Mechanism of explosive blast injury
The explosive pressure that accompanies the bursting of bombs or shells ruptures their casing and imparts a high velocity to the resulting fragments. These fragments have the potential to cause even more devastating injury to the tissues than bullets. They are unstable in flight and may tear through tissue at high speed in a tumbling fashion. These statements are particularly true of old artillery shells and terrorist bombs where the casing fragments naturally into pieces of variable size. However, the trend in conventional war is towards carefully engineered weapons which carry preformed munitions, such as notched wire or ball bearings, or have their casing etched to allow predictable fragmentation patterns resulting in a multitude of small, relatively low-energy fragments. The aim is to incapacitate, not kill, by inflicting multiple low-energy transfer wounds to two or more body systems.
In addition, all explosives are accompanied by a complex blast wave. The two main components of this wave are a blast pressure wave (known as dynamic overpressure), with a positive and negative phase, and the mass movement of air (known as blast wind).
The positive pressure phase of the blast wave lasts for only a few milliseconds, but close to an explosion it may rise to over 7000 kN/m2. As the healthy tympanic membrane ruptures at about 150 kN/m2, it is evident that the effects on the human body of such an explosion can be devastating, especially in confined areas. Like sound waves, the blast pressure waves flow over and around an obstruction and affect anyone sheltering behind a wall or in a trench. The pressure affecting such a person is known as the incident pressure (defined as the pressure level at 900 to the direction of travel of the blast shock front). Also, any person standing in front of a wall or other vertical surface facing an explosion is subjected to the added effect of a reflected pressure.The negative effect of a pressure wave is of low amplitude, lasts longer than the positive wave and is of doubtful clinical significance.
A mass movement of air or dynamic pressure results from the rapidly expanding gases at the centre of the explosion which displaces air at supersonic (greater than the speed of sound in air) speed. This has been described by an eminent blast scientist as ‘fresh air moving very fast’. The mass movement of air results in what is colloquially known as blast wind and disrupts the environment, hurling debris and people. This phenomenon results in injury patterns ranging from traumatic amputation to total body disruption. The mass movement of air may disrupt buildings, causing entrapment and crush injuries.
Blast pressure waves travel at the speed of sound in the medium being traversed. In water, velocity and distance are greater and injuries tend to be more complex and severe. For example, blast pressure waves in air rarely affect the gastrointestinal tract to any clinically significant extent in survivors; however, in water, the blast wave exerts a ‘water hammer’ effect with significant rates of gastrointestinal perforation.
When the body is impacted by a blast pressure wave, it couples into the body and sets up a series of stress waves which are capable of injury, particularly at air—fluid interfaces. Thus, injury to the ear, lungs, heart and, to a lesser extent, the gastrointestinal tract (see above) is notable. The exact mechanisms of injury at each specific tissue are still the subject of controversy but need not unduly worry readers as this topic is debated well by Cripps and Guy in Trauma and by Ryan et al. in Ballistic Trauma, as listed in the ‘Further reading’ section of this chapter.
General management of blast injuries
The structures injured by the primary blast wave, in order of prevalence, are the middle ear, the lungs and the bowel. However, the most common urgent clinical problem in survivors is usually penetrating injury caused by blast-energised debris and fragments from the casing of the exploding device (see below). Many of those exposed will have blunt, blast and thermal injuries in addition to more obvious penetrating wounds (the clinical picture is usually referred to as combined injury). The deafness of the victims of blast, due to disruption of the tympanic membrane, makes communication with them difficult and may complicate early assessment and management. Here, the primary survey and resuscitation phases of a system such as ATLS are particularly apt. The management of penetrating wounds differs little from that of missile wounds referred to earlier. The soft-tissue wounds are usually heavily contaminated with dirt, clothing and secondary missiles such as wood, masonry and other materials from the environment. Such contaminants may be driven deeply into adjacent tissue planes opened up by the force of the explosion. The propensity for wound infection in these cases is considerable and is often underestimated. Some cases are associated with multiple wounds of varying severity affecting a limb.
It may not always be practical to explore every wound at first surgery. The larger and deeper wounds should have priority of management due to the more serious consequences of infection. In many blast injuries one cannot be sure of complete wound excision and, therefore, it is imperative that all blast wounds should be left open at the end of the initial operation and delayed primary closure performed 4—6 days later.
