Triage and Evaluation of Blast-Injured Patients in Wenling Liquefied Petroleum Gas Tanker Explosion.

On June 13, 2020, a liquefied petroleum gas tanker exploded in Wenling. Here, the authors describe the mass casualty emergency response to the explosion. The authors collected the medical records of 176 inpatients at 8 hospitals in Taizhou and Hangzhou. The 176 inpatients with blast injuries comprised 70 females and 106 males, with an average age of 45.48 ± 19.96 years, and more than half of the patients were farmers. They were transported to six hospitals distributed around the explosion site in Taizhou in the initial rescue period and were grouped according to their new injury severity score as having mild, moderate, severe, or extremely severe injuries. Most patients with severe and extremely severe injuries were admitted to a superior hospital for postsecondary triage. Forty-four patients experienced primary blast injuries, 137 experienced secondary blast injuries, 37 experienced tertiary blast injuries, and 40 patients experienced quaternary blast injuries. Multiple blast injuries were suffered by 62 patients. Most patients (95.45%) suffered external injuries, with the chest, extremities, and face as the main affected areas. Burns were diagnosed in 26 adults, of whom 15.38%, 19.23%, 7.70%, and 57.69% suffered mild, moderate, severe, and extremely severe cases. Sixteen burn patients suffered from burn-blast injuries. Upper limbs and the head/face/neck area, as exposed areas, were more likely to experience a burn injury. Inhalation was the main accompanying injury. Of the eight patients who died in the prehospital session, seven had burn injuries. This report on the accident and injury characteristics of an open-air LPG-related explosion will facilitate responses to subsequent catastrophes.

Relationship between clinician documented blast exposure and pulmonary function: a retrospective chart review from a national specialty clinic.

BACKGROUND: Service member exposure to explosive blast overpressure waves is common with considerable attention to traumatic brain injury (TBI) and neuropsychological sequalae. Less is known about the impacts on the respiratory system, particularly long-term effects, despite vulnerability to overpressure. Using a national registry, we previously observed an independent relationship between self-reported blast exposure and respiratory symptoms; however, the impact on objective measures of pulmonary function is poorly understood. METHODS: 307 Veterans referred to our national specialty center for post-deployment health concerns underwent a comprehensive multi-day evaluation that included complete pulmonary function testing (PFT), occupational and environmental medicine history, neuropsychological or psychological evaluation. We developed an a priori chart abstraction process and template to classify Veterans into blast exposure groups: (1) none, (2) single-mild, or (3) multiple-mild. This template focused primarily on clinician documented notes of blast related TBI that were used as proxy for blast overpressure injury to thorax. PFT variables characterizing flow (FEV1%; %∆FEV1), volume (TLC%), diffusion (DLCO%) and respiratory mechanics (forced oscillometry) were selected for analysis. RESULTS: Veterans (40.5 ± 9.7 years; 16.3% female) were referred 8.6 ± 3.6 years after their last deployment and presented with considerable comorbid conditions and health problems (e.g., 62% post-traumatic stress, 55% dyspnea). After chart abstraction, Veterans were assigned to none (n = 208), single mild (n = 52) and multiple mild (n = 47) blast exposure groups. Among the blast exposed, clinicians documented 73.7% were < 50 m from the blast and 40.4% were physically moved by blast. PFT outcome measures were similar across all groups (p value range: 0.10-0.99). CONCLUSIONS: In this referred sample of deployed Veterans, PFT measures of flow, volume, diffusion, and respiratory mechanics were not associated with clinician documented blast exposure per the retrospective chart abstraction methodology applied. Yet, these clinical findings suggest future research should determine and assess distinction between Veteran recollections of perceived blast experiences versus overpressure wave exposure to the respiratory system.

Longitudinal auditory pathophysiology following mild blast-induced trauma.

