Biodynamics of Blast Injuries



Fig. 2.1
(a) Free-field wave—open-space wave. Classic Friedlander wave : An idealized blast overpressure waveform. (b) Simple free-field wave. A more realistic waveform. (c) Enclosed-space waveform . Blast overpressure is amplified, and positive pressure wave is prolonged



Many factors affect the likelihood and severity of blast injuries. One important factor is the medium in which the explosion takes place. For example, water molecules do not get as compressed by the blast wave as the air molecules do. Therefore, the blast wave propagates more rapidly and dissipates more slowly in a water medium causing more injury than an explosion does in an air medium [8]. Another important factor to consider is the distance at which a person or an object is from the detonation epicenter. This distance determines how exposed the victim is to the blast overpressure [9]. The blast energy dissipates and the pressure drops inversely proportional to the distance cubed. For example, if individual A is at a distance d from the detonation and individual B is at a distance 2d double that of A’s, then the BOP that individual B is exposed to is 1/8 that individual A is exposed to. A 1-kg explosive will generate blast overpressure of 500 Kpa at the site of detonation which is fatal and drops exponentially to 20 Kpa at 3 m from the center which causes minimal injury [4]. Another substantial factor that determines blast overpressure exposure is the surrounding solid surfaces. These surfaces reflect the pressure waves and amplify their forces, hence exposing people next to them to a higher blast overpressure compared to those away from them and at the same radius from the detonation center. It is the reason behind which closed-space explosions have the potential to cause more severe injuries and higher mortality that open-field explosion [10, 11].



Mechanisms of Blast Injuries


Traditionally, blast injuries have been classified into four categories according to the mechanism by which the blast wave causes these injuries. A fifth type of blast injuries has been recently suggested.

Primary blast injuries (PBI) are the direct effects of the interaction of different organs in the body with the pressure changes of the blast wave. These injuries are unique to higher order explosives which make most civilian physicians unfamiliar with them. The organ damage in PBI is produced by the interaction of the blast wave at the interface between tissues of different densities or the interface between tissues and trapped air. Consequently, gas-containing structures, like the lung, GI tract, and ear, are most commonly affected by PBI [12]. These types of injuries are the main focus of this chapter and are discussed in great details in the following section.

Secondary blast injuries occur when objects energized by the explosion strike an individual, causing either blunt or penetrating trauma (e.g., bomb fragments, shrapnel). Fragments displaced by the blast winds travel a much longer distance than that traveled by the blast overpressure. This is why secondary blast injuries can occur up to thousands of meters away from the explosion site while PBI occurs within tens of meters only [13]. Penetrating secondary blast injuries from fragmentation of the detonated weapon or the secondary fragments resulting from the explosion are a leading cause of morality in terrorist attacks not including building collapse [14].

Tertiary blast injuries occur when the victim’s body or body parts are displaced by the blast winds and then tumble impacting hard surfaces. They include injuries due to the structural collapse of buildings, crush injuries, traumatic amputations, closed head injuries, blunt abdominal trauma, tissue contusions, and fractures [15, 16].

Quaternary blast injuries involve the types of injuries that do not fit any of the three mechanisms above. They include flash burns including burns from hot gasses or fires, methemoglobinemia [17] due to inhalation of CO, inhalation of dust, smoke or cyanide, acute septicemic melioidosis [18], and psychological sequelae.

Quinary blast injuries : This recently suggested that classification is based on a case series, and it involves a “hyperinflammatory state” seen in patients postblast manifested clinically as hyperpyrexia, diaphoresis, low central venous pressure, and water retention [19].

The secondary, tertiary, and quaternary injuries are similar to injuries in civilian trauma and their management is no different than nonexplosive trauma treatment protocols whether penetrating or blunt.


Primary Blast Injuries (PBI)


As the blast overpressure reaches the individuals in proximity to the detonation epicenter, forces will be transmitted into the body causing organ damage. These forces exert their maximum concentrated effect at air-tissue interfaces. Three explosive forces that cause PBI were first described in 1950 [20]: spallation, implosion, and inertia. These forces are the components of the blast-body interaction that eventually causes tissue damage.

Spallation happens when the blast wave passes from a dense medium to a less dense medium causing the fragmentation of the dense medium into the less dense. For example, in an underwater explosion, the pressure wave passes from the water into the air causing fragmentation of the denser medium, in this case the water, into the less dense medium, in this case the air. This is manifested as an upward splash of water into the air [2, 20]. From a physiologic standpoint, a blast wave passing through the interfaces between air, alveolar tissue, and capillary wall will cause the alveolar wall to tear and the peri-alveolar capillary endothelium to be disrupted through spalling forces [21].

Implosion happens as a result of the air in air-containing organs getting compressed during the positive phase of a blast wave. Once the blast positive phase is over, the air will re-expand releasing large amounts of kinetic energy disrupting the structure containing it [22]. This is how a blast wave causes alveolar damage after air in alveoli gets compressed during the positive pressure phase and re-expands forcefully during the negative suction phase. Combined together, the spalling forces causing peri-alveolar capillary wall damage and the implosive forces causing re-expansion of air in the alveoli will force air emboli in the blood vessels leading to one of the most fatal primary blast feared complications, arterial air embolism [21]. Another example where implosive forces cause PBI is the implosion of compressed air in facial sinuses that leads to skeletal crush injuries of the naso-orbitoethmoid complex, maxillary sinuses, and nasal bones [23].

