the skull coupled with head acceleration can 

create regions of high stress concentration within the brain.
Fourth-Generation Injury Modeling | 51

Brain injury from blast 

animal models, whose 

heads were protected 

from the direct blast,100 

might be explained by 

this mechanism. Finite 

element analysis shows 

that a 20-atm blast loading against the torso produced a small, volumetric surge of blood from 

the heart of about 0.2 

mL as a result of the load 

transmitted to the heart 

through the lungs; but it 

also produced a 10-mL 

surge as a result of loading delivered through the 

abdomen (Figure 20). 

Assuming the normal 

distribution of blood 

flow, about 2 mL of the 

surge will be delivered 

to the brain. When this 

volumetric surge reaches 

the brain, the sudden 

increase of blood volume 

produces a subsequent 

pressure increase. Simulations using the L-3/

Jaycor head model estimate that an intracranial pressure of nearly 10 atm 

can result. Combined with the increased crushing effect of personal body 

armor, this mechanical pathway is being studied in the project.

Mechanical trauma caused by the blast waves, blast winds, or secondary impacts is most likely the primary cause of TBI. Nonetheless, there are 

auxiliary effects that are associated with explosives that could augment or 

aggravate the mechanical injury.

Hypoxic Effects. It is commonly observed that animals exposed to blast 

suffer disruptions in ventilation and cardiac output for 10 s following blast 

exposure and reductions of these outputs that persist for many minutes. In 

Figure 20. Schematic diagram of mechanical response model 

for binding structures in neurological cells.
52 | Blast Injury: Translating Research into Operational Medicine

addition, explosions produce noxious gases that have other acute effects 

on these processes. In our studies, the effect of toxic gas on oxygenation of 

the blood has shown that brain ischemia effects can occur in minutes under 

acute conditions. This process has been quantified with the DPM.147

Electromagnetic Pulse. The overpressure of the explosion accelerates 

hot, ionized gases in the fireball to a velocity exceeding the ambient speed 

of sound, and the rapid motion of charged particles results in a radiated 

electromagnetic pulse (EMP). Soloviev et al148,149 provide a summary of field 

data collected from conventional high explosives (1–5 kg) and a theoretical 

model that can be used for extrapolation. They conclude that, in the far 

field of these explosions, the electric field component of the EMP acts as an 

electric quadrupole—that is, the strength decreases as the fourth power of 

distance—with strength proportional to the explosive weight. 

It is well established that significant thermal effects are produced from 

continuous, incident power levels greater than 100 mW/cm2. At this flux 

of energy, the body cannot dissipate the heat rapidly enough, and tissue 

temperatures rise, leading to a wide range of physiological effects and damage. A few tests have looked at nonthermal effects on cerebral tissues of 

short duration-pulsed exposures (perhaps like repeated blast exposure) or 

modulated high-frequency exposures. Servantie et al150 saw changes in the 

electroencephalogram in rats at pulsed exposures: 0.1-μs pulses, average 

power 5 mW/cm2; and 500 to 600 pulses/s, for 10 days. Bawin et al151–154

observed changes in Ca2+ release in chicken cerebral tissue after 10 minutes 

of exposure to 0.75 mW/cm2 of modulated 450 MHz radiation, which is 

an energy dose of 450 mW-s/cm2. At 10 m from a 100-kg explosive, the 

blast wave is predicted to produce only 1% lethality, whereas Soloviev’s 

relation predicts that the EMP energy dose will be about 500 mW-s/cm2. 

Therefore, there is a possibility that blast-generated EMP, under the right 

circumstances, may augment the Ca2+ channel disruption that is initiated 

by primary mechanical injury.

Biomechanical and Physiological Response Models

The Predictive Model of the blast TBI project will build on Jaycor’s integrated 

finite element models of blast and trauma responses. Additionally, the parallel work to integrate FEM and DPM will greatly assist the blast TBI project. 

Surrogate, large and small animal testing, and clinical examination of civilian 

and military patients with TBI will provide quantitative data for each causal 

link and a validation of the overall predictive methodology.
Fourth-Generation Injury Modeling | 53

The research partnership between USAMRMC and NHTSA has advanced finite element models of the head that combine anatomical geometry 

with the mechanical properties of the tissues to give a powerful calculation 

tool. This partnership has spurred a number of studies into dynamics of the 

entire brain,155 tissue properties,156–161 and individual cells.94,162 Because of 

the availability of high-resolution anatomy and dynamic tissue properties, 

the ability to determine local mechanical stresses within the brain is well 

advanced. 

As in decades past, the USAMRMC/MOMRP foresight of developing 

fundamental mathematical tools to understand blast/trauma injury may allow 

an issue of national importance to be addressed quickly, with the potential 

for developing both a scientific understanding and a strategy for prevention 

and mitigation.

Summary

For more than 25 years, MOMRP has been a world leader in the study of 

blast-related injury. This research has produced insights, data, and predictive 

models that set standards for human exposure, guide the design of protective 

systems, and allow quick responses to the questions generated in a rapidly 

changing battle environment.

The work of MOMRP continues to address the new blast issues of the 

21st century. Together with its partners, MOMRP is researching injury to 

the central nervous system; protection of current body armor from emerging thermobaric weapons; and prediction of performance decrement, both 

physical and cognitive, under the stress of blast and other trauma.

The decision (made decades before) to use mathematical modeling as a 

lens to focus the understanding of data; to guide future experiments; and to 

project understanding to complex, real-life scenarios on the battlefield has 

resulted in a capability that is responsive to new challenges. Furthermore, 

the ability to simulate biomechanical and physiological aspects of the body 

under traumatic circumstances can be applied to interests of health, safety, 

and performance of soldiers.

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