Rocco Armonda

Explosive Blast Neurotrauma

Explosive blast traumatic brain injury (TBI) is one of the more serious wounds suffered by United States service members injured in the current conflicts in Iraq and Afghanistan. Some military medical treatments for blast TBI that have been introduced successfully in the war theater include decompressive craniectomy, cerebral angiography, transcranial Doppler, hypertonic resuscitation fluids, among others. Stateside neurosurgery, neuro-critical care, and rehabilitation for these patients have similarly progressed. With experience, military physicians have been able to clinically describe blast TBI across the entire severity spectrum. One important clinical finding is that a significant number of severe blast TBI victims develop pseudoaneurysms and vasospasm, which can lead to delayed decompensation. Another is that mild blast TBI shares clinical features with post-traumatic stress disorder (PTSD). Observations suggest that the mechanism by which explosive blast injures the central nervous system may be more complex than initially assumed. Rigorous study at the basic science and clinical levels, including detailed biomechanical analysis, is needed to improve understanding of this disease. A comprehensive epidemiological study is also warranted to determine the prevalence of this disease and the factors that contribute most to the risk of developing it. Sadly, this military-specific disease has significant potential to become a civilian one as well.

Mechanisms of Primary Blast-Induced Traumatic Brain Injury: Insights from Shock-Wave Research

Traumatic brain injury caused by explosive or blast events is traditionally divided into four phases: primary, secondary, tertiary, and quaternary blast injury. These phases of blast-induced traumatic brain injury (bTBI) are biomechanically distinct and can be modeled in both in vivo and in vitro systems. The primary bTBI injury phase represents the response of brain tissue to the initial blast wave. Among the four phases of bTBI, there is a remarkable paucity of information about the cause of primary bTBI. On the other hand, 30 years of research on the medical application of shockwaves (SW) has given us insight into the mechanisms of tissue and cellular damage in bTBI, including both air-mediated and underwater SW sources. From a basic physics perspective, the typical blast wave consists of a lead SW followed by supersonic flow. The resultant tissue injury includes several features observed in bTBI, such as hemorrhage, edema, pseudoaneurysm formation, vasoconstriction, and induction of apoptosis. These are well-described pathological findings within the SW literature. Acoustic impedance mismatch, penetration of tissue by shock/bubble interaction, geometry of the skull, shear stress, tensile stress, and subsequent cavitation formation, are all important factors in determining the extent of SW-induced tissue and cellular injury. Herein we describe the requirements for the adequate experimental set-up when investigating blast-induced tissue and cellular injury; review SW physics, research, and the importance of engineering validation (visualization/pressure measurement/numerical simulation); and, based upon our findings of SW-induced injury, discuss the potential underlying mechanisms of primary bTBI.

Blast-related traumatic brain injury

A bomb blast may cause the full severity range of traumatic brain injury (TBI), from mild concussion to severe, penetrating injury. The pathophysiology of blast-related TBI is distinctive, with injury magnitude dependent on several factors, including blast energy and distance from the blast epicentre. The prevalence of blast-related mild TBI in modern war zones has varied widely, but detection is optimised by battlefield assessment of concussion and follow-up screening of all personnel with potential concussive events. There is substantial overlap between post-concussive syndrome and post-traumatic stress disorder, and blast-related mild TBI seems to increase the risk of post-traumatic stress disorder. Post-concussive syndrome, post-traumatic stress disorder, and chronic pain are a clinical triad in this patient group. Persistent impairment after blast-related mild TBI might be largely attributable to psychological factors, although a causative link between repeated mild TBIs caused by blasts and chronic traumatic encephalopathy has not been established. The application of advanced neuroimaging and the identification of specific molecular biomarkers in serum for diagnosis and prognosis are rapidly advancing, and might help to further categorise these injuries.

Prevention of carotid angioplasty-induced bradycardia and hypotension with temporary venous pacemakers.