Blast-induced hearing difficulties affect thousands of veterans and civilians. The long-term impact of even a mild blast exposure on the central auditory system is hypothesized to contribute to lasting behavioral complaints associated with mild blast traumatic brain injury (bTBI). Although recovery from mild blast has been studied separately over brief or long time windows, few, if any, studies have investigated recovery longitudinally over short-term and longer-term (months) time windows. Specifically, many peripheral measures of auditory function either recover or exhibit subclinical deficits, masking deficits in processing complex, real-world stimuli that may recover differently. Thus, examining the acute time course and pattern of neurophysiological impairment using appropriate stimuli is critical to better understanding and intervening in bTBI-induced auditory system impairments. Here, we compared auditory brainstem response, middle-latency auditory-evoked potentials, and envelope following responses. Stimuli were clicks, tone pips, amplitude-modulated tones in quiet and in noise, and speech-like stimuli (iterated rippled noise pitch contours) in adult male rats subjected to mild blast and sham exposure over the course of 2 mo. We found that blast animals demonstrated drastic threshold increases and auditory transmission deficits immediately after blast exposure, followed by substantial recovery during the window of 7-14 days postblast, although with some deficits remaining even after 2 mo. Challenging conditions and speech-like stimuli can better elucidate mild bTBI-induced auditory deficit during this period. Our results suggest multiphasic recovery and therefore potentially different time windows for treatment, and deficits can be best observed using a small battery of sound stimuli.NEW & NOTEWORTHY Few studies on blast-induced hearing deficits go beyond simple sounds and sparsely track postexposure. Therefore, the recovery arc for potential therapies and real-world listening is poorly understood. Evidence suggested multiple recovery phases over 2 mo postexposure. Hearing thresholds largely recovered within 14 days and partially explained recovery. However, midlatency responses, responses to amplitude modulation in noise, and speech-like pitch sweeps exhibited extended changes, implying persistent central auditory deficits and the importance of subclinical threshold shifts.

Blast-induced brain injury in rats leads to transient vestibulomotor deficits and persistent orofacial pain.

Blast-induced traumatic brain injury (blast-TBI) is associated with vestibulomotor dysfunction, persistent post-traumatic headaches and post-traumatic stress disorder, requiring extensive treatments and reducing quality-of-life. Treatment and prevention of these devastating outcomes require an understanding of their underlying pathophysiology through studies that take advantage of animal models. Here, we report that cranium-directed blast-TBI in rats results in signs of pain that last at least 8 weeks after injury. These occur without significantly elevated behavioural markers of anxiety-like conditions and are not associated with glial up-regulation in sensory thalamic nuclei. These injuries also produce transient vestibulomotor abnormalities that resolve within 3 weeks of injury. Thus, blast-TBI in rats recapitulates aspects of the human condition.

Otologic Outcomes After Blast Injury: The Brussels Bombing Experience.

OBJECTIVE: After the suicide bombings in Brussels on March 22, 2016, many victims consulted our emergency department with otologic symptoms. The aim of this study was to report the otologic morbidity and outcome after acute acoustic trauma in these patients. STUDY DESIGN: Prospective cohort study. SETTING: Tertiary referral center. PATIENTS: Patients reporting subjective hearing loss, tinnitus, feeling of pressure in the ear, vertigo or hyperacusis after witnessing these bombings were included. INTERVENTION: All included patients were treated with systemic corticosteroid therapy, concurrent hyperbaric oxygen therapy (HBOT) was advised to each and every included patient. MAIN OUTCOME MEASURES: Participants underwent a routine otologic work-up including otoscopy, liminal audiometry, and subjective outcome measures related to tinnitus at baseline and at follow-up. Primary outcome was to describe the otologic morbidity after acute acoustic trauma (AAT). Secondary outcome was to evaluate the recovery of hearing loss, subjective symptoms, and tympanic membrane perforations. RESULTS: Fifty-six patients were included in our population with an average age of 27 ±â€Š13 years, and 46% women/54% men. Thirty-two patients reported subjective hearing loss, 45 reported tinnitus, 45 reported a feeling of pressure in the ear, 2 patients experienced vertigo, and 18 patients reported hyperacusis. Otoscopic examination revealed three tympanic membrane perforation (TMP). Sensorineural hearing loss (SNHL) was observed in 41% (n = 23) and mixed hearing loss in 3.6% (n = 2). No conductive hearing loss (CHL) was observed. Follow-up was obtained in 76.8%, with the last follow-up available at 47 ±â€Š74 days. Two perforations closed spontaneously, while one persistent perforation was successfully reconstructed with complete air-bone gap closure. There was a significant improvement in subjective symptoms. SNHL improvement was observed in 52.6% (10/19), mixed hearing loss improved in both patients. Improvement in hearing thresholds was seen in patients treated with steroids and in those treated with steroids and HBOT, there was no significant difference in the degree of improvement between these two groups. CONCLUSIONS: Blast-related otologic injuries have a significant impact on morbidity. Comprehensive otologic evaluation and state-of-the-art treatment may lead to a significant improvement in symptoms and hearing loss.

