This paper is another landmark by Dr. Fackler in scientific research about terminal ballistics. It explains why most of what you read about this subject in newspapers, politicized medical journals and gun magazines is grossly wrong. Dr. Fackler's research and experience bear directly on the proper treatment of different gunshot wound types.Note that the contact info below is now out of date in several important ways. -- Jeff C.]
Probably no scientific field contains more misinformation than wound ballistics. In a 1980 Journal of Trauma editorial entitled "The Idolatry of Velocity, or Lies, Damn Lies, and Ballistics," Lindsey identified many of the misconceptions and half-truths distorting the literature (1). Despite his cogent revelations, the errors he attempted to rectify are still being repeated in the literature (2-7), often embellished with unproven assumption and uninformed speculation. The body of literature generated at the wound ballistics laboratory of the Letterman Army Institute of Research over the past six years (8-14) strongly supports the points made by Professor Lindsey. The author of this paper has chosen to correct errors, as they appeared, with letters to journal editors (15-22), a time-consuming endeavor of questionable effectiveness. This critical review calls attention to the problem, corrects the most widespread and damaging misinterpretations, and lays the groundwork for improved research, understanding and clinical treatment.
Between 1875 and 1900, the study of gunshot effects had reached a high level of sophistication, thanks mainly to Theodor Kocher, whose work was the epitome of sound scientific method (23-27). However, with the advent of the high-speed movie camera in the present century, emphasis in wound ballistics shifted from sound scientific method to spectacular cinematography--a triumph of high technology over common sense. Unfortunately, a sideshow mentality seized upon the technology of the twentieth century. Flamboyance attracted more attention than sound science. Wound ballistics research was reduced to taking movies of shots into everything imaginable, and the focus of understanding narrowed to exclude every variable except projectile velocity. The exaggeration inherent in these methods so distorted the concept of temporary cavitation that, to some, it came to represent the entirety of the projectile-tissue interaction (28, 29). Rarely does the viewer find a measuring scale included in reproductions of these dramatic cinematographic frames (30). Undoubtedly, many readers have seen the Swedish film of an anesthetized pig being shot through the abdomen with an M-16 rifle that "made the rounds" about fifteen years ago. No scale or any other item was included to provide size orientation. How large was the pig? Most would assume the animal to be in the 100- to 150-kg range. It was actually a mini-pig, weighing about one tenth that much. The exaggeration of effects so introduced is obvious.
The wound produced by a particular penetrating projectile is characterized by the amount and location of tissue crush and stretch. In our laboratory, we measure the amount and location of crush (permanent cavity) and stretch (temporary cavity) on the basis of shots fired into gelatin tissue simulant. Since we have calibrated this simulant to reproduce the projectile characteristics (penetration depth, deformation, fragmentation, yaw) equivalent to those observed in living animal tissue, measurements from these shots can be used to predict approximate animal tissue disruption (8-10). These data are presented in the form of Wound Profiles (Fig 1-8), which illustrate the amount, type, and location of tissue disruption, projectile mass, velocity, construction, and shape (before and after the shot), as well as projectile deformation and projectile fragmentation pattern when applicable. The scale on each profile permits quick determination of tissue disruption dimension at any point along the penetration path for comparison with other profiles, other experimental results, or with measurements from actual wounds in a clinical setting or at autopsy. Wound profile data will be used to rectify the fallacies listed below.
The adjunct half-truth, Cavitation requires extensive debridement of tissues..." (7), lacks valid scientific support. Cavitation is nothing more than a transient displacement of tissue, a stretch, a localized "blunt trauma." It is not surprising that elastic tissues such as bowel wall, lung, and muscle are relatively resistant to being damaged by this stretch, while solid organs such as liver are not (9). Most of the muscle subjected to temporary cavity stretch survives; tissue survival has been verified in every case in which muscle was allowed to remain in situ and healing was followed to completion (43-48).
Misinterpretation of the mechanism by which the M-16 rifle causes tissue disruption perpetuated the foregoing misconceptions. The M-16 (Fig 2) was introduced in Vietnam, and many compared the increased tissue disruption it produced (12-14, 49, 50) with that caused by previous military rifles. In the Vietnam era, the major role played by bullet fragmentation in tissue disruption was not recognized (8). It is now appreciated (12-14) and documented (Fig 3) that bullet fragmentation is the predominant reason underlying the M-16's increased tissue disruption. Despite this recent evidence, a generation of surgeons and weapon developers (28) has been confused and prejudiced by the assumption that "high velocity" and "temporary cavitation" were the sole causes of tissue disruption .
