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Determining the wounding effects of ballistic projectiles to inform future injury models: a systematic review
  1. John Breeze1,2,
  2. A J Sedman2,
  3. G R James2,
  4. T W Newbery3 and
  5. A E Hepper2
  1. 1Academic Department of Military Surgery and Trauma, Royal Centre for Defence Medicine, Birmingham, UK
  2. 2Biomedical Sciences Department, Dstl, Porton Down, Salisbury, Wiltshire, UK
  3. 3Land Battlespace Systems Department, Dstl, Fort Halstead, Sevenoaks, Kent, UK
  1. Correspondence to Maj John Breeze Academic Department of Military Surgery and Trauma, Royal Centre for Defence Medicine, Birmingham Research Park, Vincent Drive, Birmingham, B15 2SQ, UK; johno.breeze{at}gmail.com

Abstract

Introduction Penetrating wounds from explosively propelled fragments and bullets are the most common causes of combat injury experienced by UK service personnel on current operations. There is a requirement for injury models capable of simulating such a threat in order to optimise body armour design.

Method A systematic review of the open literature was undertaken using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses methodology. Original papers describing the injurious effects of projectiles on skin, bone, muscle, large vessels and nerves were identified.

Results Projectiles injure these tissues by producing a permanent wound tract (PWT), comprised of a central permanent wound cavity, in conjunction with a zone of irreversible macroscopic tissue damage laterally. The primary mechanism of injury was the crushing and cutting effect of the presented surface of the projectile, with an additional smaller component due to macroscopic damage produced by the radial tissue displacement from the temporary tissue cavity (TTC). No conclusive evidence could be found for permanent pathological effects produced by the pressure wave or that any microscopic tissue changes due to the TTC (in the absence of visible macroscopic damage) led to permanent injury.

Discussion Injury models should use the PWT to delineate the area of damage to tissues from penetrating ballistic projectiles. The PWT, or its individual components, will require quantification in terms of the amount of damage produced by different projectiles penetrating these tissues. There is a lack of information qualifying the injurious effect of the temporary cavity, particularly in relation to that caused by explosive fragments, and future models should introduce modularity to potentially enable incorporation of these mechanisms at a later date were they found to be significant.

  • FORENSIC MEDICINE
  • HISTOPATHOLOGY
  • MORBID ANATOMY
  • NEUROPATHOLOGY

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Key messages

  • Penetrating wounds from explosively propelled fragments and bullets are the most common causes of combat injury experienced by UK service personnel on current operations.

  • There is a requirement for injury models capable of simulating such a threat in order to optimise body armour design.

  • Injury modellers should use the permanent wound tract to delineate the area of damage to tissues from penetrating ballistic projectiles.

  • Further experimental research is required to accurately quantify the sizes of these components for different projectiles.

Introduction

Penetrating wounds from explosively propelled fragments and bullets are the most common causes of combat injury experienced by UK service personnel on current operations.1 These projectiles can cause injury to living tissues through three potential mechanisms. The first mechanism is the crushing and cutting effect of the presented surface of the projectile, which is responsible for the production of a permanent wound cavity (PWC).2 In the second mechanism, the further passage of the projectile leads to radial acceleration of the tissue,2 ,3 which will expand, contract and oscillate after the projectile has passed through. The maximum extent of this pulsating temporary cavity produced in tissues occurs several milliseconds after the projectile has passed through that section of tissue3 and spreads out, potentially asymmetrically due to weaknesses in the tissue planes4 or projectile tumbling. The third mechanism is the pressure wave,5 occasionally also named the ‘shock’6 ,7 or ‘sonic’8 wave, which has been demonstrated experimentally in distant parts of the body.3 ,5 ,6 ,9 ,10

