Primary blast injury

Primary blast injury

Primary blast injuries result from the overpressure and are, as such, unique to blast. The e ff ect of blast overpressure is most marked at the interface between air and tissue or liquid. Tympanic membrane (TM) rupture is the most common primary blast injury . Patients may be asymptomatic or have a degree of transient hearing loss and otorrhoea. Previously , the presence of TM rupture was used as a marker for other occult blast injuries. This has been challenged recently by findings that show TM injury is not ubiquitous in the presence of more severe primary blast injury . The blast environment and orien tation of the ear canal to the shockwave are likely to determine the chance of injury . researched blast phenomenon. The exact mechanism of blast lung remains contested but it depends on the propagation of energy from the shockwave into the lung tissue, where it causes disruption. Proposed mechanisms of injury include spalling (disruption of tissues at air–liquid interfaces), implosion (com - pression and re-expansion of air-filled structures) and rapid These acceleration of tissues of di ff erent densities. Large animal models have demonstrated that the level of injury is related to the rate of c hest wall displacement, rather than the maximal 23 - depth of deflection. The severity of injury is dependent on the strength of the blast, the range from detonation and the surrounding environment. - Those working closely with explosives may wear personal armour that assists in decoupling the e ff ect of the primary blast. Current examples of such armour tend to be cumber - some. More common varieties of torso body armour pr ovide protection against penetrating injury but probably do little to - mitigate the e ff ects of primary blast. The pathophysiolog y of blast lung includes both immedi - ate and delayed responses. There is an immediate bradycardia and apnoea of variable length, which is likely to be a vagally 24 mediated reflex. The lung injury itself is typified by alveo - lar capillary rupture with subsequent intrapulmonary bleed - ing and oedema. The extent of this injury is proportional to the blast exposure and may range from microscopic petechial injury to areas of frank haemor rhage. While rarely seen in isolation, primary blast may leave lit - ). tle external evidence of injury since the skin itself is rarely a ff ected. Clinical features of blast lung include progressive hypoxia, which may not be apparent at the time of injury and is rela ted to the inflammatory response to intrapulmonary hae - morrhage and worsening oedema. Other structural lung injuries are associated with primary blast, although the prediction of these injuries by blast conditions is not consistent and is likely to be complicated by tertiary impact. Pneumothoraces may occur as a result of pleural rupture in the absence of penetrating injury . Injury to the larger vessels ma y lead to haemothoraces and the formation of alveolar–venous or bronchovenous fistulae. Air embolism due to such fistulae may cause acute hypoxia with - cardiovascular collapse and is a leading cause of death in those who do not survive until treatment. The diagnosis of blast lung is clinical with findings of hypoxia following blast exposure. Typical ‘bat-wing’ pulmo - nary infiltra tes are seen on the chest radiograph and computed tomography may discriminate these injuries from the more peripheral contusions seen in blunt trauma. Imaging may be useful in detecting associated structural lung injuries. T reatment of blast lung is largely supportive. Mechani - cal ventilation may be required but consideration should be given to the possibility of air embolism and pneumothorax that may be exacerbated. Some centres advocate the use of prophylactic bilateral pleural decompression, although ther e is little evidence to suggest an e ff ect on outcomes. Patients with significant blast lung injury are highly likely to have sustained other blast-related injuries and any management plan should consider their overall condition.

TABLE 34.3 Classi /f_i cation of blast injuries. Classi /f_i cation Injury type Examples Primary blast Overpressure Tympanic membrane injury, blast lung, intestinal blast injury Secondary blast Penetrating/ All penetrating injuries fragmentation Tertiary blast Blunt Blunt and crush injuries, traumatic amputation Quaternary blast Miscellaneous Burns, inhalation injury Quinary blast Effect of device Radiation sickness, additions infection