Inertial forces cause tissue damage based on the fact that different tissues of different densities will move at different speeds in response to blast overpressure . Similarly, different component structures of an organ of varying densities will move differently and get damaged by shear forces. The lighter structural components will move with higher acceleration than the heavier components causing major stress at the boundary [24].

It is imperative in the understanding of the blast front-body interaction to discuss the two types of waves that are generated by this interaction and that propagate through the body causing internal soft-tissue injuries: the stress waves and the shear waves.

Stress waves are longitudinal pressure waves (similar to acoustic waves) with high amplitude and velocity [25]. A shock wave can be considered a special form of stress wave that travels at supersonic speeds. These waves affect mostly organs with significant difference in the acoustic impedance of its structural components, thus affecting mainly gas-containing organs. When these stress waves reach an air-tissue interface, a component of the compressive stress wave is reflected back at the interface as a tension wave [7]. It is when these stress waves equal and exceed the tensile strength of the tissue interface that their work done on the organs becomes an irreversible work of damage [2]. A stress wave also compresses air in air-filled organs that re-expands forcefully causing damage to the walls through implosive forces. All this interprets how for example small bowel wall injury or alveolar septum injury happens in thoracic and abdominal wall PBI.

Shear waves are transverse waves with long duration and low velocity, traveling perpendicularly to the longitudinal stress waves and tangentially to body surfaces. They are generated from body wall displacement. Different solid organs with different densities move asynchronously with different inertias causing shearing of solid organs [25].


Biological Effects of Primary Blast Injuries


The true incidence of primary blast injuries is unknown despite the various reports of incidence published. This is because PBI tend to be commonly overlooked especially in situations of mass casualty where the health care teams are faced with amputations, crush injuries, burns, toxic inhalations, and penetrating trauma. Delay in the diagnosis of PBI can complicate patient care especially in patients with isolated PBI who do not manifest external body trauma [26].

Primary blast injuries involve mainly gas-containing structures, namely the pulmonary, gastrointestinal, and auditory systems. The ear is the most commonly affected organ because for primary blast injury of the ear to occur, the blast overpressure threshold required is lower than that required for lungs and the bowels to be injured [27]. However, blast injuries are not exclusive to gas-containing structures. Other systems are affected as well though less common: the heart, vascular system, eye and orbit, and central nervous system among others.

Other than specific organ injuries, PBI have a systemic effect , a global physiologic response in the form of a cardiogenic shock in the absence of hemorrhage uncompensated by vasoconstriction. It is mediated by pulmonary C-fiber receptors that are thought to initiate this vagal reflex. It usually occurs following thoracic PBI within seconds and lasts between minutes to hours but often resolves by 2 h. It is characterized by transient bradycardia, bradypnea, and hypotension [28, 29].


Pulmonary System


As with all primary blast injuries, the lungs are more likely to get injured after a blast whereby the blast overpressure is high and the positive blast phase is prolonged. Uncomplicated blast lung injury has a favorable prognosis at 1-year follow-up. Hirshberg et al. reported that people who are discharged after surviving a lung blast injury had no pulmonary complaints, normal pulmonary function tests, and resolution of the chest radiography findings at 1-year follow-up [30]. Pulmonary PBI is essentially manifested as pulmonary contusions [5]. The spallation and implosion of the stress wave at the different air-alveolar-capillary wall interfaces cause alveolar wall, capillary wall, and interalveolar space disruption [2, 22]. This causes the pooling of blood perivascularly and alveolar hemorrhage. It can range all the way from petechiae to confluent hemorrhage [31]. Also, the extravascular fluid is compressed and driven into the alveolar space which causes pulmonary edema manifested as bilateral pulmonary infiltrates on chest radiography [32]. Implosive forces can also drive air into the interstitial spaces causing interstitial emphysema [26]. Shearing forces can disrupt the bronchovascular tree and create bronchopulmonary fistulas. These tears in the air-tissue interface can lead to arterial air emboli (AAE) development either immediately after the blast causing rapid death or delayed with the initiation of positive pressure ventilation [33]. AAE when big enough can cause MI, stroke, spinal cord infarction, intestinal ischemia, and death [34]. Even when microscopic, AAE can still cause symptoms like confusion, mental status changes, vision disturbances, pain, and weakness. Clinical signs like air in the retinal arteries, tongue blanching, or livedo reticularis can be indicators of emboli [35]. Pleural tears and lacerations can also be caused by pulmonary barotrauma as a blast effect or due to positive pressure ventilation and can give rise to pneumothoraces, hemothoraces, or pneumomediastinum [7].