OBJECTIVECarotid angioplasty with stent placement is becoming an established treatment modality for patients with high-risk carotid stenosis. Unlike carotid endarterectomy, angioplasty causes direct mechanical dilation of the stenotic carotid artery and bulb. Stimulation of the sinus baroreceptors induces a reflexive response that consists of increased parasympathetic discharge and inhibition of sympathetic tone, which results in bradycardia and subsequent cardiogenic hypotension. METHODSAt a single institution, the experience with 43 patients treated from November 1994 to January 2000 with 47 angioplasty and stent procedures for occlusive carotid artery disease was retrospectively reviewed. Prophylactic temporary venous pacemakers were used to prevent hypotension from possible angioplasty-induced bradycardia. Pacemakers were set to capture a heart rate decrease below 60 beats per minute. Variables analyzed included demographics, etiology of disease, side of the lesion, the presence of symptoms, history of coronary artery disease, percent stenosis, type of stent used, number of dilations, pressure of dilation, and angioplasty balloon diameter. RESULTSTen patients were excluded because pacemakers were not used during their angioplasty procedures, and these included three emergencies and a lesion that was unrelated anatomically to the carotid sinus (petrous carotid). The remaining 37 procedures were performed in 33 patients with a mean age of 67 years, and consisted of 17 men, 16 women, 20 right and 17 left-sided lesions. The pacemakers maintained a cardiac rhythm in 23 (62%) of the 37 procedures and in no case did the pacemaker fail to respond when activated. Recurrent (56%; 10 of 18), radiation-induced (78%; 7 of 9), and medically refractory carotid stenosis (67%; 6 of 9) required intraprocedural pacing. Two patients with recurrent stenosis became hypotensive despite the aid of the pacing device but were not symptomatic. Seventy-nine percent (15 of 19) of symptomatic lesions and 57% (8 of 14) of nonsymptomatic lesions required pacing, which was statistically significant (P = 0.049). No patient experienced an operative morbidity or mortality as a consequence of the temporary pacing devices. CONCLUSIONAngioplasty-induced bradycardia is a common condition, and it is more prevalent in radiation-induced stenosis and with symptomatic lesions. Temporary venous demand pacing is a safe procedure and may prevent life-threatening, baroreceptor-induced hypotension.

Management of decompressive craniectomy defects: modern military treatment strategies.

BackgroundDecompressive craniectomy has become a critical and standard life-saving maneuver in the theater of war. The high number of patients returning with large cranial defects and complex craniofacial injuries often involving the upper orbits or associated with the sunken skin flaps are a reconstructive challenge. We present a review of our treatment protocol highlighting the evolution of decompressive craniectomy and the development of a modern cranial defect treatment algorithmic approach to reconstruct these difficult clinical cases. MethodsA review of previously published data and current data from our warfare treatment unit that reported the treatment of decompressive cranial defects from 2004 to 2011 was performed. Reported data included mechanism of injury, evacuation time, initial Glasgow Coma Scale (GCS), GCS on arrival to the continental United States, type of decompressive craniectomy, type of implants used for reconstruction, and complications such as implant infections, exposures, and removals. Secondary reconstruction techniques used to salvage failed cranioplasty cases with free tissue transfers and cranial bone or dermal fat grafts as indicated were also reviewed and outcomes were reported. ResultsFrom March 2003 to July 2011, more than 200 patients were identified who underwent cranioplasty after decompressive craniectomy. Patient average age was approximately 25 years (range, 18–53 y), and all patients were male. Average follow-up was 870 days (2.4 y). Average GCS at initial presentation was 7 and was 9 on arrival to the continental United States. Average time to evacuation to the continental United States was 6 days. Of all injuries, 46% were associated with an improvised explosive device blast. Of the patients, 90% underwent hemicraniectomies with the remaining 10% having received bifrontal craniectomies. Successful reconstruction and retention of the implant was present in 95% of the overall cohort. Contour abnormalities were the most common adverse outcome encountered (10% of patients after cranioplasty), whereas infections resulting in implant loss (5%) and seizures (<5%) were the most common complications that occurred after cranioplasty reconstruction. ConclusionsWarfare-related decompressive craniectomy defects can be safely reconstructed using custom alloplastic implants with low morbidity and mortality. Risk factors that increase the rate of infection and require implant removal included orbital extension of the craniectomy defect, proximity to facial sinuses, and large contour abnormalities with corresponding large dead spaces. Staging reconstruction of high-risk cranial defects followed by definitive cranial defect reconstruction improved the likelihood of implant retention and successful cranioplasty outcome.

Management to Optimal Parameters: Euboxia?

The critical care management of patients with traumatic brain injury (TBI) has undergone major advancements over the last several decades. Improved evidence-based research has allowed us a greater understanding of the pathophysiology and parameters that impact outcomes. Despite this, much uncertainty still remains, and further studies should be performed to identify ways to optimize parameters to achieve the best outcomes for TBI patients.

Management of Moderate and Severe TBI

The management of moderate and severe traumatic brain injury (TBI) is a complex and developing practice in the acute neurosciences. The management of such, from the field phase of illness to the tertiary definitive medical and surgical management of TBI, is discussed. Clinical syndromes and radiographic examples of brain injury are presented, along with a current review of the literature in the early critical care phase of moderate and severe brain injury management. We discuss an algorithm for managing the challenging patient, and discuss areas of needed future research.