Dietary Zinc Modulates Matrix Metalloproteinases in Traumatic Brain Injury.

Animal models of mild traumatic brain injury (mTBI) provide opportunity to examine the extent to which dietary interventions can be used to improve recovery after injury. Animal studies also suggest that matrix metalloproteinases (MMPs) play a role in tissue remodeling post-TBI. Because dietary zinc (Zn) improved recovery in nonblast mTBI models, and the MMPs are Zn-requiring enzymes, we evaluated the effects of low- (LoZn) and adequate-Zn (AdZn) diets on MMP expression and behavioral responses, subsequent to exposure to a single blast. MMP messenger RNA expression in soleus muscle and frontal cortex tissues were quantified at 48 h and 14 days post-blast. In muscle, blast resulted in significant upregulation of membrane-type (MT)-MMP, MMP-2, tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 at 48 h post-injury in rats consuming AdZn. At 14 days post-blast, there were no blast or dietary effects observed on MMP levels in muscle, supporting the existence of a Zn-responsive, functional repair and remodeling mechanism. In contrast, blast resulted in a significant downregulation of MT-MMP, TIMP-1, and TIMP-2 and a significant upregulation of MMP-3 levels at 48 h post-injury in cortex tissue, whereas at 14 days post-blast, MT-MMP, MMP-2, and TIMP-2 were all downregulated in response to blast, independent of diet, and TIMP-1 were significantly increased in rats fed AdZn diets despite the absence of elevated MMPs. Because the blast injuries occurred while animals were under general anesthesia, the increased immobility observed post-injury in rats consuming LoZn diets suggest that blast mTBI can, in the absence of any psychological stressor, induce post-traumatic stress disorder-related traits that are chronic, but responsive to diet. Taken together, our results support a relationship between marginally Zn-deficient status and a compromised regenerative response post-injury in muscle, likely through the MMP pathway. However, in neuronal tissue, changes in MMP/TIMP levels after blast indicate a variable response to marginally Zn-deficient diets that may help explain compromised repair mechanism(s) previously associated with the systemic hypozincemia that develops in patients with TBI.

Nano-Pulsed Laser Therapy Is Neuroprotective in a Rat Model of Blast-Induced Neurotrauma.

We have developed a novel, non-invasive nano-pulsed laser therapy (NPLT) system that combines the benefits of near-infrared laser light (808 nm) and ultrasound (optoacoustic) waves, which are generated with each short laser pulse within the tissue. We tested NPLT in a rat model of blast-induced neurotrauma (BINT) to determine whether transcranial application of NPLT provides neuroprotective effects. The laser pulses were applied on the intact rat head 1 h after injury using a specially developed fiber-optic system. Vestibulomotor function was assessed on post-injury days (PIDs) 1-3 on the beam balance and beam walking tasks. Cognitive function was assessed on PIDs 6-10 using a working memory Morris water maze (MWM) test. BDNF and caspase-3 messenger RNA (mRNA) expression was measured by quantitative real-time PCR (qRT-PCR) in laser-captured cortical neurons. Microglia activation and neuronal injury were assessed in brain sections by immunofluorescence using specific antibodies against CD68 and active caspase-3, respectively. In the vestibulomotor and cognitive (MWM) tests, NPLT-treated animals performed significantly better than the untreated blast group and similarly to sham animals. NPLT upregulated mRNA encoding BDNF and downregulated the pro-apoptotic protein caspase-3 in cortical neurons. Immunofluorescence demonstrated that NPLT inhibited microglia activation and reduced the number of cortical neurons expressing activated caspase-3. NPLT also increased expression of BDNF in the hippocampus and the number of proliferating progenitor cells in the dentate gyrus. Our data demonstrate a neuroprotective effect of NPLT and prompt further studies aimed to develop NPLT as a therapeutic intervention after traumatic brain injury (TBI).

[Antimicrobial anti-inflammatory photodynamic and light-emitting-diode phototherapy of the consequences of the gunshot and mine-blast injury to the face, head, and neck including damage to the ENT organs]. / Antimikrobnaia protivovospalitel'naia fotodinamicheskaia i svetodiodnaia fototerapiia posledstvii ognestrel'noi i minno-vzryvnoi travmy golovy i shei.

