3.1.1 Introduction

Blunt—usually direct—trauma may result in soft-tissue injury, which initially is often underestimated because it presents with a less dramatic clinical appearance than penetrating trauma. The extent of the injury may increase as pathophysiological processes continue for days after injury (chapter 10.3.3). Understanding the susceptibility of skin, muscle, nerves, and vascular structures to blunt or crushing occurrences enables the surgeon to thoroughly assess the condition of the injured area in order to formulate a treatment plan. This chapter describes such mechanisms, with emphasis on direct impact and crush injuries. As with any other type of injury, there is a substantial range of severity, from simple contusion to closed lacerations to devastating crush injuries. While closed injuries may not carry the same risk of infection as their penetrating or open crushing counterparts, they may have equally poor outcomes due to vascular injury or massive muscle necrosis.

3.1.2 Direct trauma

The most frequent cause of blunt trauma leading to significant soft-tissue damage is a direct blow, most often covering a larger area of impact than seen in penetrating injuries and with variable disruption of the integument. If the injury results from a more focal point of impact, disruption of the skin occurs, with possible concomitant vascular or neurologic injury. In a larger impact area, the energy is dissipated. Thus, open injuries are less frequent. However, this impact can still cause significant damage.

In a validated rat model, Crisco et al [1] found that the degree of damage incurred depended upon both the mass and velocity of the impacting object as well as the radius of curvature or dimensions of this object. They discovered a predictable time course of pathology, which follows initial injury. Immediately after impact, the gross appearance of the damaged muscle demonstrated marked hemorrhage and edema near the surface, which extended radially from the point of impact ( Fig 3.1-1 ). Microscopically, this area showed intracellular formation of vacuoles within intact myofibrils and clear myofibril disruption of varying extent. There was no immediate change in quantities of collagen, and no early markers of fibroblast migration.

There appear to be three distinct zones of injury ( Fig 3.1-2 ): the central or gap zone, directly beneath the point of impact; the regenerative zone, where edema develops over the initial few days, and the uninjured, surviving zone. These zones depend upon the amount of energy imparted to the soft tissue as well as its relationship to the surrounding hard tissues. A relationship also exists between muscle mass and the possibility for muscle displacement. Studies have demonstrated that a muscle, which is contracted at the time of injury, sustains less severe damage than muscle in a relaxed state. In the latter case, the zone of direct injury tends to be displaced and deeper. The degree of damage initially present may clinically be difficult to determine. In severe injury, clear disruption can lead to hematoma, whereas lesser damage will rather create intramuscular hemorrhage.

A blunt impact creates damage that is highly dependent upon the material properties of the recipient tissue. When a considerable soft-tissue envelope is present, the impact creates shearing forces within adipose tissue, the underlying muscle, and neurovascular structures, which will dissipate some of the energy. However, when the soft-tissue envelope is minimal, skin and bone will typically be the first to fail. In case skin and bone remain intact even though the imparted energy is severe, a closed, complete laceration may occur. This is marked by failure and retraction of the muscle mass away from the zone of injury (chapter 10.3), resulting in an obvious defect. If linear structures are present, these are subjected to similar shear forces. Nerve tissue has very little tolerance in regard to stretching and prolonged compression.

Vascular injury has been described in conjunction with blunt trauma [2]. The degree of trauma inflicted in order to cause vascular injury is often severe enough to also cause associated limb loss, hemorrhage, and even life-threatening injury to the trunk, or a systemic inflammatory response. In these situations, careful clinical assessment, including peripheral neurovascular examination as well as an ankle-brachial index test, are mandatory. The nature of such an arterial injury is rather an avulsion (intimal tear) than a true crush and, therefore, loss of pulses is not consistently complete. Diagnosis requires awareness and detailed assessment. An ankle-brachial index (ABI) less than 0.9 has been found to be 100% correlated with occult lower-extremity vascular injury in healthy subjects [3].

