Stop the Bleed: Is Mass Education the Best Approach?

The Stop the Bleed (STB) course teaches trainees prehospital hemorrhage control with a focus on mass education. Identifying populations most likely to benefit can help save on the significant cost and limited resources. In this study, we attempted to identify those populations and performed a cost analysis. Trainees underwent STB education and completed a survey on completion to assess demographics and prior experiences where STB skills could have been useful. Five hundred seventy-one trainees categorized as first responders (14%), students (56%), and the working public (30%) completed the survey. Most trainees found the lecture and simulation helpful, 96 per cent and 98 per cent, respectively. There were significant differences among groups who had previously been in situations where the STB course would have been helpful (88% first responders versus 40% students versus 43% public workers) (P < 0.001). Teaching a class of 10 students costs approximately $455; the cost can be as high as $1246 for a class of 50 students. Most STB trainees found the course helpful. First responders are most likely to be exposed to situations where course information could be helpful. Focusing on specific high-yield groups rather than mass education might be a more efficient approach to STB education.

Dorsal column sensory axons degenerate due to impaired microvascular perfusion after spinal cord injury in rats.

The mechanisms contributing to axon loss after spinal cord injury (SCI) are largely unknown but may involve microvascular loss as we have previously suggested. Here, we used a mild contusive injury (120 kdyn IH impactor) at T9 in rats focusing on ascending primary sensory dorsal column axons, anterogradely traced from the sciatic nerves. The injury caused a rapid and progressive loss of dorsal column microvasculature and oligodendrocytes at the injury site and penumbra and an ~70% loss of the sensory axons by 24 h. To model the microvascular loss, focal ischemia of the T9 dorsal columns was achieved via phototoxic activation of intravenously injected rose bengal. This caused an ~53% loss of sensory axons and an ~80% loss of dorsal column oligodendrocytes by 24 h. Axon loss correlated with the extent and axial length of microvessel and oligodendrocyte loss along the dorsal column. To determine if oligodendrocyte loss contributes to axon loss, the glial toxin ethidium bromide (EB; 0.3 µg/µl) was microinjected into the T9 dorsal columns, and resulted in an ~88% loss of dorsal column oligodendrocytes and an ~56% loss of sensory axons after 72 h. EB also caused an ~75% loss of microvessels. Lower concentrations of EB resulted in less axon, oligodendrocyte and microvessel loss, which were highly correlated (R(2) = 0.81). These data suggest that focal spinal cord ischemia causes both oligodendrocyte and axon degeneration, which are perhaps linked. Importantly, they highlight the need of limiting the penumbral spread of ischemia and oligodendrocyte loss after SCI in order to protect axons.

Intravenous infusion of magnesium chloride improves epicenter blood flow during the acute stage of contusive spinal cord injury in rats.

Vasospasm, hemorrhage, and loss of microvessels at the site of contusive or compressive spinal cord injury lead to infarction and initiate secondary degeneration. Here, we used intravenous injection of endothelial-binding lectin followed by histology to show that the number of perfused microvessels at the injury site is decreased by 80-90% as early as 20 min following a moderate T9 contusion in adult female rats. Hemorrhage within the spinal cord also was maximal at 20 min, consistent with its vasoconstrictive actions in the central nervous system (CNS). Microvascular blood flow recovered to up to 50% of normal volume in the injury penumbra by 6 h, but not at the epicenter. A comparison with an endothelial cell marker suggested that many microvessels fail to be reperfused up to 48 h post-injury. The ischemia was probably caused by vasospasm of vessels penetrating the parenchyma, because repeated Doppler measurements over the spinal cord showed a doubling of total blood flow over the first 12 h. Moreover, intravenous infusion of magnesium chloride, used clinically to treat CNS vasospasm, greatly improved the number of perfused microvessels at 24 and 48 h. The magnesium treatment seemed safe as it did not increase hemorrhage, despite the improved parenchymal blood flow. However, the treatment did not reduce acute microvessel, motor neuron or oligodendrocyte loss, and when infused for 7 days did not affect functional recovery or spared epicenter white matter over a 4 week period. These data suggest that microvascular blood flow can be restored with a clinically relevant treatment following spinal cord injury.

Patient-specific orthotopic glioblastoma xenograft models recapitulate the histopathology and biology of human glioblastomas in situ.

