Hydrostatic Shock: Wikipedia Article

[Michael Courtney]

As for the resultant rise in ICP (intra-cranial pressure), you'd need a sustained- not fleeting- pressure of 20-30 mm Hg to disrupt cognitive function. And the effects would take too long to manifest themselves to alter the outcome of a firefight.

Research from a broad variety of fields has shown that brief pressure transients of 15-30 PSI are sufficient to temporarily disrupt consiousness and are associated with mild traumatic brain injury and concussion. 30 mm Hg is less than 1 PSI, so you are talking about much smaller pressures than are actually reaching the brain as a result of a bullet impact that produces 800-1000 PSI in the chest.

The fact is, raised ICPs are only witnessed (in the context of smallarms) after direct head-trauma, not after thoracic or abdominal wounds. It's just a fact. Check with any reputable neurosurgeon who's treated gunshot victims.

You're talking about measured ICPs in the hospital after the event. We are talking about very brief (milliseconds) pressure transients that are present during the actual bullet impact (and for milliseconds afterward).

Similarly, if effects of hydrostatic shock can damage the brain from afar, how come anyone ever survives a penetrating head wound from a bullet? (Admittedly rare, but I've known a few). Doesn't the Kellie-Monroe principle apply?

Remote damage necessary to produce incapacitation is comparable to the same level of mild concussion that causes temporary incapacitation in sports injuries to the head. It's a much lower level of damage than that associated with a significant permanent neurological disfunction, much less death.

Michael Courtney

 

[Michael Courtney]

And if- as proponents of 'hdrostatic shock' claim, these pressure-waves travel via major blood vessels (and apart from via cerebro-spinal fluid in the case of the spine being hit, there doesn't seem to be any other credible mechanism)- why aren't the lungs / heart damaged?

Transmission via the major blood vessels is probably the dominant hypothesis, but transmission via the cerobro-spinal fluid and soft tissues have also been suggested. These alternatives require the pressure wave to pass through either the spine or cranium, so they are less appealing, but they have not been ruled out either by experimental data or compelling theoretical considerations. The waves have sufficiently high frequency components that significant amplitude could be transmitted through bone.

No immediate trauma, no thrombo-embolytic events, no raised troponin-T, no disruption of cardiac pacing. Most significantly, there's no loss of blood-pressure autoregulation (and resultant neurogenic cardiac shock), although such a pressure-wave would presumably impinge on baro-receptors which are sensitive to, er, pressure.

It is known that the pressure wave magnitudes required to damage vascular tissue, muscle, and lung tissue are much higher than magnitudes that are required to damage neural tissue.

We believe it is an open question whether hits to the thoracic cavity can interfere with blood-pressure autoregulation. A reference to published data to the contrary would certainly be a valuable contribution.

The fact is, if hydrostatic pressure-waves occur during smallarms injury, they seem to have little clinical effect.

First of all, it is possible to for mild traumatic brain injury to cause temporary incapacitation without having significant clinical effects.

Secondly, it should be recognized that the BPW threshold for easily observable effects is above the level of BPW produced in most handgun injuries presenting in emergency rooms. Some service caliber loads produce BPW levels above 1000 PSI, but most do not. In addition, many military rifle wounds do not produce BPW levels above 1000 PSI unless the bullet tumbles and fragments early in the wound channel. (The threshold for easily observable BPW effects is 1000 PSI near the center of the chest.)

Thirdly, how many survivors of hits meeting the selection criteria for remote BPW effects receive thorough evaluations for mild TBI?

Michael Courtney

 

[Michael Courtney]

@ Dr. Courtney: I seem to recall that at some point in the past, you posted some equations that estimated the magnitude of the hydraulic shock that would result from impact of a projectile given its velocity and the diameter of the meplat. I have not been able to find that post (maybe it was on some other forum? but I thought it was here.)

Could you re-post those equations? Thanks!

I think you may be remembering a post from someone else. We parameterize BPW magnitude in terms of impact energy, penetration depth, and fraction of retained mass.

If all the mass is retained, the pressure magnitude is

p = 5E/pi d,

where E is the impact energy (in ft-lbs), d is the penetration depth (in feet), and p is the peak pressure wave (in PSI) on the surface of a 1" diameter cylinder centered on the wound axis.

Michael Courtney

 

[Feanaro]

It is somewhat dubious, and IIRC against wikipedia policy, to cite oneself in an academic article.

There is nothing wrong with self-citation, either in Wikipedia or academia.

I do think the "Myth?" section suffers from some weasel words though. For example, "Because subtle damage in neural tissues was difficult to detect, denials of "hydrostatic shock" (remote neural effects) as a real wounding mechanism persisted for some time." The implication is that they no longer persist, presumably because they are incorrect. I don't recall Fackler, for example, recanting his position.

However, considering that Courtney et al. are on the complete opposite side of the fence, it's more unbiased than most such rewrites.

 

[Michael Courtney]

For example, "Because subtle damage in neural tissues was difficult to detect, denials of "hydrostatic shock" (remote neural effects) as a real wounding mechanism persisted for some time." The implication is that they no longer persist, presumably because they are incorrect. I don't recall Fackler, for example, recanting his position.

