Under The Microscope: THE MECHANICS OF MISSILE INJURY

 

Though the majority of missile wounds are caused by firearms, other devices such as crossbows, captive-bolt guns, air weapons and even catapults can launch lethal projectiles. In the bombing deaths now so commonly associated with terrorism, missile fragments cause more deaths than the blast effects, so, overall, an understanding of projectile trauma is essential.

With the exception of deceleration injuries, all mechanical trauma, whether punching, stabbing or kicking, is caused by the transfer of energy from an external moving object to the tissues and nowhere is this more obvious than in shooting. For damage to occur, some or all of the kinetic energy of the missile has to be absorbed by the target tissues, where it is dissipated as heat, noise and mechanical disruption. When a missile passes completely through soft tissues, it may retain much of its original kinetic energy and fail to transfer any appreciable amount to the tissues, which may remain relatively intact apart from the immediate bullet track. If the latter is in a limb muscle, there may be no serious effects if major blood vessels are not involved, though the same track in brain, lung or heart may prove fatal. To ensure transfer of energy to the tissues, some missiles are especially designed or modified to slow up or stop within the body. Soft-headed bullets will flatten on impact and some are designed to fragment. The 'dumdum' bullet, which has a scored nose, and the military missile with an air-cavity within the tip are intended to splay open on impact to increase the 'braking' or deceleration effect, and transfer more energy for disruption.

Explosive-tipped bullets, such as those used in the assassination attempt on President Reagan, are not designed to cause damage by the tiny detonation, but drastically to deform the missile to cause maximum deceleration. Weapons designed to be fired in confined spaces, such as those for combating hijack attempts in an aircraft, may be of relatively low velocity and have a deceleration feature incorporated to ensure the absence, of an exit wound, and thus limited travel of the missile to avoid puncture of the pressurized passenger cabin. The trajectory of the missile also determines how much and how fast its energy is given up to the target. Shotgun pellets are spherical, so the orientation of impact is not relevant, but all conical bullets may acquire an erratic course in the tissues. They may tumble end-over-end, especially when nearing the limit of range; they may 'wag' or 'yaw' from side to side of their axial trajectory; the base may rotate around the axis, with the tip remaining on the straight path; and they may 'precess' or 'nutate' with com- plex spiral or circular movements about the axis. Whatever the deviation, it offers more contact between the projectile and the tissues, allowing more transfer of energy and thus greater tissue damage. The amount of kinetic energy possessed by a projectile accords to the familiar formula of half the product of the missile mass and the square of its velocity. Modern military science takes advantage of the squaring of the velocity to develop weapons that have a missile of small mass but exceedingly high velocity to provide the maximum kinetic energy for tissue damage. The mode of injury depends on the velocity of the missile.

The mode of injury depends on the velocity of the missile. Relatively slow projectiles are those travelling at up to the speed of sound in air (340 metres/second or 1100 feet/second), which of course includes all  non-explosively propelled missiles like crossbow bolts and air-rifle pellets, as well as most revolver bullets. These mechanically thrust aside the tissues along a track only slightly wider than the missile. The tissues are lacerated or crushed, secondary damage occurs from rupture of blood vessels and other structures, and secondary and tertiary damage is caused by displaced bone and cartilage fragments. Above the speed of sound in air, a missile passing through tissue sends a shock wave of compression ahead of the laceration track, this wave being propagated at about the speed of sound in water (1500 metres/second or 4800 feet/second). Though this wave lasts only for a brief period, it raises the tissue pressure to extreme values, up to thou- sands of kilopascals. In tissues like brain, liver and muscle, this can cause severe disruption within a wide zone around the bullet track, and can be propagated down hollow fluid- containing vessels to cause distant vascular damage.

High-velocity projectiles produce yet another phenomenon, that of cavitation. The missile accelerates the molecules of the tissues adjacent to the track, so that they continue to move cantingly outwards even after the missile has travelled onwards. This forms a cavity around the track that is far wider than the diameter of the projectile. It reaches a maximum size within milliseconds and then pulsates with decreasing amplitude so that a fusiform cavity rapidly follows in the wake of the bullet. When the bullet stops or leaves the organ, the cavity rapidly subsides, but the track of damage persists in a tubular zone much wider than the actual missile.

In most of the shooting cases seen by forensic pathologists, death will have occurred rapidly but, where it is delayed, secondary damage from infarction, local necrosis of muscle and organs, and infection must always be borne in mind. High-velocity weapons in particular can cause vascular damage at a distance from direct trauma, stretching and thrombosis, leading in turn to ischaemic lesions such as infarcts.

 

Acknowledgements:

www.aived.nl    AIVD – @Erik Akerboom ©

www.politie.nl  Politiekorpschef  @Janny Knol©

www.politie.nl WEB Politie - @Henk van Essen©

 

Bibliography:

1.    Criminal Investigations – Crime Scene Investigation.2000

2.    Forensic Science.2006

3.    Techniques of Crime Scene Investigation.2012

4.    Forensics Pathology.2001

5.    Pathology.2005

6.    Forensic DNA Technology (Lewis Publishers,New York, 1991).

7.    The Examination and Typing of Bloodstains in the Crime Laboratory (U.S. Department of Justice, Washington, D.C., 1971).

8.    „A Short History of the Polymerase Chain Reaction". PCR Protocols. Methods in Molecular Biology.