Pulmonary contusions are usually bilateral in closed-space explosions but tend to be worse on the side of the impact of the blast wave in open-field explosions [5]. The ribs protect the lung parenchyma from the full force of the blast overpressure. This results in stripes of hemorrhagic congestion corresponding to the intercostal spaces where there is no rib protection. These parallel bands of ecchymoses used to be called mistakenly “rib markings” as they were thought to be occurring under the ribs but were proven to occur along the intercostal spaces with the ribs providing protection to the underlying parenchyma. Perimediastinal lung parenchyma especially the azygos lobe and lung regions in the costophrenic angles are more severely involved by the blast injury. This unequal distribution is justified by the reflection and augmentation of the stress wave within the chest [7].

Specific ultrastructural manifestations have been reported in lung primary blast injury. On light microscopy, pulmonary capillaries are seen dilated [36]. On electron microscopy, increased pinocytosis, blebbing, and ballooning in pulmonary capillary endothelial and type I epithelial cells are seen in experiments done on rats exposed to a blast. Also, loss of structure or enlargement was noted in the lamellated bodies of type II epithelial cells [37]. These changes occurred not only in areas of the lung with apparent damage but also in apparently normal regions of lung parenchyma. So patients with no clinical or radiologic evidence of injury could still have sustained a lung blast.

At the macroscopic level, respiratory mucosa is very sensitive to blast effect. Damage occurs at overpressures below those that would cause parenchymal lung injury . Mucosal injury includes loss of cilia and flattening of epithelial cells. More severe injury can also occur with stripping of the mucosal epithelium off the basal lamina the so-called stripped epithelium lesion, with the resultant intraluminal hemorrhage. This stripping of the epithelium is postulated to be due to the spalling forces at the epithelial tissue-air surface. These injuries generally resolve spontaneously and should be sought while examining a patient subjected to a blast. Their presence is an indicator of possible primary parenchymal lung blast injury and other organ blast injuries [38].

Clinically, the triad of dyspnea, cough, and hypoxia is referred to as “blast lung syndrome ” and is due to ventilation mismatch, vascular shunting, and impaired gas exchange [39]. Focal pulmonary edema and hemorrhage in the alveoli cause ventilation perfusion mismatch with increased intrapulmonary shunt, hypoxia, reduced lung compliance, and increased work of breathing [40]. Clinical symptoms include dyspnea, cough, hemoptysis, chest pain, or discomfort. Clinical signs include tachypnea, cyanosis, reduced breath sounds and dullness to percussion, coarse crepitations, rhonchi, subcutaneous emphysema, features of hemopneumothorax or pneumothorax, retrosternal crunch, or retinal artery emboli.

Any blast-exposed patient is worth a chest radiograph. Bilateral pulmonary infiltrate is typically seen on chest radiography in primary blast injuries [32]. Usually, these infiltrates develop within few hours, become maximal at 24–48 h, and tend to resolve within a week. Infiltrates that continue to worsen beyond 48 h may be indicative of pneumonia or adult respiratory distress syndrome [7]. Pneumothorax, hemopneumothorax, interstitial emphysema, subcutaneous emphysema, pneumomediastinum, or pneumoperitoneum might be evident on chest radiography. Most blast injuries develop immediately, but sometimes, progressive vascular leak and inflammatory changes develop over 12–24 even up to 48 h contributing to delayed presentation [31]. Hence, patients with pulmonary symptoms and negative chest radiographs should be observed for 8 h before discharge [14]. However, the majority of patients with blast lung injury will manifest radiologic or clinical findings on admission [41]. If the symptoms are persistent or severe with a negative chest radiograph then a chest CT should be done [42]. A study showed that the ratio of PaO2 to FiO2, the presence or absence of chest radiograph infiltrates, and bronchopleural fistulas can help identify the severity of the lung injury in terms of mortality or progression to adult respiratory distress syndrome (ARDS) and help determine the respiratory management [43].

Management of primary blast injuries of the lung can be quiet challenging. On one side, these patients are most often hemodynamically unstable requiring volume resuscitation yet excessive fluid resuscitation can lead to or exacerbate pulmonary edema in patients suffering from contusions [32]. To optimize the patient’s respiratory status adequate pain management and noninvasive ventilation techniques are used. Avoiding positive pressure ventilation (PPV) as much as possible could not be emphasized enough. Positive pressure ventilation especially with high positive end-expiratory pressure (PEEP) is thought to increase the risk of pulmonary barotrauma, namely pneumothorax and arterial air emboli [9, 44]. Drainage of air, fluid, and blood through chest tube thoracostomy is very important in optimizing the pulmonary status of the patient and helps minimize the need for PPV. Prophylactic chest tube thoracostomy is recommended for patients who suffer from severe lung blast injury that will need positive pressure ventilation or need air transportation [45]. In blast lung injuries, lung compliance is poor and if positive pressure ventilation is to be needed then protective measures must be used like low PEEP, low O2 saturation, low tidal volumes, and permissive hypercapnia [43, 46]. Reversion to spontaneous breathing by intermittent mechanical ventilation and continuous positive airway pressure should be done as soon as the patient’s pulmonary status allows it.

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Nov 17, 2017 | Posted by in MUSCULOSKELETAL MEDICINE | Comments Off on Biodynamics of Blast Injuries
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