traumatic
The pathophysiological device of neural damage related to traumatic brain injury TBI have traditionally been divided into primary ones that happen at the moment of impact and secondary ones that happen minutes to days following the trauma and are generally the result of the host response. Although these are similar in general in military and civilian TBI, the military setting includes two mechanical mechanisms of injury much more frequently penetrating ballistic injury and blast injury.
The reader is directed to recent reviews of the mechanical physics and biological effects of ballistic projectile injury. In penetrating brain injury, a foreign object penetrates the bony skull and traverses into and sometimes through the brain substance. This causes physical disruption of neurons, glial cells, and fiber tracts. Ischemia and hemorrhage may add to the damage. Penetrating ballistic injury e.g. rifle shot tends to produce high energy transfer to the tissues.
The severity of tissue damage is a function of the kinetic energy lost by the projectile within the body. This has become more prominent in recent conflicts, and is a distinct type of primary traumatic injury, with sufficiently distinct physical characteristics and potentially biological effects to be categorized separately. Briefly, the mechanical offend of blast injury is categorized as primary, secondary, tertiary, or quaternary.
PATHOPHYSIOLOGICAL DEVICE
The pathophysiological processes traumatic involved with military TBI are, in principle at least, very similar to those of civilian TBI, even for models of pure or largely blast TBI. It is still the norm to identify a separation of primary injury induced at the moment of the physical insult and secondary injury induced by host cellular responses including excitotoxicity, oxidant damage, and inflammation or by physiological insults like ischemia, hypoxemia, hypo- or hypercapnia, intracranial hypertension, and hypo- or hyperglycemia, Neuronal, axonal, glial damage, necrotic and apoptotic cell mechanisms have been suggested in neuronal damage.
Individual reports have inconsistently portrayed selective axonal or hippocampal vulnerability after blast injury. Two distinct features of blast injury have been noted, mostly in case series. The first is the formation of early and extreme edema, which is accompanied by severe disruption of the blood-brain barrier. This has, in some studies, been correlated with microglial activation and inducible nitric oxide synthase upregulation, followed by resulting oxidant and nitric oxide mediated microvascular damage. The second is a more significant part of severe vascular injury, with high vasospasm and delayed pseudoaneurysm. The pathophysiology for this is not well understood, but one has speculated that this could be due to the transmission of the blast wave down the vascular tree.
EPIDEMIOLOGY
Historically, in war-related injuries, 15–20% of the traumatic injuries are above the clavicles. The estimate in contemporary and current wars is comparable, and a substantial percentage of such injuries consist of TBI. TBI has been estimated to account for a 0.14 percent hospital admission rate among all deployed troops in US statistics. In whatever classification system is utilized, troops with TBI seem to constitute a higher percentage of US casualties in Iraq and Afghanistan than those in other recent wars. According to head, face, and neck injuries, at least 22 percent of injured soldiers sent home from these wars have latest traumatic brain injury.
According to one recent medical study using post-deployment screening instruments, 12 percent of soldiers coming back had incurred injuries with loss of consciousness. TBI is invariably a significant cause of death; 42 percent of British servicemen killed by enemy action in Afghanistan and Iraq during April 2006-March 2007 sustained a non-survivable head injury, whereas 43 percent of lethal penetrating injuries in Somalia were to the neck or head.
But the UK figures indicate that it was a less important cause of survivable injury in the first Gulf War, only one of 24 head injuries needed craniotomy, and although 17 percent of 224 Afghan cases included the head and neck, only two craniotomies and two neck explorations were needed. These findings indicate that, in UK experience, head injury is often the cause of death from military trauma, but in survivors, the incidence of major head injury necessitating brain injury surgical operation is very low.
IMAGING AND MOLECULAR BIOMARKERS
In the case of traumatic brain injury, most of the literature has centered on biomarkers in CSF or blood using conventional or novel methods. Two strategies have been pursued to identify biomarkers. The first involves the measurement of specific molecules that have been proposed by pathophysiological knowledge. For instance, calpain degradation is observed in necrotic cell death, whereas caspase activation is a characteristic of apoptotic cell death. Identification of calpain breakdown products or indicators of caspase activation have thus been employed as biomarkers of these two processes in tissue.
A second strategy is data-driven, including screening biological samples for differences between patients with traumatic injury and controls, TBI severities, TBI, apoptotic cell death, brain injury outcomes. Both strategies have promise but have not yet produced a clinically validated biomarker for any use. Biomarkers studied in TBI are enumerated, and readers who desire more information are referred to a series of outstanding recent review articles. This includes electronic cognitive test systems to detect concussion and mild TBI in soldiers following blast injury.
These remote assessments can include web-based programs, laptop computers, and/or hand-held data management systems. Early detection of mild TBI in this manner can allow safe and effective triage, and assist in evacuation or return to active duty decisions. Acute and subacute management of injured soldiers can be facilitated by video teleconferencing and electronic medical record sharing with TBI specialists occasionally during the performance of surgical procedures.
These interactions also help in continuity of care, by engaging clinical specialists at base hospitals involved in initial care, and thus completely familiar with the nuances of management in individual patients. Telemedicine is also applicable for rehabilitation, and for supporting home care, but this is beyond the scope of the present article. It is noteworthy that such methods can not only maximize care in individual patients but also facilitate staff training.
Conclusion
Post-traumatic epilepsy can be another significant late morbidity in this group. PTE typically occurs within five years of head traumatic brain injury, with an estimated risk of 53 percent risk in penetrating TBI, 10 to 25 percent in combat-related closed-head injury with abnormal brain imaging, and approximately 5 percent in moderately severe closed-head injury with normal CT imaging. The effect of mild TBI related to blast exposure on the development of late PTE is not well understood.
There is a rising prevalence of military traumatic brain injury and such injuries are observed in war-torn civilians or terrorist attacks. Blast-induced mild TBI has been described as the signature injury of the Iraq and Afghanistan wars. The assessment encompasses schemes that are usual in civilian practice but, in shared with civilian TBI, pays scant attention to the information provided by current imaging, especially diffusion tensor magnetic resonance imaging, and new biomarkers. The logistics of clinical care delivery in the field may have a part to play in maximizing outcomes.
Clinical management shares a great deal in common with civilian TBI but intracranial pressure monitoring is not consistently available, and protocols must be adapted to accommodate this. Further, severe initial edema has resulted in the expanding use of decompressive craniectomy, and blast TBI can be followed by an increased rate of vasospasm and pseudoaneurysm development. Visual and/or auditory impairments are frequent and there is a high risk of post-traumatic epilepsy. TBI is infrequently an isolated diagnosis in this context, and recurrent post-concussive symptoms are frequently accompanied by post-traumatic stress disorder and pain, a combination of findings that have been referred to as the polytrauma clinical triad.
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