The objective of the present study was the enhancement of the effectiveness of the treatment of the consequences of the gunshot wounds and mine-blast injuries inflicted to the face, head, and neck encountered in the otolaryngological practice as well as the prevention of the formation of the large demarcation areas in the injured tissues and the preparation of these tissues for the further restorative treatment. Anti-microbial and anti-inflammatory photodynamic therapy (PDT) as well as light-emitting-diode (LED) phototherapy were carried out in 20 patients who suffered gunshot wounds and mine-blast injuries to the face, head, and neck. The photodynamic therapy was performed with the use of an aqueous solution of methylene blue at a concentration of 0.1%, the 'Alod-1' infrared laser ('Granat' modification, Russia), and the 'AFS-Solaris' light-emitting diode-based phototherapeutic apparatus (Russia). The analysis of the results of the study has demonstrated the high efficiency of the proposed approach that made it possible to prevent the development of severe septic complications, reduce the amount of drug therapy, significantly shorten duration of the treatment, and create the conditions for the earlier rehabilitation and further plastic and cosmetic restoration of the tissue structures.

Palovarotene inhibits connective tissue progenitor cell proliferation in a rat model of combat-related heterotopic ossification.

Heterotopic ossification (HO) develops in the extremities of wounded service members and is common in the setting of high-energy penetrating injuries and blast-related amputations. No safe and effective prophylaxis modality has been identified for this patient population. Palovarotene has been shown to reduce bone formation in traumatic and genetic models of HO. The purpose of this study was to determine the effects of Palovarotene on inflammation, progenitor cell proliferation, and gene expression following a blast-related amputation in a rodent model (n = 72 animals), as well as the ability of Raman spectroscopy to detect early HO before radiographic changes are present. Treatment with Palovarotene was found to dampen the systemic inflammatory response including the cytokines IL-6 (p = 0.01), TNF-α (p = 0.001), and IFN-γ (p = 0.03) as well as the local inflammatory response via a 76% reduction in the cellular infiltration at post-operative day (POD)-7 (p = 0.03). Palovarotene decreased osteogenic connective tissue progenitor (CTP-O) colonies by as much as 98% both in vitro (p = 0.04) and in vivo (p = 0.01). Palovarotene treated animals exhibited significantly decreased expression of osteo- and chondrogenic genes by POD-7, including BMP4 (p = 0.02). Finally, Raman spectroscopy was able to detect differences between the two groups by POD-1 (p < 0.001). These results indicate that Palovarotene inhibits traumatic HO formation through multiple inter-related mechanisms including anti-inflammatory, anti-proliferative, and gene expression modulation. Further, that Raman spectroscopy is able to detect markers of early HO formation before it becomes radiographically evident, which could facilitate earlier diagnosis and treatment. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:1135-1144, 2018.

Controlled Low-Pressure Blast-Wave Exposure Causes Distinct Behavioral and Morphological Responses Modelling Mild Traumatic Brain Injury, Post-Traumatic Stress Disorder, and Comorbid Mild Traumatic Brain Injury-Post-Traumatic Stress Disorder.

The intense focus in the clinical literature on the mental and neurocognitive sequelae of explosive blast-wave exposure, especially when comorbid with post-traumatic stress-related disorders (PTSD) is justified, and warrants the design of translationally valid animal studies to provide valid complementary basic data. We employed a controlled experimental blast-wave paradigm in which unanesthetized animals were exposed to visual, auditory, olfactory, and tactile effects of an explosive blast-wave produced by exploding a thin copper wire. By combining cognitive-behavioral paradigms and ex vivo brain MRI to assess mild traumatic brain injury (mTBI) phenotype with a validated behavioral model for PTSD, complemented by morphological assessments, this study sought to examine our ability to evaluate the biobehavioral effects of low-intensity blast overpressure on rats, in a translationally valid manner. There were no significant differences between blast- and sham-exposed rats on motor coordination and strength, or sensory function. Whereas most male rats exposed to the blast-wave displayed normal behavioral and cognitive responses, 23.6% of the rats displayed a significant retardation of spatial learning acquisition, fulfilling criteria for mTBI-like responses. In addition, 5.4% of the blast-exposed animals displayed an extreme response in the behavioral tasks used to define PTSD-like criteria, whereas 10.9% of the rats developed both long-lasting and progressively worsening behavioral and cognitive "symptoms," suggesting comorbid PTSD-mTBI-like behavioral and cognitive response patterns. Neither group displayed changes on MRI. Exposure to experimental blast-wave elicited distinct behavioral and morphological responses modelling mTBI-like, PTSD-like, and comorbid mTBI-PTSD-like responses. This experimental animal model can be a useful tool for elucidating neurobiological mechanisms underlying the effects of blast-wave-induced mTBI and PTSD and comorbid mTBI-PTSD.