incidence of abdominal injury due to air blast has not been extensively examined, although a recent review of multiple incidents, including a variety of blast conditions, showed that abdominal injury is not common – seen in around 3% of inci 25 dents. Damage is dependent on coupling of the blast overpressure and the shockwave to a stress wave that travels through the abdomen. The e ff ect of shockwave dispersal is most marked at tissue–air interfaces. As such, the hollow organs are those most commonly injured. The caecum is probably most sensi tive to intestinal blast injury . Conversely , the small bowel and its extensive mesentery may be more susceptible to large shear waves causing mesenteric tearing. The presentation of primary blast injury to the bow el may be delayed relative to the acute onset of blast lung. Abdomi nal symptoms may be absent initially with progression to pain and frank peritonitis, should perforation and contamination occur. Given the lack of external injury , indications for opera tive intervention are largely clinical, as with conventional blunt abdominal trauma. The patient should be assessed anaesthet ically with particular consideration to the e ff ect of anaesthesia and ventilation on any concomitant blast lung injury . The most common operative finding of intestinal blast 25 is subserosal haemorrhage. Tearing of the mucosal surface with bleeding into the lumen of the tract may occur following repeated exposure to relatively lower blast overpressures. As in blunt injury , there is a propensity for mural haematomas to progress to perforation as a result of tissue necrosis. Full- thickness injuries to the bowel with immediate perforation can occur with a greater exposure to blast overpressure. The surgical management of blast bowel injury is that of any penetrating and blunt trauma, with primary repair or resection as indicated. Surgical judgement is essential regarding the find ings of non-perforated but contused bowel. A damage control approach to such injuries may allow for repeat assessment later, but in a physiologically well patient, in whom a relook would not be justified, the surgeon must decide to resect a segment or risk future progression of these lesions to perforation. The solid organs are more resistant to primary blast. Paren chymal disruption due to the shockwave has been described at very high levels of overpressure, although the experimental data for these injuries are sparse. Injury , with subsequent bleed ing, may result from rapid distractions of organ attachments and mesenteries. These blast conditions are more likely to be encountered in enclosed conditions and di ff erentiation of pri mary from tertiary injuries is di ffi cult. Primary blast injury

Primary blast injuries result from the overpressure and are, as such, unique to blast. The e ff ect of blast overpressure is most marked at the interface between air and tissue or liquid. Tympanic membrane (TM) rupture is the most common primary blast injury . Patients may be asymptomatic or have a degree of transient hearing loss and otorrhoea. Previously , the presence of TM rupture was used as a marker for other occult blast injuries. This has been challenged recently by findings that show TM injury is not ubiquitous in the presence of more severe primary blast injury . The blast environment and orien tation of the ear canal to the shockwave are likely to determine the chance of injury . researched blast phenomenon. The exact mechanism of blast lung remains contested but it depends on the propagation of energy from the shockwave into the lung tissue, where it causes disruption. Proposed mechanisms of injury include spalling (disruption of tissues at air–liquid interfaces), implosion (com - pression and re-expansion of air-filled structures) and rapid These acceleration of tissues of di ff erent densities. Large animal models have demonstrated that the level of injury is related to the rate of c hest wall displacement, rather than the maximal 23 - depth of deflection. The severity of injury is dependent on the strength of the blast, the range from detonation and the surrounding environment. - Those working closely with explosives may wear personal armour that assists in decoupling the e ff ect of the primary blast. Current examples of such armour tend to be cumber - some. More common varieties of torso body armour pr ovide protection against penetrating injury but probably do little to - mitigate the e ff ects of primary blast. The pathophysiolog y of blast lung includes both immedi - ate and delayed responses. There is an immediate bradycardia and apnoea of variable length, which is likely to be a vagally 24 mediated reflex. The lung injury itself is typified by alveo - lar capillary rupture with subsequent intrapulmonary bleed - ing and oedema. The extent of this injury is proportional to the blast exposure and may range from microscopic petechial injury to areas of frank haemor rhage. While rarely seen in isolation, primary blast may leave lit - ). tle external evidence of injury since the skin itself is rarely a ff ected. Clinical features of blast lung include progressive hypoxia, which may not be apparent at the time of injury and is rela ted to the inflammatory response to intrapulmonary hae - morrhage and worsening oedema. Other structural lung injuries are associated with primary blast, although the prediction of these injuries by blast conditions is not consistent and is likely to be complicated by tertiary impact. Pneumothoraces may occur as a result of pleural rupture in the absence of penetrating injury . Injury to the larger vessels ma y lead to haemothoraces and the formation of alveolar–venous or bronchovenous fistulae. Air embolism due to such fistulae may cause acute hypoxia with - cardiovascular collapse and is a leading cause of death in those who do not survive until treatment. The diagnosis of blast lung is clinical with findings of hypoxia following blast exposure. Typical ‘bat-wing’ pulmo - nary infiltra tes are seen on the chest radiograph and computed tomography may discriminate these injuries from the more peripheral contusions seen in blunt trauma. Imaging may be useful in detecting associated structural lung injuries. T reatment of blast lung is largely supportive. Mechani - cal ventilation may be required but consideration should be given to the possibility of air embolism and pneumothorax that may be exacerbated. Some centres advocate the use of prophylactic bilateral pleural decompression, although ther e is little evidence to suggest an e ff ect on outcomes. Patients with significant blast lung injury are highly likely to have sustained other blast-related injuries and any management plan should consider their overall condition.