Injury models capable of simulating the threat from penetrating ballistic injury are desired to optimise body armour design. Such models require an accurate understanding of the interaction between projectile parameters (mass, velocity, density, shape, deformation, etc) and the severity of tissue damage to underpin the ability to make robust injury predictions. Traditionally, injury models have taken the form of physical models, which have been based primarily on animals and tissue simulants2 (Figure 1), although postmortem human subjects have been used intermittently. Although original ballistic experimentation using such physical models will inevitably still be necessary for the foreseeable future, the use of computer simulations (numerical injury models) will alleviate many of the limitations of physical models such as restrictions in the number of shots that can be taken, the facilities required to undertake such experiments and understandable ethical considerations in animal experimentation. Historically numerical injury models used by the Ministry of Defence have simulated penetrating injuries using algorithms that predict the probability of a soldier being incapacitated.1 These existing algorithms treat large body areas as a single homogenous entity in which the head and neck are considered as a single unit for instance, and do not reflect the underlying anatomy. A newer approach, currently being applied in neck wounds, is to use a high fidelity (HF), finite element approach, in which the body area is broken down into its constitutive anatomical components expressed as discrete elements, each of which uses algorithms representative of that individual tissue type.1 Although such an HF approach has the potential to provide more robust injury predictions than either its physical or numerical predecessors, it is dependent on its ability to accurately represent the manner in which a ballistic projectile interacts with the individual tissue types of that model. The primary tissue types that require characterisation in early iterations of such a model are blood vessels, nerves, muscle, skin and bones.1 The aim of this review is to determine how these mechanisms engender wounding in these living tissues in order to enable them to be appropriately represented within future HF injury models.

Figure 1

Demonstration of the potential wounding effects due to a fragment simulating projectile using a gelatin tissue stimulant. (A) Projectile immediately prior to impact, (B) Maximum extent of temporary cavity and (C) Permanent cavity when projectile has come to rest.

Method

A systematic review of the open literature from 1900 to present was undertaken using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses methodology.11 The following databases were searched: PubMed, ProQuest, Web of Science and Google Scholar in addition to an internet search using Google, Internet Explorer and Firefox. The following keywords were used: wound tract, permanent, temporary, ballistic, fragment, bullet, tissue, soap, gelatin, simulant, cavity, projectile, sonic, shock, trauma and explosive. Only primary sources providing original experimental data were included and any identified in a non-English language were translated. The British Library was finally able to perform a search of its internal records using the same keywords and documents from its archives were copied. The references from articles were also hand searched and requested if not already identified. Secondary sources were excluded and the wounding effects were subdivided into experiments using bullets and explosive fragments. The reported effects of how these three potential injury mechanisms engender wounding in isolated skin, muscle, bone, blood vessels and nerves were determined.

Results

A total of 151 papers and 21 books were identified using database searching and a further 19 papers through examining the references found in these sources; nine papers were translated into English. In all, 83 papers and seven books included pertinent information (Figure 2) and no other systematic reviews on the subject were identified. There was clear agreement in all publications that the resultant damage to all tissue types consists of a centralised PWC,12 ,13 all tissues within which would be assumed to be destroyed.2 ,12 ,14 ,15 Surrounding the PWC is tissue damage that is both macroscopic and microscopic, and which may be reversible or irreversible.8 ,13 The combination of the PWC and any surrounding irreversible tissue damage should be termed the permanent wound tract (PWT).12 ,16 The PWT is the result of both the cutting and crushing effect of the projectile in all tissues,2 ,12 ,17 ,18 in combination with the temporary cavity formation in some tissues.6 ,13 ,1822

Figure 2

Results of systematic review using Preferred Reporting Items for Systematic Reviews and Meta-Analyses methodology (numbers of publications in brackets).