It is indeed surprising that only Lindsey questioned the attribution of the marked increase in tissue disruption to a rather modest 10% increase in velocity. Surely, someone should have noticed that the largest increase of projectile velocity in the history of small-arms development (a 50% increase--made possible by the invention of the copper-jacketed bullet near the end of the nineteenth century) was accompanied by a marked decrease in soft tissue disruption (51, 52). This decrease was predicted by Kocher, whose work had taught him the importance of projectile deformation (26, 27); new smaller-caliber bullets did not deform upon striking tissue as did previous large caliber soft lead bullets (Fig 1).
To further confuse the issue, pressures of up to 100 atmospheres are incorrectly attributed to temporary cavitation by many authors (39, 40, 55-57). These authors appear to have confused the sonic pressure wave with the pressure generated in tissues by temporary cavitation. Temporary cavity tissue displacement can cause pressures of only about 4 atmospheres (31). A careful reading of Harvey's paper (31) should correct this confusion.
Probably the most exaggerated account of temporary cavity effect in the literature appears in High Velocity Missile Wounds by Owen-Smith (36). His Fig 2.20 on page 35 shows a lesion in a pig's colon caused by a "standard bullet fired at 770 m/s (2500 ft/s)." Concerning this wound, he states "there are microscopic changes of cell death extending 20 cm from the edge of the hole in the colon; this is why such an area must be resected if it has been damaged by a rifle bullet." Perusal of the source document of this picture (58), however, reveals that a deforming soft-point hunting bullet was used for this shot. In describing the effect of this shot, the source document states, "...haemorrhage extended macroscopically to a diameter (my emphasis) of 20 cm." When the 8-cm hole diameter is subtracted, a 6-cm distance (rather than the 20 cm reported by Owen-Smith) from the edge of the hole on each side adds up to the "diameter of 20 cm" reported by Scott in the source document. Furthermore, photographs of bowel defects caused by bullets must be viewed with caution. Folding back the bowel wall around the edges of the hole can make tissue defects appear larger. If colon tissue at a distance of 20 cm from the bullet hole is killed, as asserted by Owen-Smith, what happens to the loops of small bowel and other organs that are within 20 cm of the bullet hole? Are they killed too? If so, this would equate to destruction of most of the abdominal contents by every penetrating "high-velocity" bullet. Clearly, this conclusion is inconsistent with well established available facts. A study done in our laboratory (9), for example, showed damage to a pig colon caused by a nondeforming military bullet traveling at 911 m/s (2989 ft/s) that was only slightly larger than the dimensions of the bullet that had caused it.
It should be noted, however, that stretch from temporary cavity tissue displacement can disrupt blood vessels or break bones at some distance from the projectile path (40), just as they can be disrupted by blunt trauma. We can produce this in the laboratory by careful choice of projectile and projectile trajectory in tissue (48), but in practice this happens only very rarely. Data from the Vietnam conflict show that the great majority of torso and extremity wounds were attributable to the damage due to the permanent cavity alone (59).
Data from ballistics studies 10, 13, 14) show quite clearly that:
A large slow projectile (Fig 7) will crush (permanent cavity) a large amount of tissue, whereas a small fast missile with the same kinetic energy (Fig 4) will stretch more tissue (temporary cavity) but crush little. If the tissue crushed by a projectile includes the wall of the aorta, far more damaging consequences are likely to result than if this same projectile "deposits" the same amount of energy beside this vessel.
Many body tissues (muscle, skin, bowel wall, lung) are soft and flexible--the physical characteristics of a good shock absorber. Drop a raw egg onto a cement floor from a height of 2 m; then drop a rubber ball of the same mass from the same height. The kinetic energy exchange in both dropped objects was the same at the moment of impact. Compare the difference in effect; the egg breaks while the ball rebounds undamaged. Most living animal soft tissue has a consistency much closer to that of the rubber ball than to that of the brittle egg shell. This simple experiment demonstrates the fallacy in the common assumption that all kinetic energy "deposited" in the body does damage.
The assumption that "kinetic energy deposit" is directly proportional to damage done to tissues also fails to recognize the components of the projectile-tissue collision that use energy but do not cause tissue disruption. They are 1) sonic pressure wave, 2) heating of the tissue, 3) heating of the projectile, 4) deformation of the projectile, and 5) motion imparted to the tissue (gelatin bloc displacement for example).
