Blast injuries and Brain Trauma: An Overview

Bomb explosions are most common in warzones but are also frequently encountered in countries riven with sectarian violence such as Iraq and Syria.  Bomb blast injuries are also seen in isolated terrorist attacks such as those that have recently affected Pakistan. Medical students in Pakistan should be familiar with the topic of bomb blast injury and its effects on humans. Bomb blast trauma ranges from mild to extremely severe depending on the energy dissipated by the explosion, the distance of the victim from the epicenter of the blast, the orientation of the victim and the environment in which the blast occurs.  Enclosed spaces such as a bus or a subway train create more severe trauma than open space [1]. There has been a ten-fold rise in terrorist attacks over recent decades [2]. The incidence of blast-induced TBI is therefore increasing in civilian populations. These events pose unique challenges for civilian medical services. Hospitals face resource constraints and triage dilemmas in mass causality situations, and practitioners must contend with the unique surgical challenges blast injuries pose, including extensive tissue devitalization, burns and polytrauma.  There are four mechanisms of blast-induced injury. Primary blast injury results from the pressure wave passing through the body causing injury to the internal organs.  Secondary blast injury results from fragments of the bomb penetrating the body. Tertiary blast injury is caused by the energy of the blast, which may physically throw the human body against walls or other fixed structures. Quaternary blast injury represents thermal, chemical or other miscellaneous injuries sustained during the blast [3-5].

Explosions cause an initial high pressure shock wave as the blast radiates outward, followed by a “blast wind” as air is drawn to the original detonation point (Figure 1) [5,6]. This shockwave causes primary blast injury via barotrauma: that is, damage caused by the effects of pressure changes too drastic for the body to accommodate [6]. When a blast wave passes through the human body it causes tissues to oscillate. The degree of pressure that results from the vibrating tissues is determined by an inherent property of the tissue called its acoustic impedance. Damage from the shockwave typically occurs at air-fluid interfaces or in gas filled organs because these have large acoustic impedance mismatches, subjecting these areas to dynamic pressure changes [7]. Medical personnel should be cognisant of this mechanism, as it explains why the lungs, bowel, and tympanic membranes are very susceptible to primary blast injury [8]. Tympanic membrane rupture is the most common primary blast injury [8]. It occurs at a blast pressure of just 5 pounds per square inch above atmospheric pressure [9]. Tympanic membrane integrity is sensitive to the point of being a screening tool for blast injury [6] and predictor of prognosis. Rupture of the eardrum results in temporary deafness, as opposed to dislocation of the ossicles or injury to the cochlea; two associated but more severe injuries that result in permanent hearing loss. Blast Lung Injury (BLI) is the single most important prognostic variable in immediate survival [10]. Blast Lung injury may manifest as pulmonary contusions, pulmonary hemorrhage, pneumothorax, alveolar-venous fistulae and air embolism. The first sign is often oxygen desaturation, sometimes in the absence of other signs [6]. Blast injuries to the abdomen present on a spectrum from minor submucosal bleeding to full thickness disruption and perforation. The characteristic lesion is a mural hematoma [11-13]. Delayed perforation may occur up to 14 days after the explosion and is probably ischemia related [12-14]. Rupture of solid abdominal viscera may occur. Traumatic limb amputations and multiple soft tissue wounds and fractures are also common. The classic appearance of fragment injuries is a small entry wound with severe internal damage from cavitation effect, associated with devitalized tissue and gross contamination [1].

Explosions cause an initial high pressure shock wave as the blast radiates outward, followed by a “blast wind” as air is drawn to the original detonation point (Figure 1) [5,6]. This shockwave causes primary blast injury via barotrauma: that is, damage caused by the effects of pressure changes too drastic for the body to accommodate [6]. When a blast wave passes through the human body it causes tissues to oscillate. The degree of pressure that results from the vibrating tissues is determined by an inherent property of the tissue called its acoustic impedance. Damage from the shockwave typically occurs at air-fluid interfaces or in gas filled organs because these have large acoustic impedance mismatches, subjecting these areas to dynamic pressure changes [7]. Medical personnel should be cognisant of this mechanism, as it explains why the lungs, bowel, and tympanic membranes are very susceptible to primary blast injury [8]. Tympanic membrane rupture is the most common primary blast injury [8]. It occurs at a blast pressure of just 5 pounds per square inch above atmospheric pressure [9]. Tympanic membrane integrity is sensitive to the point of being a screening tool for blast injury [6] and predictor of prognosis. Rupture of the eardrum results in temporary deafness, as opposed to dislocation of the ossicles or injury to the cochlea; two associated but more severe injuries that result in permanent hearing loss. Blast Lung Injury (BLI) is the single most important prognostic variable in immediate survival [10]. Blast Lung injury may manifest as pulmonary contusions, pulmonary hemorrhage, pneumothorax, alveolar-venous fistulae and air embolism. The first sign is often oxygen desaturation, sometimes in the absence of other signs [6]. Blast injuries to the abdomen present on a spectrum from minor submucosal bleeding to full thickness disruption and perforation. The characteristic lesion is a mural hematoma [11-13]. Delayed perforation may occur up to 14 days after the explosion and is probably ischemia related [12-14]. Rupture of solid abdominal viscera may occur. Traumatic limb amputations and multiple soft tissue wounds and fractures are also common. The classic appearance of fragment injuries is a small entry wound with severe internal damage from cavitation effect, associated with devitalized tissue and gross contamination [1].