TABLE 34.3 Classi /f_i cation of blast injuries. Classi /f_i cation Injury type Examples Primary blast Overpressure Tympanic membrane injury, blast lung, intestinal blast injury Secondary blast Penetrating/ All penetrating injuries fragmentation Tertiary blast Blunt Blunt and crush injuries, traumatic amputation Quaternary blast Miscellaneous Burns, inhalation injury Quinary blast Effect of device Radiation sickness, additions infection

incidence of abdominal injury due to air blast has not been extensively examined, although a recent review of multiple incidents, including a variety of blast conditions, showed that abdominal injury is not common – seen in around 3% of inci 25 dents. Damage is dependent on coupling of the blast overpressure and the shockwave to a stress wave that travels through the abdomen. The e ff ect of shockwave dispersal is most marked at tissue–air interfaces. As such, the hollow organs are those most commonly injured. The caecum is probably most sensi tive to intestinal blast injury . Conversely , the small bowel and its extensive mesentery may be more susceptible to large shear waves causing mesenteric tearing. The presentation of primary blast injury to the bow el may be delayed relative to the acute onset of blast lung. Abdomi nal symptoms may be absent initially with progression to pain and frank peritonitis, should perforation and contamination occur. Given the lack of external injury , indications for opera tive intervention are largely clinical, as with conventional blunt abdominal trauma. The patient should be assessed anaesthet ically with particular consideration to the e ff ect of anaesthesia and ventilation on any concomitant blast lung injury . The most common operative finding of intestinal blast 25 is subserosal haemorrhage. Tearing of the mucosal surface with bleeding into the lumen of the tract may occur following repeated exposure to relatively lower blast overpressures. As in blunt injury , there is a propensity for mural haematomas to progress to perforation as a result of tissue necrosis. Full- thickness injuries to the bowel with immediate perforation can occur with a greater exposure to blast overpressure. The surgical management of blast bowel injury is that of any penetrating and blunt trauma, with primary repair or resection as indicated. Surgical judgement is essential regarding the find ings of non-perforated but contused bowel. A damage control approach to such injuries may allow for repeat assessment later, but in a physiologically well patient, in whom a relook would not be justified, the surgeon must decide to resect a segment or risk future progression of these lesions to perforation. The solid organs are more resistant to primary blast. Paren chymal disruption due to the shockwave has been described at very high levels of overpressure, although the experimental data for these injuries are sparse. Injury , with subsequent bleed ing, may result from rapid distractions of organ attachments and mesenteries. These blast conditions are more likely to be encountered in enclosed conditions and di ff erentiation of pri mary from tertiary injuries is di ffi cult. Primary blast injury