The popular format for determination of "kinetic energy deposit" uses a chronograph to determine striking velocity and another to determine exit velocity. A 15-cm thick block of tissue simulant (gelatin or soap) is the target most often used. This method has one big factor in its favor; it is simple and easy to do. As for its validity, the interested reader is referred to wound profiles shown in Figs 1-7. Comparing only the first 15 cm of the missile path with the entire missile path as shown on the profiles shows the severe limitation of the 15-cm block format. The assumption by weapons developers that only the first 15 cm of the penetrating projectile's path through tissue is of clinical significance (64) may simplify their job, but fails to provide sufficient information for valid prediction of the projectile's wounding potential. The length of bullet trajectories through the human torso can be up to four times as long as those in these small blocs. Even if this method were scientifically valid, its use has been further flawed by nearly all investigators who have included the M-16 rifle bullet in those projectiles tested. This method assumes that the projectile's mass remains constant through both chronographs. The M-16 routinely loses one third of its mass in the form of fragments which may remain in the target (see Fig 2). The part of the bullet that passes through the second chronograph screens weighs only about two-thirds as much as the intact bullet that passed through the first set of screens. No provision is made for catching and weighing the projectile to correct for bullet fragmentation when it occurs. The failure to correct for loss of bullet mass can cause large errors in "energy deposit" data (8).
Surgeons sometimes excise tissue from experimental missile wounds that is, in their judgment, nonviable and compare the weight of tissue excised with the "kinetic energy deposited" (65). A surgeon's judgment and his technique of tissue excision is very subjective, as shown by Berlin et al (66), who found in a comparison that "One surgeon excised less tissue at low energy transfers and rather more at high energy transfers than the other surgeon, although both surgeons used the same criteria when judging the tissues." None of these experiments included control animals to verify that tissue the surgeon had declared "nonviable" actually became necrotic if left in place. Interestingly, all studies in which animals were kept alive for objective observations of wound healing report less lasting tissue damage than estimated from observation of the wound in the first few hours after it was inflicted (43-47, 67, 68). In a study of over 4,000 wounded in WW II it was remarked, "It is surprising to see how much apparently nonvital tissue recovered" (69).
Anyone yet unconvinced of the fallacy in using kinetic energy alone to measure wounding capacity might wish to consider the example of a modern broadhead hunting arrow. It is used to kill all species of big game, yet its striking energy is only about 50 ft-lb (68 Joules)-- less than that of the .22 Short bullet. Energy is used efficiently by the sharp blade of the broadhead arrow. Cutting tissue is far more efficient than crushing it, and crushing it is far more efficient than tearing it apart by stretch (as in temporary cavitation).
Duct-sealing compound (73), clay (2,74), soap (66, 72), gelatin (28-30, 38), and water-soaked phone books or newspapers (74) are commonly used tissue simulants. Information from each has been presented in the literature with the implication that it yields valid predictive information about wounding effects in living animals. Contrary to the assumptions that these materials are equivalent to animal tissue, bullet deformation caused by impact with them can vary widely. Recently, for example, we tested a 9-mm soft point pistol bullet that showed no deformation at all when shot into fresh swine cadaver leg muscle or into our 10% gelatin (shot at 4 degrees C), but expanded to a diameter of 15 mm when shot into duct-sealing compound (75).
Nonelastic tissue simulants (duct-sealing compound, clay, soap) can also mislead by their dramatic preservation of the maximum temporary cavity. Such demonstrations give a false impression that these cavities represent the potential for tissue destruction rather than the potential for tissue stretch. The latter may be absorbed by most living tissues with little or no lasting damage.
In the battlefield setting the surgeon cannot know, with certainty, all the properties of the wounding projectile (shape, mass, construction type, striking velocity). In a majority of civilian cases information about the wounding weapon is not available (76). Fortunately, such information is not necessary for the proper treatment of gunshot wounds. In fact, it is the author's opinion that the patient will be better off if his medical care provider doesn't know anything about the wounding weapon at all. The provider might then, without bias, use objective data from his physical examination and roentgenographic studies to make more valid treatment decisions.
When a penetrating projectile does cause significant tissue disruption, that disruption is usually very obvious. For example, in an uncomplicated extremity wound caused by the M-16 rifle (Fig 2), if the bullet yaws significantly and fragments, this will be evident in the form of a large exit hole. If no significant yaw occurs, the exit will closely resemble the entrance hole, and little or no functional disturbance will be evident because of minimal tissue disruption. If, on the other hand, the bullet breaks up very early in its path through the tissue, it is possible that the entrance and exit holes could be small despite marked tissue disruption within the limb (such a pattern is typical of a soft point bullet (Fig 7); occasionally this pattern may also be produced by the M-16 bullet. The situation should pose no diagnostic problem; marked functional disturbance with swelling will be obvious on physical examination, and the bullet fragmentation with soft tissue disruption will be obvious on biplanar x-rays. As in the therapy of any other form of trauma, objective data should guide treatment decisions.