9.    Molecular Cloning: A Laboratory Manual (3rd ed.). Cold Spring Harbor,N.Y.: Cold Spring Harbor Laboratory Press.2001

10.   "Antibodies as Thermolabile Switches: High Temperature Triggering for the Polymerase Chain Reaction". Bio/Technology.1994

11.   Forensic Science Handbook, vol. III (Regents/Prentice Hall, Englewood Cliffs, NJ, 1993).

12.   "Thermostable DNA Polymerases for a Wide Spectrum of Applications: Comparison of a Robust Hybrid TopoTaq to other enzymes". In Kieleczawa J. DNA Sequencing II: Optimizing Preparation and Cleanup. Jones and Bartlett. 2006

13.   Nielsen B, et al., Acute and adaptive responses in humans to exercise in a warm, humid environment, Eur J Physiol 1997

14.   Molnar GW, Survival of hypothermia by men immersed in the ocean. JAMA 1946

15.   Paton BC, Accidental hypothermia. Pharmacol Ther 1983

16.   Simpson K, Exposure to cold-starvation and neglect, in Simpson K (Ed): Modem Trends in Forensic Medicine. St Louis, MO, Mosby Co, 1953.

17.   Fitzgerald FT, Hypoglycemia and accidental hypothermia in an alcoholic population. West J Med 1980

18.   Stoner HB et al., Metabolic aspects of hypothermia in the elderly. Clin Sci 1980

19.   MacGregor DC et al., The effects of ether, ethanol, propanol and butanol on tolerance to deep hypothermia. Dis Chest 1966

20.   Cooper KE, Hunter AR, and Keatinge WR, Accidental hypothermia. Int Anesthesia Clin 1964

21.   Keatinge WR. The effects of subcutaneous fat and of previous exposure to cold on the body temperature, peripheral blood flow and metabolic rate of men in cold water. J Physiol 1960

22.   Sloan REG and Keatinge WR, Cooling rates of young people swimming in cold water. J Appl Physiol 1973

23.   Keatinge WR, Role of cold and immersion accidents. In Adam JM (Ed) Hypothermia – Ashore and Afloat. 1981, Chapter 4, Aberdeen Univ. Press, GB.

24.   Keatinge WR and Evans M, The respiratory and cardiovascular responses to immersion in cold and warm water. QJ Exp Physiol 1961

25.   Keatinge WR and Nadel JA, Immediate respiratory response to sudden cooling of the skin. J Appl Physiol 1965 

26.   Golden F. St C. and Hurvey GR, The “After Drop” and death after rescue from immersion in cold water. In Adam JM (Ed). Hypothermia – Ashore and Afloat, Chapter 5, Aberdeen Univ. Press, GB 1981.

27.   Burton AC and Bazett HC, Study of average temperature of tissue, of exchange of heat and vasomotor responses in man by means of bath coloremeter. Am J Physiol 1936

28.   Adam JM, Cold Weather: Its characteristics, dangers and assessment, In Adam JM (Ed).Hypothermia – Ashore and Afloat, Aberdeen Univ. Press, GB1981.

29.   Modell JH and Davis JH, Electrolyte changes in human drowning victims.Anesthesiology 1969

30.   Bolte RG, et al., The use of extracorporeal rewarming in a child submerged for 66 minutes. JAMA 1988

31.   Ornato JP, The resuscitation of near-drowning victims. JAMA 1986

32.   Conn AW and Barker CA: Fresh water drowning and near-drowning — An update.1984;

33.   Reh H, On the early postmortem course of “washerwoman’s skin at the fingertips.” Z Rechtsmed 1984

34.   Gonzales TA, Vance M, Helpern M, Legal Medicine and Toxicology. New York, Appleton-Century Co, 1937.

35.   Peabody AJ, Diatoms and drowning – A review, Med Sci Law 1980

36.   Foged N, Diatoms and drowning — Once more.Forens Sci Int 1983

37.   "Microscale chaotic advection enables robust convective DNA replication.". Analytical Chemistry. 2013

38.   Sourcebook in Forensic Serology, Immunology, and Biochemistry (U.S. Department of Justice, National Institute of Justice, Washington, D.C.,1983).

39.   C. A. Villee et al., Biology (Saunders College Publishing, Philadelphia, 2nd ed.,1989).

40.   Molecular Biology of the Gene (Benjamin/Cummings Publishing Company, Menlo Park, CA, 4th ed., 1987).

41.   Molecular Evolutionary Genetics (Plenum Press, New York,1985).

42.   Human Physiology. An Integrate. 2016

43.   Dumas JL and Walker N, Bilateral scapular fractures secondary to electrical shock. Arch. Orthopaed & Trauma Surg, 1992; 111(5)

44.   Stueland DT, et al., Bilateral humeral fractures from electrically induced muscular spasm. J. of Emerg. Med. 1989

45.   Shaheen MA and Sabet NA, Bilateral simultaneous fracture of the femoral neck following electrical shock. Injury. 1984

46.   Rajam KH, et al., Fracture of vertebral bodies caused by accidental electric shock. J. Indian Med Assoc. 1976

 

47.   Wright RK, Broisz HG, and Shuman M, The investigation of electrical injuries and deaths. Presented at the meeting of the American Academy of Forensic Science, Reno, NV, February 2000

48. Broor SL, Kumar A, Chari ST, et al. 1989. Corrosive oesophageal strictures following acid ingestion: clinical profile and results of endoscopic dilatation.

49. Baud FJ, Barriot P, TOGS V, et al. 199 1. Elevated blood cyanide concentrations in victims of smoke inhalation.

50. Blackwell M, Robbins A. 1979. Arsine (arsenic hydride) poisoning in the workplace