The wide range of pathology seen in blast-induced TBI includes concussion, brain contusion, petechial hemorrhage, subdural hematoma, intracerebral hematoma, intraventricular hemorrhage, subarachnoid hemorrhage, brain swelling, raised intracranial pressure and penetration of metal and bone fragments into the brain and breaches of the skull resulting in cerebrospinal fluid (CSF) leak [1, 15] The brain is particularly prone to direct damage from the primary blast injury at CSF-brain interfaces, resulting in bubble formation, cavitation of brain tissues, capillary damage and axonal pathway disruption [15, 19, 20]. The blast wave can also indirectly affect the brain. It causes a rush of blood from the trunk to the brain vasculature, causing high cerebral blood pressure to disrupt the microcirculation and blood brain barrier [21]. Two studies suggest that wearing torso body armor may actually lessen blast-induced brain trauma [22, 23]. The orbits and nasal sinuses may act as an anatomical funnel for the primary blast wave, focusing injury on the orbito-frontal cortex [24]. At a cellular level, blasts cause free-radical mediated oxidative stress, contributing to the injury [25]. Extra cranial and intracranial vascular injury may also occur, including carotid and vertebral artery dissection, rupture and thrombosis or late pseudo aneurysm formation. Temporally, explosions may immediately cause a short period of apnea accompanied by bradycardia and hypotension, which is believed to reflect the blast waves effect on the brain stem or a vago-sympathetic reflex activated from the chest [9,26,27]. In the first few hours after the blast, brain swelling typically occurs – a combination of cerebral edema and vascular engorgement – but may occur several days after the injury. At 24-48 hours post injury, Armonda and colleagues found 47.4% of 57 patients with TBI’s, mostly from bomb blasts, had traumatic vasospasm which on average lasted two weeks [28].

Mild TBI patients typically have a GCS of 13-15, although GCS is a relatively unreliable indicator as many will have a GCS of 15. Both blast and non-blast mild traumatic brain injury can be followed by headaches, cognitive dysfunction, attention difficulties, and impaired balance.  The Military Acute Concussion Evaluation (MACE) is a clinical tool for mild traumatic brain injury screening [30]. It is composed of two sections; the patient’s history and the Standardized Assessment of Concussion, which is also validated for sports injuries [31]. Eye tracking and balance testing may be useful clinical adjuncts, as balance disturbance results from vestibular and otolith dysfunction [32, 33] In comparison, moderate or severe TBI typically present with a corresponding GCS of 9-12 and 3-8 respectively. These patients require CT neuroimaging (Figure 2) for investigating the extent of damage and planning surgery, and many require angiography to check for concomitant extra cranial and intracranial vascular injury. Blast-induced mild TBI often results in normal brain CT’s and MRI’s. Diffusion tensor imaging which is sensitive for white matter fibre tracking has thus far proven inconsistent as an investigational tool for mild TBI’s [34]. PET, functional MRI, serum biomarkers and blast dosimeters placed on combat helmets are current areas of research [35-37].

The ‘ABC’ principles of Advanced Trauma Life Support (ATLS) apply directly to the early resuscitation of the bomb blast victim. Hemorrhage control is required to prevent exsanguination and fractures must be stabilized, as must the cervical spine in suspected neck injury [1]. The patient should be intubated if the GCS is < 9. ‘Damage control resuscitation’ is practiced to rapidly correct physiologic derangements such as hypotension, hypothermia and acidosis, the “lethal triad”. Untreated, these may increase mortality through coagulopathy.