The corollary postulate, "low-velocity projectiles cause insignificant damage,Õ can also lead to disaster. The author was consulted recently about a case in which gas gangrene had developed in a leg wound caused by a .38 Special pistol (a "low-velocity" projectile). Surgical exploration of the wound had been delayed until 40 hours after the injury, and the first antibiotic had been administered four hours after the operation. It was the author's opinion that treatment had been inappropriate, but could not be considered negligent, since the literature contains many recommendations such as "...the majority of low velocity gunshot wounds of the extremities may be safely treated without recourse to the operating room" (41), and "Debridement is unnecessary for wounds caused by bullets whose muzzle energy is less than 400 foot pounds" (42). If antibiotic coverage had been started soon after the wound occurred, and if the bias obtained from the literature had not misled the surgeon to delay surgical exploration of the wound, this lethal infection most certainly would have been avoided.
Light bullets of high velocity lose velocity rapidly in flight--a basic physical phenomenon (11). Perhaps the aforementioned weapon problems could have been avoided if weapons designers had been less influenced by the mystique of "high velocity" and more influenced by basic physics of projectiles in flight. They might have realized that the older M-16 bullet was too light to be effective at longer ranges and used a heavier bullet in the first place. It is difficult to be optimistic for the future when these weapons developers still use the scientifically discredited "kinetic energy deposit" method to estimate wounding effects.
An extensive body of misinformation has been promulgated (28,29), based on the assumption that the temporary cavity produced by a handgun bullet is the sole factor determining its "incapacitation" effect on the human target. These studies were done to aid law enforcement agencies in their choice of weapons. The investigators superimposed temporary cavity measurements, derived from shots into gelatin blocs, on a computer man" diagram of the human body. They judged relative damage by the anatomic regions "included" in the cavity. A "Relative Incapacitation Index" for each bullet was then calculated from these data. The superimposition of the temporary cavity on a region to determine the anatomic structures it encompasses reveals a serious misunderstanding of wounding mechanisms. By definition, no tissue is included "in" the temporary cavity: tissue is pushed aside by it. Using the permanent cavity in this fashion would make sense, but the permanent cavity is totally ignored in the calculation of the Relative Incapacitation Index. Not surprisingly, this Relative Incapacitation Index has been criticized (17, 79, 80), but reliance on its supposed validity continues to endanger the lives of those who must depend on the reliable performance of their weapon. These Relative Incapacitation Index studies were supported by the US Government (Dept. Of Justice), causing many to assume their validity, and compounding the detrimental effects of the misinformation.
Misinterpretation of war trauma experience has misled many writers. Such experience is anecdotal. Rarely if ever is the weapon, type of bullet, distance from muzzle to target, and absence of intermediate targets known with certainty on the battlefield as it is in the wound ballistics laboratory. Memory mixes all types of war wounds together, assumptions on treatment efficacy are made despite lack of follow-up information, and statements from higher headquarters concerning treatment rendered in the field of action are frequently based on inaccurate data and incorrect assumptions. In sum, a lot of error is reported as fact.
Physicians writing in the field of wound ballistics need to acquire sufficient expertise in weapon technology so that they are not completely dependent on ballistics engineers or other "experts" for information. Ballistics engineers writing in the field must acquire sufficient expertise about the living animal so that they at least know the pertinent questions to ask. Unless the "knowledge gap" between the physical and biological sciences is bridged at least partially by those who work in this field, an enormous potential for inaccuracy is likely to continue.
Recognizing the projectile-tissue interaction as a simple mechanical collision and comprehending how tissue is disrupted (crush and stretch) in this collision, coupled with wound profiles illustrating how much crush and stretch occurs at any depth of projectile penetration, should give the reader sufficient background to recognize any perpetuation of past errors or creation of new ones in the future. It is not surprising that attempts to teach wound ballistics using formulae or tables of velocity and kinetic energy have been counterproductive. These methods have diverted attention from the actual tissue disruption and made the subject appear unnecessarily complicated.
An intelligent surgeon, knowing nothing about gunshot wounds except that they are contaminated, would most likely treat them quite appropriately. He would base his treatment decisions on objective data from the physical examination and x-ray studies, as he would in treating any other form of trauma. The surgeon who has read and accepted what is written in the wound ballistics literature could become a menace, doing more harm with his treatment than was done by the bullet. It is encouraging to note from the author's own experience as a combat surgeon and contacts with others that most treatment of penetrating injuries rendered on the field of battle was governed more by the common sense and good training of the surgeon than by what is written in the wound ballistics literature.
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