Cutting and crushing effects

This is the primary mechanism in the formation of the PWC and any macroscopic damage lateral to it.12 Macroscopic tissue damage is found laterally to the PWC and is caused by both the cutting and crushing effect of the projectile in combination with the tissue distortion generated by the temporary cavity. Macroscopic damage can be reversible or irreversible, with the area immediately adjacent to the PWC generally having irreversible changes (referred to as the contusion zone12 or zone of massive quakes16) and the outer layer (concussion zone) having reversible changes.12 Clinically, however, such discrete zones are rarely found12 and do not form in regular circles around the projectile path. Damage is usually patchy and not necessarily correlated to distance from the path of the projectile,8 reflecting that the clinical effect is dependent on both tissue type and architecture.12 ,13 Macroscopic damage will heal completely in some tissue types but this effect is likely to be rare, especially in complicated military wounds and in the presence of infection and contamination. Although irreversible macroscopic tissue damage (IMTD) in muscle may lead to scarring,12 ,13 in many cases there will be little residual clinical effect should the area of scarring be small or other muscles may compensate. Structures such as arteries and nerves would likely suffer IMTD but again the clinical effect would be dependent on the size of the damaged area. Bones will be damaged through a direct hit by a projectile if it exceeds the threshold velocity required for perforation of the cortex.23 Any ballistic projectile with enough energy to completely traverse bone will destroy any substance within its path,24 thereby producing a PWC in bone.25 Such a tract will likely result in fracture of the bone at that location.2325

Temporary cavity effects

The temporary cavity results in a transient, rapid strain of tissues that may, depending on the mechanical characteristics of the tissue, produce injury. Dense homogenous tissues, particularly if enclosed by a connective capsule or casing such as the liver or brain, suffer the greatest injury from the temporary cavity.18 Conversely, elastic tissues with a high strain to failure such as lungs and large arteries resist the destructive effects of the temporary cavity well.26 Two papers stated that the temporary cavity did not cause macroscopic damage to isolated large nerves6 ,20 and five papers stated that it did not cause macroscopic damage to isolated large arteries.6 ,13 ,19 ,21 ,22 All of these papers pertained to bullets and no evidence was found on explosive fragments. A single paper demonstrated macroscopic large artery damage due to the temporary cavity produced by a bullet27 but the effect was only demonstrated in projectiles of velocities exceeding 1000 m.s−1 as they passed the vessel and was not seen in the concurrent in vivo experiments those authors conducted.

The temporary cavity can cause microscopic damage to muscle,16 arteries8 ,28 and nerves. The resultant area has been described as the concussion zone,12 ,22 the zone of extravasation2 ,6 ,29 and the zone of molecular quake.16 Muscle within this area, in the absence of missile or bone fragmentation, generally only sustains minor injury,14 ,15 ,27 ,30 ,31 although this was contested by one author.32 Microscopic changes to all of the layers in the arterial wall have been demonstrated in blood vessels2729 ,33 up to 50 mm from the most lateral aspect of macroscopic tissue damage.34 Although some authors have felt that this microscopic arterial damage has warranted debridement of macroscopically normal sections of the artery lateral to the PWT,27 ,33 it is generally agreed that there is no correlation between microscopic arterial damage and long term morbidity.28 ,35

Skin is damaged by both the direct crushing effect of the projectile2 ,12 ,36 as well the rapid radial tissue displacement produced by the temporary cavity,2 ,18 demonstrated by the stellate exit wounds in tumbling projectiles3 ,12 ,37 ,38 that can be greater than the largest dimensions of the projectile.

Indirect bone fractures can occur at a distance from the projectile path18 and have been demonstrated to be due to strain placed on the bone by the radial tissue displacement produced by the temporary cavity formation18 ,22 ,25 ,3840 and not the preceding pressure wave as previously postulated.41 Experimentally indirect fractures have been shown to be caused by both bullets2 ,18 ,25 ,40 ,42 and fragments.39 ,41 However, clinically their occurrence is rare18 so that defining an incidence is difficult.43

Evidence was found for peripheral nerve and spinal cord damage from missiles that do not touch it directly,20 ,4447 which was felt to be secondary to microscopic damage to small blood vessels supplying large nerves.18 Although temporarily impaired neuronal conduction due to microscopic axonal damage was experimentally demonstrated up to 18 mm from the PWC,44 or 3 mm from the most lateral point of macroscopically damaged tissue,44 there was no evidence that this caused long term morbidity.20 ,45 ,46