A significant majority of scientific authors who have published peer-reviewed views on remote pressure wave effects support the reality of remote pressure wave effects. Since the Suneson et al. papers were published in 1990, only a small minority have published assertions that remote neural effects are not real.

In 1989 and 1991, Fackler published two papers in which he strongly opposed the idea of remote pressure wave effects, calling them a "myth." By 1996, several other studies had been published supporting remote wounding effects, and Fackler had retreated to the position that "To date, no study has scientifically or objectively demonstrated any change in the human gunshot victim that cannot be explained by the well-recognized wounding mechanisms of tissue crush resulting from a direct hit by the penetrating projectile or tissue displacement from temporary cavitation."

This represented a significant retreat in his earlier position because he is emphasizing the lack of demonstration in humans (rather than animal models). (Apparently, he was not aware of references 3, 4, 38, and 39 even though they had already been published.)

To our knowledge, Fackler's 1996 paper was the last significant peer-reviewed denial of remote wounding effects of ballistic pressure waves. It contained the flawed reference to lithotriptors not damaging tissue which was later shown to be in error. It also came before a number of later papers further documenting the role of ballistic pressure waves (refs 15, 16, 17, 19) which include both experimental studies supporting the earlier Suneson results and further case studies in humans. In addition, since Fackler's 1996 paper, a number of scientists in the field of blast injury have referenced the BPW literature favorably demonstrating a broad consensus of support in the scientific community.

To our knowledge, no one has published an peer-reviewed objection to Wang's 2004 paper demonstrating remote BPW effects in dogs or to Sturtevant's 1998 paper documenting remote BPW effects in a case study or to Treib et al's 1996 paper doing the same.

Sure, some former IWBA members continue to defend the Fackler's outdated views on internet forums, but these are not considered reliable sources in either the scientific literature or by Wikipedia's standards of verifiability. Twelve years of silence in the scientific literature is significant in light of the fact that research has continued to be published in support of remote BPW effects. In addition, even most of the former IWBA members tend to emphasize the unreliability of remote BPW effects as an incapacitation mechanism rather than asserting the much stronger view that the remote BPW effects do not exist at all.


Michael Courtney

 

[st_albert]

I think you may be remembering a post from someone else. We parameterize BPW magnitude in terms of impact energy, penetration depth, and fraction of retained mass.

If all the mass is retained, the pressure magnitude is

p = 5E/pi d,

where E is the impact energy (in ft-lbs), d is the penetration depth (in feet), and p is the peak pressure wave (in PSI) on the surface of a 1" diameter cylinder centered on the wound axis.

Thanks. I probably did remember it wrong, but the above equation is on the right track. I presume that your equation is parsed as follows:

p = 5E/(pi*d) , right?

Then, this says that the shape of the projectile does not affect the peak pressure, EXCEPT for its influence on d, the penetration depth. A projectile which slows down faster (more negative dv/dt) should have a smaller d (total penetration distance?) and since we're assuming mass is constant, the pressure at unit area should be proportional to the magnitude of dv/dt. Correct me if I'm not following this right -- it's been a while since I studied physics.

Anyway, the derivation I (mis) remebered had to do with quantifying the effect of projectile shape on the magnitude of deceleration (hence the peak pressure?). Broadly, the more blunt the projectile the faster it decelerates, so the higher the pressure peak and the shorter the penetration distance, other things being equal.

Thus it would seem you'd get a bigger hydrostatic effect with a wadcutter bullet than with a round-nose design, given the same impact energy and, let's say same sectional density.

Sorry to blather on about this, and I probably should have taken it to email or pm, but I thought the effect of bullet shape might be of interest to others.

Albert

Edited to add: Aack! Silly me, I should have read the footnotes at wikipedia. This is already discussed in one of your papers, Courtney and Courtney, "Ballistic pressure wave contributions to rapid incapacitation in the Strasbourg goat tests", http://arxiv.org/ftp/physics/papers/0701/0701267.pdf

 

[Michael Courtney]

Thanks. I probably did remember it wrong, but the above equation is on the right track. I presume that your equation is parsed as follows:

p = 5E/(pi*d) , right?

Then, this says that the shape of the projectile does not affect the peak pressure, EXCEPT for its influence on d, the penetration depth.

This formula gives an accurate estimate for expanding JHP's which retain 100% of their mass. It over-estimates pressure wave magnitudes for bullets which do not expand and underestimates pressure wave magnitudes for bullets that fragment.

A projectile which slows down faster (more negative dv/dt) should have a smaller d (total penetration distance?) and since we're assuming mass is constant, the pressure at unit area should be proportional to the magnitude of dv/dt. Correct me if I'm not following this right -- it's been a while since I studied physics.

Right.

Anyway, the derivation I (mis) remebered had to do with quantifying the effect of projectile shape on the magnitude of deceleration (hence the peak pressure?). Broadly, the more blunt the projectile the faster it decelerates, so the higher the pressure peak and the shorter the penetration distance, other things being equal.

Thus it would seem you'd get a bigger hydrostatic effect with a wadcutter bullet than with a round-nose design, given the same impact energy and, let's say same sectional density.

This approach is technically sound, but the utility is limited because most self-defense loads expand so that both the shape and frontal area are dynamic. We wanted a way to estimate the peak retarding force (thus the pressure wave magnitude) without knowing the shape and frontal area of the penetrating projectile at every instant.

Michael Courtney