‘Damage Control surgery’ is a priority during initial neurosurgical intervention and is applicable to moderate or severe injuries [1]. Decompressive craniectomies are a pillar of neurosurgical management, and are indicated in patients with a GCS<9, CT evidence of brain swelling, penetrating brain fragments or intracranial hematomas [1,15]. In the case of bilateral hematomas a bilateral craniectomy is required.  The craniotomy is normally a large fronto-temporo-parietal flap. After opening the dura, subdural hematomas are removed, and hemostatic control gained from coagulation and tamponade of bleeding vessels. Any superficial penetrating fragments are removed. Lobectomy is considered if there is extensive devitalization of cerebral tissue, and temporal lobectomy may be indicated if there is evidence of upper brain stem compression with a dilated pupil [1]. For patients with a GCS<9 a ventriculostomy (external ventricular drain) with CSF venting will help control the ICP, and if available, an intraparenchymal ICP monitor may also be placed to continuously measure the ICP. The dura must be closed watertight, to avoid CSF leak and secondary infection. The dura over the skull base is particularly prone to breach by penetrating fragments [1]. Scalp closure over the injured area is the goal, as dura and bone should not remain exposed. Secondary operations or complex cranio-facial reconstructions are performed at a later date as, having stabilized the patient, mass casualty situations frequently mean surgeons must then prioritize other emergency cases. Neurosurgeons, maxillofacial, ear, nose and throat (ENT) and ophthalmological surgeons may all be involved in the repair and reconstruction of complex craniofacial injuries following bomb blast.

The management of mild presentations focuses on observation, additional blast exposure prevention, and psychological care. American military guidelines state that personnel with mild TBI should not return to the battlefield until there is resolution of concussion, as literature shows that additional brain trauma during this time might result in prolonged recovery or permanent disability [38]. Some soldiers will display symptoms of post-concussive syndrome – headache, fatigue, sensitivity to external stimuli, sleep disturbance and concentration difficulties [39] – for which a double-blinded, placebo controlled study has found acetylcysteine effective [40].  The same principles of management can be applied in the civilian situation.

Patients with mild TBI have an increased risk of post-traumatic stress disorder (PTSD) [41-43]. During studies of US Army Special Operations, Kontos and colleagues noted that PTSD symptoms occurred in 14.6% of participants with mild TBI, and they concluded that PTSD symptoms were more prevalent in patients whose mild TBI was blast related. The researchers also observed a dose-response gradient between number of bomb blasts and mild TBI and PTSD, suggesting that repeated exposures may result in permanent disability [18]. It is not known whether civilian victims of a bomb blast injury show similar rates of PTSD and other mental health issues following bomb blast injury. PTSD has been shown to occur even with amnesia of the original blast incident [41,43]. One possible explanation is that the parts of the brain implicated in PTSD (basal frontal, anterior, and mesial temporal lobes) are vulnerable in bomb blasts [43,44]. In addition, many of the features of PTSD overlap with post-concussive syndrome, making the distinction between the two difficult at times [41]. Chronic pain in blast-induced TBI patients is also common, and one study of 340 patients found that 42% of blast trauma victims exhibited the triad of chronic pain, PTSD and post-concussive syndrome [45,46].

The prognosis for blast-induced TBI correlates with Glasgow Coma Scale scores on admission [47, 48]. 64% of patients presenting with a GCS between 6 and 8 had attained functional independence at 2 years, double the percentage of patients presenting with a GCS of 3-5 in one study [47].  The mortality for blast-induced TBI is heavily dependent on whether the injury occurs in a military or civilian setting. In a retrospective study [49] of 604 patients, military patients with either an isolated blast-induced TBI or penetrating severe TBI had mortality rates of 7.7% and 5.6% respectively, lower than in patients who sustained similar injuries in a civilian setting (21% and 47.0%).  Although this discrepancy is in part because of lower neurosurgical intervention rates in civilian settings, it may also result from the higher rate of gunshot wounds in a civilian setting.  Blast-induced TBI patients may show improvements over a 1-2 year period [47, 48]

Blast-induced TBI is becoming more common in a civilian setting. Patient presentation varies, dependent on the exact mechanism of injury; primary (barotrauma), secondary (penetration), tertiary (acceleration affects) or quaternary (burns and miscellaneous).  The Primary blast wave causes damage to the tympanic membranes, lungs, bowel and in the brain. Blast-induced TBI’s are graded into mild, moderate and severe, which roughly correlate with GCS and have different clinical courses. Mild blast-induced TBI’s are acutely managed like mild non-blast TBI’s. Moderate and severe blast-induced TBI pose a tangible risk to life and are often complicated by poly trauma. In the acute setting decompressive craniotomies are common life-saving interventions, but many patients will require additional surgery once they have been acutely stabilized. Mild TBI has an excellent prognosis, though associated with psychological sequelae. The mortality in severe and moderate blast-induced TBI is influenced by whether the injury is sustained in a military or civilian setting.

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