3.1.3 Crush injury

Crush injury occurs when force is applied over an extended period of time to an immobilized portion of the body. Localized ischemia may occur as vessels are occluded by the external pressure. Crush injury of muscles is often associated with systemic effects of the ischemia, and may result in severe electrolyte imbalance, and myoglobinuria. The systemic effects have been described extensively, and are directly related to the severity and duration of tissue damage. They are manifested as an ischemic phase followed by reperfusion of the damaged area once the pressure is relieved (ischemia reperfusion injury) ( Fig 3.1-3 ). Products of cellular death are then circulated, causing direct toxicity to end organs such as the brain, the lungs or the kidneys. Less frequently, a physical disruption of linear structures, such as vessels and nerves, is observed, precluding tissue reperfusion.

Crushing often exceeds the elasticity of the skin, causing it to burst ( Fig 3.1-4 ). Tissues most sensitive to sustained pressure, such as vessels and nerves, fail early. Therefore, neurologic deficits and perfusion failure are often observed and can be directly related to trauma or secondarily to ischemia ( Fig 3.1-5 ). The clinical presentation of a prolonged crush injury is one of massive local soft-tissue damage, deformity, and associated fractures in the presence of a systemically unstable patient. In order to assess the involved damage correctly, the time interval between injury and rescue must be known, as it plays a large role in the development of subsequent reperfusion effects.

The pathophysiology at the site of injury is similar to blunt injury described above, however, with a substantially wider zone of injury. Actual muscle disruption occurs and hematomas will develop. In the setting of associated vascular injury, compartment syndrome may be imminent, but even without direct vascular injury, the reperfusion of ischemic muscle results in massive edema with delayed presentation of compartment syndrome. One study demonstrated the typical findings of severe blunt injury coupled with extreme capillary dilation beginning 2–4 days after crushing that was mediated by high nitric oxide levels [4]. Nitric oxide was shown to cause the characteristic hyperperfusion, and may have an additional destructive effect on compromised muscle due to increased blood flow, edema formation, and circulation of toxic mediators arising from areas of ischemia. The clinical impact is seen in a brisk response to bleeding when crushed muscle is debrided, and frequent difficulty in obtaining hemostasis.

3.2.1 Introduction

Penetrating injuries comprise a wide spectrum of soft-tissue injuries, from low-energy stab wounds to the systemic devastation of war-related blast injuries. Their severity is closely related to the affected structures and location, the degree of energy dissipation, and the behavior of the penetrating object within the tissue as well as the propensity for contamination. These determinants are critical for the amount of damage, lethality or long-term morbidity. While clinical treatment and evaluation of these injuries will be described subsequently, it is imperative to first understand the mechanisms leading to these injuries, and the associated pathology. This knowledge of the injury needs to include the degree to which these events impact the victim systemically as well as the associated injuries that are typically seen in such contexts. This section will discuss such aspects, beginning with a basic overview of ballistic injuries, respectively the study of the impact of a projectile on the human body.

3.2.2 Ballistic injury

In order to fully understand the effect of ballistic trauma, one must know the meaning of several terms rarely used in clinical practice except in the field of penetrating injury. Ballistics encompasses three discrete aspects of the trajectory of a projectile during its flight. Internal ballistics relates to the behavior of a bullet within its firing tube or at the instant of explosion. External ballistics describes the flight path from tube to the object of impact, and terminal ballistics refers to the events upon impact. Terminal ballistics correlates to wound ballistics whenever it relates to living tissue upon impact. As the projectile passes through tissue, the area directly damaged is called the permanent cavity. The term temporary cavity has been used to describe the tissues that are stretched in response to a cavity being formed as the bullet becomes unstable and tumbles. Terminal or wound ballistics will be the focus of this section.

The ultimate damage that a projectile inflicts upon its target is directly related to the quantity of kinetic energy it transfers to that target, which is a function of the composition, configuration, and stability of the projectile at impact as well as the characteristics and location of the organs hit by the projectile. Kinetic energy follows the equation KE = 1/2 mv², where m = the mass of the projectile and v = the velocity of the projectile [5]. Projectile mass can vary greatly from extremely small blast fragments to the 3.5 g round of the M16 military rifle to an artillery round weighing several kilograms. Throughout the history of studying ballistic injuries much emphasis has been placed upon velocity. In fact, while velocity is extremely important in laboratory settings, its significance to the study of human wounding patterns is much more ambiguous. In real life, velocity at the time of impact, is difficult to assess and depends upon the shape and composition of the projectile, the distance it has travelled as well as friction or drag from the surrounding air or material traversed. While arbitrarily defined, the most universally agreed upon terms for this subject define high muzzle velocity to be greater than 609.6 m/s (ie, 2000 ft/s). This velocity has previously been accepted as the point at which cavitation occurs within soft tissue. These factors are important in order to understand the behavior of a projectile immediately prior to impact. The most important consideration with respect to the damage caused by a projectile is the amount of kinetic energy imparted to the tissue rather than the velocity of the missile alone. This kinetic energy may not always be completely expended within the target. When a projectile has completely passed through a body, resulting in a perforated wound, it still retains part of its kinetic energy.

