Mechanism and Emergency Management of Blast Eye/Orbital Injuries

Sabri T Shuker


Expert Rev Ophthalmol. 2008;3(2):229-246. 

In This Article

Blast Biological Effects & Mechanism

An explosion of solid or liquid chemical materials rapidly releases energy and produces a large volume of gaseous product. Weapons depend on high- and low-explosive potentials, thermobaric ‘enhanced-blast explosives' and nuclear detonations, which all provide a change in potential energy to kinetic energy in a very short period of time, resulting in a blast wave. The spherical front of this blast wave exhibits a discontinuous increase in pressure, density and temperature, known as a shock front. A blast wave can inflict several types of bodily injuries through one or more of the following distinct mechanisms, each of which is responsible for a different type of blast injury. These mechanisms fall into five categories, which are as follows.

The leading edge of a blast wave, which consists of few millimeters of overpressurized air, is called the blast front and it moves rapidly in all directions from the epicenter of the explosion.[101]

In 2003, Thach reported that small changes in atmospheric pressure can lead to high-velocity winds.[1] For instance, a peak pressure of as little as 0.25 psi can generate wind speeds of up to 125 mph. Comparing these winds with the overpressurized blast wave that moves rapidly away from the center of detonation and which can be as high as 3.7–18.6 miles/s (6000– 30,000 m/s; or 13,421–67,108 mph), for high explosives and 900 ft/s (270 m/s) for low explosives, it is a blast wind (not blast wave). Stewart (2006), stated that when a high explosive detonates, it is converted almost instantaneously into a gas at very high pressure and temperature.[2] For example, the major ingredient in composition C-4 or cyclotrimethylene trinitramine (RDX) can generate an initial pressure of over 4 × 106 psi.[3] These high-pressure gases rapidly expand from the original volume and generate a marked pressure wave – the blast wave – that moves outward in all directions as a thin layer of compressed air. The displaced air then compresses and forms a vacuum returning to the point of detonation (negative wave).

Temperatures from the explosive gases can reach 3000°C in the center zone, especially in thermobaric explosion. Victims close to the detonation can sustain third-degree burns that can be fatal, and the temperature produced by thermobaric is greater than in high explosive.[102] For a single, sharp-rising blast wave caused by detonation of a high explosive, the damage to human structures is a function of the peak pressure and the duration of the initial positive phase. The greatest energy transfer occurs at points where tissue density changes.[4]

When a blast front reaches a victim in spherical shape, as in improvised explosive devices (IEDs), or in cone shape, as in some mine explosions, it causes an enormous, almost instantaneous rise in ambient pressure, filling the space with high-pressure gases in 0.001 s. Because explosive gases continue to expand from their point of origin, a longer negative underpressure (relative vacuum) follows the peak positive overpressure. Both the positive overpressure and the negative underpressure are capable of causing significant primary blast injury (Stewart [2006]) (Figure 1).[2]

Air blast shock wave (pressure/time).

The sudden pressure change caused by the blast wave can damage living tissue through four mechanisms: spalling, implosion, acceleration–deceleration and pressure differentials. Kluger (2003) stated that an overpressure of 1.8 psi generates glass shards capable of penetrating the abdominal wall and 3 psi overpressure can throw the human body, causing fatality 1% of the time.[5] Lung injury with 1% mortality is observed at 35 psi overpressure, but results in 99% fatality at 65 psi. A charge of 25 kg TNT will induce a 150 psi peak overpressure for 2 ms that travels at 3000–8000 m/s and more explosive will prolong the duration of the blast front, adding to the wounding potential. The blast wind movement induced by the explosion depends on the air density and the blast wind velocity: the higher the velocity the greater the generation of casualties. By single or multiple biophysics, effects of blast wave impact causes variable wound patterns and this demonstrates how a complex consequence of blast effect acts. A great deal remains to be discovered concerning how biological structures primarily respond to blasts, both in terms of responses of individual tissues and tissue microbiology to vibratory energy and why some anatomical tissues are more susceptible to primary blast than others.

The air-filled organs and air–fluid interfaces are the organs damaged by dynamic pressure changes at tissue density (i.e., air–fluid) borders due to the interaction of a high-frequency stress wave and a lower frequency shear wave. One or the other of these waves predominates, depending on the characteristics and location of the blast. Rupture of the tympanic membranes, pulmonary damage and air immobilization and rupture of hollow viscera are the most important primary forms of blast injury.[6–10] Ocular/orbital anatomical region containing liquid and other tissue media bounded by thin bone plate walls of air-containing sinuses are also vulnerable.

During a blast in the open, scaling is affected by factors such as topography and conditions of burst and energy transfer. These augment or attenuate the blast wave in an unpredictable manner. Scaling of blast intensity indoors, inside buildings or bus shelters are more lethal and have tissue destructive effects attributable to the uncertain – almost infinite – possibilities that are inherent in reflection from walls of varying geometry and structure. The same effects apply to the body tissue structure and its architecture.[4,11–15]

Blast injury has an overall lethality of approximately 7.8% in open air. This jumps to 49% when the blast occurs in confined spaces (Boffard and MacFarlane [1993][16]).

Secondary blast injury is much more common than primary blast injury. Indeed, secondary blast injury is the most common cause of death in blast victims. Up to 10% of blast survivors will have significant eye injuries.[17]

Penetrating fragments made of different kinds and shapes of objects ranging from conventional shell fragments to car fragments, ground particles, sand and pebbles or other components may cause devastating damage to the eye and body.

In conventional war, the most common weapons responsible for ocular injuries are shell fragments from rockets, grenades, mines and other nonmagnetic particles. Wong et al. (1997) declared that combat eye-penetrating foreign bodies are approximately 55% nonmagnetic, reflecting the nonferrous composition of mines and secondary missiles.[18]

In urban explosions, secondary blast causative factors are different inside populated cities. Glass fragments from windows are notorious for causing ocular injuries. They often do not kill, but can cause blindness and ruptured globes. At the speed that explosively propelled fragments of glass travel, there is no time for the blink reflex to operate.

Propelling of the body against walls or objects, or crush injuries and blunt trauma from building collapse resulting in crush injures to any part of the body including the eyes/orbital and facial bone trauma constitutes the tertiary blast effect.

Asphyxia through inhalation of fumes from toxic, burnt materials and burns by high thermal explosive effects on the cornea are the key factors in the quaternary blast effect.

The quinary blast effects includes the toxic substances that are absorbed through wounds or by inhalation (Kluger et al. [2006];[6] Wong et al. [1997][18]).


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