Executive summary: The Brain Injury and Mechanism of Action of Hyperbaric Oxygen for Persistent Post-Concussive Symptoms after Mild Traumatic Brain Injury (mTBI) (BIMA) Study.

The Brain Injury and Mechanism of Action of Hyperbaric Oxygen for Persistent Post-Concussive Symptoms after Mild Traumatic Brain Injury (mTBI) (BIMA) study, sponsored by the Department of Defense and held under an investigational new drug application by the Office of the Army Surgeon General, is one of the largest and most complex clinical trials of hyperbaric oxygen (HBO2) for post-concussive symptoms (PCS) in U.S. military service members.

Baseline neurological evaluations in a hyperbaric trial of post-concussive syndrome.

Standard neurologic examinations may not detect abnormalities in U.S. military service members with persistent post-concussive symptoms following mild traumatic brain injury. The Brain Injury and Mechanisms of Action of Hyperbaric Oxygen for Persistent Post-Concussive Symptoms after Mild Traumatic Brain Injury Study (BIMA) enrolled 71 participants September 2012-May 2014. Participants received: comprehensive neurological and oculomotor exam; balance testing (Berg Balance Scale-BBS; Romberg Test-RT, Sharpened Romberg Test-SRT); olfactory function (Brief Smell Identification Test-BSIT). Two trained neurologists conducted the examinations at a central facility in Colorado Springs. Median age was 32 years (range 21-53), 99% male, 82% Caucasian, 49% PTSD, 28% most recent qualifying injury three months to one year prior to enrollment, 32% blast injuries only, and 73% multiple injuries. Some participants presented with abnormal facial sensation (15%), abnormal tandem gait (13%), and tremor (11%). 54% had abnormal near point of convergence (abnormal range 13-80 cm). 86% scored ≥ 55 on the BBS, with no participant scoring ⟨ 50. 49% scored ⟨ 30 seconds on the best trial of the SRT. RT was abnormal in 10%. 15% of participants scored ≤ 9 (out of 12) on BSIT, about twice what is expected in a normal population. The neurological examination found abnormalities across a range of testing, with convergence insufficiency and SRT having the most sensitivity. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT01611194; https://clinicaltrials.gov/show/NCT01611194.

Baseline EEG abnormalities in mild traumatic brain injury from the BIMA study.

The Brain Injury and Mechanisms of Action of HBO2 for Persistent Post-Concussive Symptoms after Mild Traumatic Brain Injury (BIMA), sponsored by the Department of Defense, is a randomized, double-blind, sham-controlled trial of hyperbaric oxygen (HBO2) in service members with persistent post-concussive symptoms following mild TBI, undergoing comprehensive assessments. The clinical EEG was assessed by neurologists for slow wave activity, ictal/interictal epileptiform abnormalities, and background periodic discharges. There is scant literature about EEG findings in this population, so we report baseline clinical EEG results and explore associations with other evaluations, including demographics, medication, neurological assessments, and clinical MRI outcomes. Seventy-one participants were enrolled: median age 32 years, 99% male, 49% comorbid PTSD, 28% with mTBI in the previous year, 32% blast injuries only, and 73% multiple injuries. All participants reported medication use (mean medications = 8, SD = 5). Slowing was present in 39%: generalized 37%, localized 8%, both 6%. No other abnormalities were identified. Slowing was not significantly associated with demographics, medication or neurological evaluation. Participants without EEG abnormalities paradoxically had significantly higher number of white matter hyperintensities as identified on MRI (p = 0.003). EEG slowing is present in more than one-third of participants in this study without evidence of associations with demographics, medications or neurological findings. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT01611194; https://clinicaltrials.gov/show/NCT01611194.

Orbital compressed air and petroleum injury mimicking necrotizing fasciitis.