Upon impact with a human target, a projectile, whether it is a high-velocity bullet, a low-velocity shotgun pellet, arrow, or even a knife blade, will begin to transfer motion or kinetic energy to the target. The degree of damage is ultimately proportional to this transfer of energy, but is very much affected by additional forces acting upon the projectile. It becomes important to understand the behavior of the projectile within the tissue in order to understand the factors determining energy transfer. A nonspherical projectile with forward momentum meets a countering force acting to decelerate it—this is called friction or drag—which acts upon the leading surface. If the long axis of a nonspherical projectile is aligned with the direction of flight, this simply slows the projectile. However, if the bullet deviates from its track, the deceleration force turns into momentum and begins to tilt it out of the original direction of flight. This is defined as yaw. As yaw increases, the surface of the projectile imparting energy to the target is larger. This is known as the base-immersion phenomenon ( Fig 3.2-1 ). A common misconception is that yaw plays a significant role during flight prior to impact. If a projectile is spinning, such as occurs with the spiral grooves of a modern rifle, then yaw can be counteracted by gyroscopic forces that tend to minimize this deviation. For a variable distance after leaving the rifle tube, a bullet may have significant yaw, but this tends to decrease up to the time of impact. At impact, however, yaw can become more pronounced due to the marked difference in tissue density compared to air, and the bullet thus becomes unstable. In many situations the bullet completely rotates into a base-forward attitude within the second medium. Projectile studies in ballistic gelatin have demonstrated a consistent reversal at a penetration depth that is characteristic for each projectile [6]. The clinical significance of this effect lies in the explosive transfer of energy at the point when the bullet flips. This point can substantially be affected by previous impact with external objects—tree limbs, windows, clothing—or internally by contact with bone, fascial planes or tissues of different densities such as muscle and lung tissue. In such situations, the bullet may either impact with an enlarged surface and be deformed or else fragment into smaller missiles, each causing its own wound track. Occasionally, fragmentation of a primary projectile or impact with movable objects can propel multiple secondary projectiles. The path of destruction that the bullet leaves behind after it has passed is called the permanent cavity, and is divided into three zones ( Fig 3.2-2 ): the central zone of permanent cavity, the intermediate zone of extravasation, and the peripheral zone of concussion [7].

The concept of cavitation pertains to a stretching of the soft tissue as the projectile travels through it. While cavitation, or stretching of soft tissues, has been demonstrated at all velocities, the marked expansion of this cavity consistently develops at velocities of over 609.6 m/s (ie, 2000 ft/s). This effect does not create the irreversible destruction that is seen from direct trauma within the permanent cavity, but certain tissues such as brain, nerves, and bone are less tolerant than more elastic tissues such as lung and liver. The cavity is very transient, but does create a vacuum, and it is this vacuum that can impel foreign debris and contamination into the cavity. Ballistic gelatin is a homogeneous material and readily demonstrates the phenomenon of cavitation ( Fig 3.2-3 , 3.2-4 ). Cavitation is markedly reduced in living tissue due to the anisotropic properties of fascia and connective tissues. Therefore, cavitation does not have as profound an effect as previously theorized. It may still be implicated in the stretch injuries seen in nerve and vascular tissues in close proximity to the permanent cavity.

The notion that a projectile is sterile and wound contamination will not occur has been disproven [8]. In fact, in cavitation situations, the vacuum associated with the temporary cavity has been demonstrated to draw external material and even bacteria into that cavity. Sometimes this vacuum effect is also referred to as blowback.