Primary blast injuries result from the overpressure and are, as such, unique to blast. The e ff ect of blast overpressure is most marked at the interface between air and tissue or liquid. Tympanic membrane (TM) rupture is the most common primary blast injury . Patients may be asymptomatic or have a degree of transient hearing loss and otorrhoea. Previously , the presence of TM rupture was used as a marker for other occult blast injuries. This has been challenged recently by findings that show TM injury is not ubiquitous in the presence of more severe primary blast injury . The blast environment and orien tation of the ear canal to the shockwave are likely to determine the chance of injury . researched blast phenomenon. The exact mechanism of blast lung remains contested but it depends on the propagation of energy from the shockwave into the lung tissue, where it causes disruption. Proposed mechanisms of injury include spalling (disruption of tissues at air–liquid interfaces), implosion (com - pression and re-expansion of air-filled structures) and rapid These acceleration of tissues of di ff erent densities. Large animal models have demonstrated that the level of injury is related to the rate of c hest wall displacement, rather than the maximal 23 - depth of deflection. The severity of injury is dependent on the strength of the blast, the range from detonation and the surrounding environment. - Those working closely with explosives may wear personal armour that assists in decoupling the e ff ect of the primary blast. Current examples of such armour tend to be cumber - some. More common varieties of torso body armour pr ovide protection against penetrating injury but probably do little to - mitigate the e ff ects of primary blast. The pathophysiolog y of blast lung includes both immedi - ate and delayed responses. There is an immediate bradycardia and apnoea of variable length, which is likely to be a vagally 24 mediated reflex. The lung injury itself is typified by alveo - lar capillary rupture with subsequent intrapulmonary bleed - ing and oedema. The extent of this injury is proportional to the blast exposure and may range from microscopic petechial injury to areas of frank haemor rhage. While rarely seen in isolation, primary blast may leave lit - ). tle external evidence of injury since the skin itself is rarely a ff ected. Clinical features of blast lung include progressive hypoxia, which may not be apparent at the time of injury and is rela ted to the inflammatory response to intrapulmonary hae - morrhage and worsening oedema. Other structural lung injuries are associated with primary blast, although the prediction of these injuries by blast conditions is not consistent and is likely to be complicated by tertiary impact. Pneumothoraces may occur as a result of pleural rupture in the absence of penetrating injury . Injury to the larger vessels ma y lead to haemothoraces and the formation of alveolar–venous or bronchovenous fistulae. Air embolism due to such fistulae may cause acute hypoxia with - cardiovascular collapse and is a leading cause of death in those who do not survive until treatment. The diagnosis of blast lung is clinical with findings of hypoxia following blast exposure. Typical ‘bat-wing’ pulmo - nary infiltra tes are seen on the chest radiograph and computed tomography may discriminate these injuries from the more peripheral contusions seen in blunt trauma. Imaging may be useful in detecting associated structural lung injuries. T reatment of blast lung is largely supportive. Mechani - cal ventilation may be required but consideration should be given to the possibility of air embolism and pneumothorax that may be exacerbated. Some centres advocate the use of prophylactic bilateral pleural decompression, although ther e is little evidence to suggest an e ff ect on outcomes. Patients with significant blast lung injury are highly likely to have sustained other blast-related injuries and any management plan should consider their overall condition.

TABLE 34.3 Classi /f_i cation of blast injuries. Classi /f_i cation Injury type Examples Primary blast Overpressure Tympanic membrane injury, blast lung, intestinal blast injury Secondary blast Penetrating/ All penetrating injuries fragmentation Tertiary blast Blunt Blunt and crush injuries, traumatic amputation Quaternary blast Miscellaneous Burns, inhalation injury Quinary blast Effect of device Radiation sickness, additions infection

incidence of abdominal injury due to air blast has not been extensively examined, although a recent review of multiple incidents, including a variety of blast conditions, showed that abdominal injury is not common – seen in around 3% of inci 25 dents. Damage is dependent on coupling of the blast overpressure and the shockwave to a stress wave that travels through the abdomen. The e ff ect of shockwave dispersal is most marked at tissue–air interfaces. As such, the hollow organs are those most commonly injured. The caecum is probably most sensi tive to intestinal blast injury . Conversely , the small bowel and its extensive mesentery may be more susceptible to large shear waves causing mesenteric tearing. The presentation of primary blast injury to the bow el may be delayed relative to the acute onset of blast lung. Abdomi nal symptoms may be absent initially with progression to pain and frank peritonitis, should perforation and contamination occur. Given the lack of external injury , indications for opera tive intervention are largely clinical, as with conventional blunt abdominal trauma. The patient should be assessed anaesthet ically with particular consideration to the e ff ect of anaesthesia and ventilation on any concomitant blast lung injury . The most common operative finding of intestinal blast 25 is subserosal haemorrhage. Tearing of the mucosal surface with bleeding into the lumen of the tract may occur following repeated exposure to relatively lower blast overpressures. As in blunt injury , there is a propensity for mural haematomas to progress to perforation as a result of tissue necrosis. Full- thickness injuries to the bowel with immediate perforation can occur with a greater exposure to blast overpressure. The surgical management of blast bowel injury is that of any penetrating and blunt trauma, with primary repair or resection as indicated. Surgical judgement is essential regarding the find ings of non-perforated but contused bowel. A damage control approach to such injuries may allow for repeat assessment later, but in a physiologically well patient, in whom a relook would not be justified, the surgeon must decide to resect a segment or risk future progression of these lesions to perforation. The solid organs are more resistant to primary blast. Paren chymal disruption due to the shockwave has been described at very high levels of overpressure, although the experimental data for these injuries are sparse. Injury , with subsequent bleed ing, may result from rapid distractions of organ attachments and mesenteries. These blast conditions are more likely to be encountered in enclosed conditions and di ff erentiation of pri mary from tertiary injuries is di ffi cult.