Arquitectura del sistema de una red GSM

Huguier proposed that the mechanism of destruction by which projectiles damage tissues involved a sudden catastrophic rise in pressure (Huguier, 1848, cited by Payne, 1997). Firing into both liver and muscle (projectile information unavailable), Huguier suggested that energy imparted by the moving projectile caused water present in these tissues to be dispersed in a hydrodynamic fashion. This was during a period of time when the notion of the use of ‘explosive bullets’ in the battlefield had been proposed (Besant- Matthews, 2000). According to Horsely (1894), the explosive effects that were seen could be explained by the fluidity of the particles in the impacted part of the body being

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displaced. Horsley (1894) cited that work carried out by Kocher between 1874 and 1876 supported Huguier’s original theory, with Kocher described by Wilson (1921) as the pioneer of accurate observations on the wounding effects of high velocity bullets. It was Woodruff (1898) however, who first coined the concept of cavitation (a hydrodynamic process) for wound ballistics (Wilson, 1977).

As already discussed, tissue that comes into contact with a moving projectile is damaged by crushing and lacerating. While a projectile is traversing living tissues, it also causes the tissues surrounding the projectile’s path to accelerate away, due to high pressures created (Janzon, 1997). This results in the splashing and stretching of the margins of the tissues surrounding the projectile’s path. This is the start of a temporary cavity formation (Besant-Matthews, 2000) (Figure 2-8).

The pressure imparts momentum to the tissues in both a forward and radial fashion; tissues that are pushed forward are accelerated by the bullet; tissues moved radially acquire approximately one tenth of the projectile’s velocity (Belkin, 1979). As well as the propagation due to pressure, energy is transferred in the form of stored (potential) energy due to the elastic deformity of the tissues (Janzon, 1997). This explains why the particles in the tissue keep moving after the projectile has passed (Adams, 1982). Tissues are stretched and distorted, but because the tissues in a living target are neither wholly nor uniformly elastic, the extent of the damage is determined by the level of elasticity in combination with the tissue’s respective density and air content. The energy that is imparted by the missile is also a determinant (Barach et al., 1986).

Tissues with greater elasticity are better equipped at resisting the disruptive effects of the temporary cavity. Elastic tissue such as skeletal muscle, blood vessels and skin may rebound back after being pushed away during penetration (Jenkins and Dougherty, 2005). Tissues with little or no elasticity can be damaged in a method that is explosive in character (Adams, 1982). The effect of tissue density has been discussed; however, its effect is also important in temporary cavitation. Energy is absorbed by tissue in proportion to its density. Lung tissue is high in elasticity and low in density, and hence the temporary cavity effects are typically much smaller in size when compared to temporary cavities in organs such as the liver and spleen (Wilson, 1977). As previously stated, denser tissue causes greater drag on a projectile. Using Newton’s third law, the forces acting on the tissues have to be equalled out by the tissues accelerating away with equal force. This

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explains why the temporary cavity is usually largest when the projectile expands or is yawing at 90 °; these are instances where the drag and energy transfer is greatest.

Once the tissues have been extended up to and beyond their elastic limit, the cavity will reach its maximum size. Belkin (1979) stated this is 30 times or more the size of the permanent cavity, while Di Maio (1999) believes it is in the region of 11-12.5 times the diameter of the projectile. When at its maximum size, the cavity has a sub-atmospheric pressure present within it, sucking in air and matter from the outside environment through both the entry and exit wound (Adams, 1982; Janzon, 1997). Due to this sub-atmospheric pressure, the cavity collapses after a matter of milliseconds, setting up a positive pressure (Belkin, 1979; Adams, 1982). This causes a cycle of decreasing expansions and collapses of the cavity, the pulsations of which add to the disruption of the surrounding tissues (Belkin, 1979). The whole process of the temporary cavitation is in the order of 5-10 milliseconds from propagation to collapse (Krauss, 1957; Hiss and Kahana, 2000).

After the final pulsation, the permanent cavity will be what remains, with the evidence that there was a temporary cavity found in the ‘zones of contusion’ and ‘concussion’, the final two zones of a ballistic wound (Wang et al., 1988). Although there is no clear-cut difference between the two zones, the borders will be irregular; the zone of contusion will contain areas of devitalised tissue together with haemorrhage within and between tissues. Conversely, the zone of concussion will contain wholly normal tissue, with microscopic evidence of damage, such as swollen myofibres and bleeding between fibres (Wang et al., 1988; Bowyer et al., 1997b). The shape of the temporary cavity will depend on the shape, presentation and yaw of the projectile, and generally mimics the shape of the permanent cavity (Belkin, 1979).

It had been claimed that low velocity projectiles (hand-gun rounds, less than 500m/s) did not cause a temporary cavity and that only high velocity impacts did, however, this is not the case, the temporary cavitation is just on a smaller scale in lower velocity impacts (Besant-Matthews, 2000; Hiss and Kahana, 2000).

The importance of the temporary cavitation is a debated subject. Some have considered it the most important factor in wounding mechanisms (e.g. Sellier and Kneubuehl, 1994; Janzon, 1997). Others have hypothesised that it is not as important as the permanent cavity and have questioned attempts that have been made to treat the temporary cavity effects, rather than actual injuries, believing this resulted in the

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unnecessary removal of viable tissues (Lindsey, 1980; Fackler and Kneubuehl, 1990). This suggestion turned into advice from Cooper and Ryan (1990), who stated that not all tissue affected by the temporary cavitation process is necessarily damaged by it. Through cavitation can produce star-shaped damage radiating from the permanent track (Janzon et

al., 1997). The effect of cavitation will ultimately depend on the properties of the tissue

in which the cavitation occurred.