Regional management of blast injuries
Here one is particularly concerned with identifying specific injuries caused by the primary blast wave.
Blast damages the hearing in three ways. There may be rupture of the tympanic membrane, dislocation of the ossicles or widespread disruption of the inner ear. The latter is sometimes accompanied by permanent deafness. It should be remembered that the likelihood of ear damage depends on the angle between the incident blast wave and the external auditory meatus. Although deafness is a certain indicator of exposure to significant blast loading, its absence does not imply the absence of blast injury to other systems.
Injury to the lung parenchyma is complex and the exact mechanisms are still the subject of debate. Undoubtedly, the impacting primary blast wave may cause a rapid inward movement of the chest wall and result in underlying pulmonary contusion, but this is not the principal mechanism in the severe and progressive acute lung injury picture seen in small numbers of survivors. In these casualties it is probable that the initial blast wave couples into the chest resulting in stress waves which spread out, reflect and reinforce at tissue interfaces. At air—fluid interfaces they may result in considerable disruption. This is particularly notable at the alveolar—capillary membrane and leads to capillary leakage resulting in a spreading haemorrhagic alveolar contamination.
An inflammatory cascade now ensues resulting in a post-blast respiratory insufficiency (PBRI), which is virtually indistinguishable from adult respiratory distress syndrome (ARDS) following generalised sepsis or fat embolism syndrome (FES), and posing a difficult clinical problem in critical care units. PBRI varies from a mild and localised area of pulmonary contusion injury to a fulminating and rapidly fatal condition involving both lungs. This rapid and progressive condition is relatively rare, as casualties sufficiently close to suffer extreme blast loading to the chest wall are usually killed by multiple penetrating wounds or are dismembered by blast winds. In severe cases, respiratory insufficiency may be further precipitated by overtransfusion with electrolyte solutions. The clinical picture is typical — patients develop a cough with frothy blood-stained sputum, dyspnoea and a feeling of apprehension, bordering on a foreboding of impending doom — they are often right. A pulse oximeter will show a resistant low saturation, with values well below 90 per cent. Blood gas analysis confirms arterial hypoxia and a raised carbon dioxide partial pressure (PCO9.Chest radio-graphs in the initial stages may show localised contusion injury but, as the inflammatory cascade builds, radiographic evidence becomes generalised with bilateral fluffy infiltrates spreading out from the hilum of both lungs.
Specific clinical management of an established case remains controversial. There is still little hard evidence to guide clinicians. However, most agree with the guidelines listed in below
Postblast respiratory insufficiency (PBRI) — clinical guidelines
• Work within the ABCDE system of the ATLS system
• Avoid overhydration while maintaining vital organ perfusion
• Administer high-flow oxygen (12 litres/minute) with mask and rebreathing bag
• Carry out arterial blood analysis to assess need for further measures
• Resort to mechanical ventilation early to ensure adequate oxygenation
• Use positive end-expiratory pressure (PEEP) carefully while avoiding excessive peak and plateau pressures
- Corticosteroids should be avoided
Injury to gas-filled viscera is more common in underwater explosions than air blasts. Perforation of the stomach, small intestine and caecum is most common. The clinical presentation is one of increasing abdominal pain accompanied by signs of peritonism and often gas under the diaphragm. In the presence of clear physical signs urgent laparotomy is indicated. In cases where signs are few but the risks are high, ultrasonography, CT, diagnostic peritoneal lavage and laparoscopy should be considered. There is no single modality agreed by all. Serological assessment of gut-associated enzymes is still an experimental tool and no reliable serum marker of intestinal injury is available.
The eye should be examined in both the primary and secondary surveys, yet injury is easily missed. Conjunctival haemorrhage following blast exposure may herald a more serious underlying problem of penetration of the globe by blast-energised debris or fragments. The pupil must be carefully examined and any abnormality, distortion of the iris or the presence of a hyphema, for example, should be investigated by an ophthalmologist.
Factors that increase the morbidity and mortality following bomb blast injuries are associated chemical and thermal burns, and the inhalation of toxic gases and smoke.