BACKGROUND: Orbital injury secondary to petroleum-based products is rare. We report the first case, to our knowledge, of a combined compressed air and chemical orbital injury, which mimicked necrotizing fasciitis. CASE REPORT: A 58-year-old man was repairing his motorcycle engine when a piston inadvertently fired, discharging compressed air and petroleum-based carburetor cleaner into his left eye. He developed surgical emphysema, skin necrosis, and a chemical cellulitis, causing an orbital compartment syndrome. He was treated initially with antibiotics and subsequently with intravenous steroid and orbital decompression surgery. There was almost complete recovery by 4 weeks postsurgery. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Petroleum-based products can cause severe skin irritation and necrosis. Compressed air injury can cause surgical emphysema. When these two mechanisms of injury are combined, the resulting orbitopathy and skin necrosis can mimic necrotizing fasciitis and cause diagnostic confusion. A favorable outcome is achievable with aggressive timely management.

Mild traumatic brain injury from primary blast vs. blunt forces: post-concussion consequences and functional neuroimaging.

INTRODUCTION: Primary blast forces may cause dysfunction from mild traumatic brain injury (mTBI). OBJECTIVE: To investigate the effects of primary blast forces, independent of associated blunt trauma and post-traumatic stress disorder, on sensitive post-concussive measures. METHODS: This study investigated post-concussive symptoms, functional health and well-being, cognition, and positron emission tomography (PET) neuroimaging among 12 Iraq or Afghanistan war veterans who sustained pure blast-force mTBI, compared to 12 who sustained pure blunt-force mTBI. RESULTS: Both groups had significantly lower scores than published norms on the Rivermead Post-Concussion Questionnaire (RPQ) and the SF36-V Health Survey. Compared to the Blunt Group, the Blast Group had poorer scores on the Paced Auditory Serial Addition Test (PASAT) and greater PET hypometabolism in the right superior parietal region. Only the Blast Group had significant correlations of their RPQ, SF36-V Mental Composite Score, and PASAT scores with specific regional metabolic changes. CONCLUSION: This pilot study suggests that pure blast force mTBI may have greater post-concussive sequelae including deficits in attentional control and regional brain metabolism, compared to blunt mTBI. A disturbance of a right parietal-frontal attentional network is one potential explanation for these findings.

A phase I study of low-pressure hyperbaric oxygen therapy for blast-induced post-concussion syndrome and post-traumatic stress disorder.

This is a preliminary report on the safety and efficacy of 1.5 ATA hyperbaric oxygen therapy (HBOT) in military subjects with chronic blast-induced mild to moderate traumatic brain injury (TBI)/post-concussion syndrome (PCS) and post-traumatic stress disorder (PTSD). Sixteen military subjects received 40 1.5 ATA/60 min HBOT sessions in 30 days. Symptoms, physical and neurological exams, SPECT brain imaging, and neuropsychological and psychological testing were completed before and within 1 week after treatment. Subjects experienced reversible middle ear barotrauma (5), transient deterioration in symptoms (4), and reversible bronchospasm (1); one subject withdrew. Post-treatment testing demonstrated significant improvement in: symptoms, neurological exam, full-scale IQ (+14.8 points; p<0.001), WMS IV Delayed Memory (p=0.026), WMS-IV Working Memory (p=0.003), Stroop Test (p<0.001), TOVA Impulsivity (p=0.041), TOVA Variability (p=0.045), Grooved Pegboard (p=0.028), PCS symptoms (Rivermead PCSQ: p=0.0002), PTSD symptoms (PCL-M: p<0.001), depression (PHQ-9: p<0.001), anxiety (GAD-7: p=0.007), quality of life (MPQoL: p=0.003), and self-report of percent of normal (p<0.001), SPECT coefficient of variation in all white matter and some gray matter ROIs after the first HBOT, and in half of white matter ROIs after 40 HBOT sessions, and SPECT statistical parametric mapping analysis (diffuse improvements in regional cerebral blood flow after 1 and 40 HBOT sessions). Forty 1.5 ATA HBOT sessions in 1 month was safe in a military cohort with chronic blast-induced PCS and PTSD. Significant improvements occurred in symptoms, abnormal physical exam findings, cognitive testing, and quality-of-life measurements, with concomitant significant improvements in SPECT.

Morphological changes of the neural cells after blast injury of spinal cord and neuroprotective effects of sodium beta-aescinate in rabbits.