Pressure wave effects

Strong opinion was found dividing between papers suggesting the pressure wave contributes to wound injury5 ,10 ,4852 and those that it does not.9 ,19 ,37 ,44 Our review demonstrated that this opinion was based upon five papers describing original experimental data.5 ,10 ,51 ,53 ,54 Microscopic changes in neuronal tissue at a distance from the point of ballistic impact were demonstrated by Suneson et al10 ,51 ,53 in vivo, which those authors ascribed to the effect of the pressure wave. They also felt this mechanism was responsible for causing decreased oxygen consumption in cultured nerve cells in vitro.5 This has been cited as evidence that pressure waves are responsible for neurological symptoms,48 ,52 despite the lack of clinical data supporting the histological findings. It has been suggested that proponents of the damaging effects of pressure wave52 have also incorrectly reported the results of previous experimental data54 as well as ascribing pressure waves as the cause for a pathology that would be more correctly explained by the effects of the temporary cavity.55 Overall, insufficient evidence was found to demonstrate that microscopic changes induced by pressure wave in vitro cause significant clinical damage.

Discussion

The aim of this review was to qualify how projectiles damage the primary constituents of anatomical structures associated with mortality to enable them be appropriately represented within the planned injury models. Overall, 48 of the 59 original papers identified used experimental data derived from bullets; in contrast, there was a relative paucity of experimental data derived from explosive fragments (16/59 of papers). Although strongly expressed opinion was found as to the potential wounding effects of the pressure wave,5 ,10 ,4852 our review of the literature could not find objective evidence that this mechanism causes significant injury that either warrants, or enables, modelling at this stage.

Although the stretching effect of the temporary cavity is responsible for a small portion of the PWC and macroscopic damage lateral to that, the primary mechanism for this damage was the cutting and crushing effect of the presented surface of the projectile. The temporary cavity can damage skin and result in indirect fractures of bone, which are both outcomes that will require quantifying in an injury model. Indirect vertebral fractures are particularly important as they may damage the adjacent spinal cord directly18 or through the production of secondary fragments.42 Although the temporary cavity was found to result in microscopic tissue damage to isolated arteries, muscles and large nerves lateral to the PWT, no experimental evidence was found to demonstrate that these changes translated to permanent damage. It was recognised that experimental testing of the effects of the temporary cavity generally used isolated tissues and that it is the method of attachment of these structures to their surroundings that may result in damage from this mechanism, such as tearing the attachment of an artery at a fixed point (eg, its entry into a bony foramen). The temporary cavity clearly has varying injurious effects dependent on tissue type and architecture6 ,13 ,22 ,27 ,56 and we would therefore encourage the term temporary tissue cavity (TTC) instead of temporary wound cavity to differentiate the effect of this mechanism in tissues rather than simulants.

The clinical result of the crushing and cutting effect of a projectile in all tissues, in conjunction with the rapid radial displacement of the TTC in selected tissues, is the production of the PWT. The literature indicates that it is comprised of the central PWC, together with a zone of irreversible tissue damage lateral to the PWC that heals by scarring,8 ,24 although precise definitions vary between authors.3 ,12 ,31 As only macroscopic tissue damage was demonstrated to be potentially irreversible, a clearer term would be to call this zone of damage lateral to the PWC the zone of IMTD. It is therefore our belief that the planned numerical injury models should use the PWT (defined as the PWC and the zone of IMTD) to delineate the area of potential damage to tissues (Figure 3).

Figure 3

Clinical appearance of wound tract (a=permanent wound cavity, b=macroscopic damaged tissue likely to form irreversible macroscopic tissue damage, dotted line=likely extent of permanent wound tract).

Accurate quantification of these components is required for injury models that simulate the passage of a projectile through individual anatomical components and tissue types. Animal muscle, particularly that derived from pigs, has been demonstrated to reproduce the penetration and retardation effects of fragments into human muscle12 ,31 but no agreed surrogate exists for other anatomical components such as skin or bone. Large numbers of test subjects are required to overcome the inherent variation in such testing37 ,38 and therefore tissue simulants have historically been used to reduce experimental variation and overcome the ethical implications of using animal models.