Frequent discrepancies between preclinical and clinical results of anticancer agents demand a reliable translational platform that can precisely recapitulate the biology of human cancers. Another critical unmet need is the ability to predict therapeutic responses for individual patients. Toward this goal, we have established a library of orthotopic glioblastoma (GBM) xenograft models using surgical samples of GBM patients. These patient-specific GBM xenograft tumors recapitulate histopathological properties and maintain genomic characteristics of parental GBMs in situ. Furthermore, in vivo irradiation, chemotherapy, and targeted therapy of these xenograft tumors mimic the treatment response of parental GBMs. We also found that establishment of orthotopic xenograft models portends poor prognosis of GBM patients and identified the gene signatures and pathways signatures associated with the clinical aggressiveness of GBMs. Together, the patient-specific orthotopic GBM xenograft library represent the preclinically and clinically valuable "patient tumor's phenocopy" that represents molecular and functional heterogeneity of GBMs.

Uncovertebral hypertrophy is a significant risk factor for the occurrence of heterotopic ossification after cervical disc replacement: survivorship analysis of Bryan disc for single-level cervical arthroplasty.

OBJECTIVES: The purpose of this study is to investigate the incidence of heterotopic ossification (HO) in the Bryan cervical arthroplasty group and to identify associations between preoperative factors and the development of HO. METHODS: We performed a retrospective review of clinical and radiological data on patients who underwent single-level cervical arthroplasty with Bryan prosthesis between January 2005 and September 2007. Patients were postoperatively followed-up at 1, 3, 6, 12 months and every year thereafter. The clinical assessment was conducted using Odom's criteria. The presence of HO was evaluated on the basis of X-ray at each time-point according to the McAfee classification. In this study, we focused on survivorship of Bryan prosthesis for single-level arthroplasty. The occurrence of ROM-affecting HO was defined as a functional failure and was used as an endpoint for determining survivorship. RESULTS: Through the analysis of 19 cases of Bryan disc arthroplasty for cervical radiculopathy and/or myelopathy, we revealed that ROM-affecting HO occurs in as many as 36.8% of cases and found that 37% of patients had ROM-affecting HO within 24 months following surgery. The overall survival time to the occurrence of ROM-affecting HO was 36.4 ± 4.4 months. Survival time of the prosthesis in the patient group without preoperative uncovertebral hypertrophy was significantly longer than that in the patient group with preoperative uncovertebral hypertrophy (47.2 months vs 25.5 months, p = 0.02). Cox regression proportional hazard analysis illustrated that preoperative uncovertebral hypertrophy was determined as a significant risk factor for the occurrence of ROM-affecting HO (hazard ratio = 12.30; 95% confidential interval = 1.10-137.03; p = 0.04). CONCLUSION: These findings suggest that the condition of the uncovertebral joint must be evaluated in preoperative planning for Bryan cervical arthroplasty.

Evaluation of congenital lumbosacral malformations and neurological findings in patients with low back pain.

AIM: To investigate the correlation of congenital lumbosacral abnormalities with neurological signs in young patients with low back pain (LBP) MATERIAL AND METHODS: The study included 401 patients with LBP that lasted longer than 2 weeks. All cases were screened by standard lumbosacral x-rays for the presence of the most common congenital vertebral abnormalities i.e. spina bifida occulta (SBO) and transitional vertebra (TV). Patients were divided into two groups according to presence of a neurological sign. Patients with a neurological sign were referred for computerized tomography and/or magnetic resonance imaging. RESULTS: Sixty-two patients had a neurological sign. Congenital vertebral abnormalities were detected in 52 patients (12.1%); 34 of these (8.5%) were spina bifida, whereas 18 (4.5%) were transitional vertebra. SBO was most commonly observed at the S1 level (30 patients). No correlation for SBO or TV was determined in patients with and without neurological signs but these groups showed significant difference for disc herniation in CT or MRI (P=0.001). Congenital abnormalities had no correlation with disc herniation in CT or MRI. CONCLUSION: LBP in young adults with TV or SBO showed no correlation with neurological signs. Therefore patients with prolonged LBP that present with neurological signs may be scheduled for CT and/or MRI, but reevaluation of the patient with psychometric tests is recommended if there is no neurological sign.