OBJECTIVE: Explosive blast neurotrauma is becoming more and more common not only in the military population but also in civilian life due to the ever-present threat of terrorism and accidents. However, little attention has been offered to the studies associated with blast wave-induced spinal cord injury in the literatures. The purpose of this study is to report a rabbit model of explosive blast injury to the spinal cord, to investigate the histological changes, focusing especially on apoptosis, and to reveal whether beta-aescinate (SA) has the neuroprotective effects against the blast injury. METHODS: Adult male New Zealand white rabbits were randomly divided into sham group, experimental group and SA group. All rabbits except the sham group were exposed to the detonation, produced by the blast tube containing 0.7 g cyclotrimethylene trinitramine, with the mean peak overpressure of 50.4 MP focused on the dorsal surface of T9-T10 level. After evaluation of the neurologic function, spinal cord of the rabbits was removed at 8 h, 1, 3, 7, 14 or 30 days and the H&E staining, EM examination, DNA gel electrophoresis and TUNEL were progressively performed. RESULTS: The study demonstrated the occurrence of both necrosis and apoptosis at the lesion site. Moreover, the SA therapy could not only improve the neurologic outcomes (P<0.05) but also reduce the loss of motoneuron and TUNEL-positive rate (P<0.05). CONCLUSIONS: In the rabbit model of explosive blast injury to the spinal cord, the coexistent apoptotic and necrotic changes in cells was confirmed and the SA had neuroprotective effects to the blast injury of the spinal cord in rabbits. This is the first report in which the histological characteristics and drug treatment of the blast injury to the spinal cord is demonstrated.

Case report: Treatment of mild traumatic brain injury with hyperbaric oxygen.

Two United States Air Force Airmen were injured in a roadside improvised explosive device (IED) blast in Iraq in January 2008. Both airmen suffered concussive injuries and developed irritability, sleep disturbances, headaches, memory difficulties and cognitive difficulties as symptoms of mild traumatic brain injury (mTBI). Six months after injury, repeat Automated Neuropsychological Assessment Metrics (ANAM) testing showed deterioration, when compared to pre-injury baseline ANAM assessment, in all measured areas (simple reaction time, procedural reaction time, code substitution learning, code substitution delayed, mathematical processing, and matching to sample). The airmen were treated with hyperbaric oxygen in treatments of 100% oxygen for one hour at 1.5 atmospheres absolute, resulting in rapid improvement of headaches and sleep disturbances, improvement in all symptoms and resolution of most symptoms. Repeat ANAM testing after completion of the hyperbaric treatments - nine months after initial injury - showed improvement in all areas, with most measures improving to pre-injury baseline levels. The airmen received no other treatment besides medical monitoring. Repeat neuropsychologic testing confirmed the improvement. We conclude that the improvement in symptoms and ANAM performance is most likely attributable to HBO treatment.

Characteristics of and strategies for patients with severe burn-blast combined injury.

BACKGROUND: Severe burn-blast combined injury is a great challenge to medical teams for its high mortality. The aim of this study was to elucidate the clinical characteristics of the injury and to present our clinical experiences on the treatment of such cases. METHODS: Five patients with severe burn-blast combined injuries were admitted to our hospital 77 hours post-injury on June 7, 2005. The burn extent ranged from 80% to 97% (89.6% +/- 7.2%) of TBSA (full-thickness burns 75% - 92% (83.4% +/- 7.3%)). All the patients were diagnosed as having blast injury and moderate or severe inhalation injury. Functions of the heart, liver, kidney, lung, pancreas and coagulation were observed. Autopsy samples of the heart, liver, and lungs were taken from the deceased. Comprehensive measures were taken during the treatment, including protection of organ dys function, use of antibiotics, early anticoagulant treatment, early closure of burn wounds, etc. All the data were analyzed statistically with t test. RESULTS: One patient died of septic shock 23 hours after admission (four days after injury), the others survived. Dysfunction of the heart, liver, lungs, pancreas, and coagulation were found in all the patients on admission, and the functions were ameliorated after appropriate treatments. CONCLUSIONS: Burn-blast combined injury may cause multiple organ dysfunctions, especially coagulopathy. Proper judgment of patients' condition, energetic anticoagulant treatment, early closure of burn wounds, rational use of antibiotics, nutritional support, intensive insulin treatment, timely and effective support and protection of organ function are the most important contributory factors in successful treatment of burn-blast combined injuries.