It is generally agreed that the dimensions of the temporary cavity produced by projectiles traversing both ballistic gelatin30 ,37 ,38 and ballistic soap56 are believed to be similar to that produced in homogenous muscle. However, the same close relationship between the permanent cavity produced in a simulant compared with that produced in homogenous muscle is more controversial, primarily due to their differing elasticity.6 ,7 Fackler et al, probably the most enduringly respected opinion on the subject, specifically stated that the permanent cavity volume in simulants should not be used to estimate that in animals,30 although they did agree with other authors12 that their shapes are representative of one another.

The PWT represents a demarcation between a zone of IMTD and reversible tissue damage.57 Demarcating between viable and non-viable tissue therefore remains a subjective clinical decision.7 ,13 Clinical criteria have been well validated in their accuracy and include colour,58 consistency, contractility37 ,38 and capillary bleeding.38 For this reason, it has been suggested that the mass of surgically debrided tissue (mSDT) is a better metric of the PWT.12 ,32 ,37 ,38 ,56 ,59 ,60 Jussila et al60 performed a meta-analysis of results from different porcine studies, relating mSDT to various potentially measurable variables. All had very poor correlation, with the highest correlation (still only 0.29) being found for an equation relating mSDT to dissipated kinetic energy per millimetre of wound channel (Ed/lw). However, that equation is not applicable to future models wanting to determine tissue damage at points along a wound track as it uses the total mSDT and does not normalise it by varying lengths of PWT. Using the tabulated mean data values provided by Jussila et al60 but normalising them by the mean wound tract lengths, as would be required for this injury model approach, produced an even weaker correlation of 0.11 (Figure 4).

Figure 4

(A) Mean values for mass of surgically debrided tissue (mean mSDT) versus dissipated energy per unit length of wound channel (Ed/lw) obtained from tabulated data found in Jussila et al;60 (B) Mean values of mSDT expressed per unit length of permanent wound track (mean mSDT/lw) versus mean dissipated energy per unit length of wound channel (mean Ed/lw).

Future research

Of the methods identified in the literature, the mSDT is the one more closely aligned with the definition of the PWT and enables distinctions between tissues other than homogenous muscle to be made. Also, using experienced trauma surgeons to differentiate between non-viable and viable tissue is analogous to the method that would be undertaken on injured soldiers in an operating theatre. However, current experimental data are insufficient to use this method and further original animal experimentation would be required to implement it. CT is an emerging technology in the field of wound ballistics61 and has been used to measure the dimensions of the permanent cavity in both gelatin61 and porcine tissue62 (Figure 5). However, no comparisons between the cavities found in simulants to that in animals were found, such that this method currently lacks experimental validation, although this is an approach we would recommend in the future. The use of data derived from simulants therefore remains the only practical method of attempting to quantify these wounding effects; although this method is potentially accurate to measure the temporary cavity, it will inevitably underestimate the permanent cavity, particularly in inelastic tissues.

Figure 5

Experimental permanent wound tract produced by fragment simulating projectile fired into porcine tissue as visualised on a CT scan (width of permanent wound cavity demonstrated).

Conclusions

Injury models should use the PWT to delineate the area of damage to tissues from penetrating ballistic projectiles. The PWT, or its individual components, will require quantification in terms of the amount of damage produced by different projectiles penetrating these tissues. Model developers should be aware that there is a lack of information relating to injurious effect of the temporary cavity, particularly in relation to that caused by explosive fragments, and future models should introduce modularity to potentially enable incorporation of these mechanisms if they are later found to be significant.

References

Footnotes

  • Contributors Planning: JB; Conduct: JB, AS, GRJ and TN; Reporting: JB, AS, GRJ, TN and AH; Guarantor: JB.

  • Funding None.

  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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