Traumatic vertebral artery injury: proposal for classification of the severity of trauma and likelihood of fatal outcome.

Vertebral artery injury (VAI) occurs after (blunt) trauma as well as spontaneously. The risk of incurring VAI from a blunt trauma probably parallels the severity of trauma, often referred to as major- and minor-trauma. However, the literature does not provide concrete definitions of these terms. This study aims to define minor- and major-trauma and to analyze the likelihood of fatal outcome in VAI. For this purpose, classification criteria of major- and minor-trauma were developed and a PubMed database search was performed for articles on VAI published prior to 2013. The definitions of minor- and major-trauma, derived mainly from radiological screening criteria in cervical spine injury and based on the mechanism leading to the injury, were used in the analysis of the literature. The search produced 241 VAI cases with sufficiently detailed data for the comparison of major-trauma (52 cases, 50 lethal), minor-trauma (8 cases, none lethal), and no-trauma (182 cases, 69 lethal). The numbers of lethal cases in the total study population and subgroups differed significantly between the groups (Fisher's exact test) and the likelihood ratios (LRs) of lethal outcome were substantially higher in the major-trauma group compared to the other groups. The highly significant p values show that the proposed criteria differentiate between trauma types with regard to fatal outcome. The presented results can assist in the evaluation of forensic cases of VAI.

Molecular characterization of the vascular features of focal nodular hyperplasia and hepatocellular adenoma: a role for angiopoietin-1.

UNLABELLED: Focal nodular hyperplasia (FNH) and hepatocellular adenoma (HCA) are two hepatic nodular lesions of different etiologies. FNH, a polyclonal lesion, is assumed to be a regenerative reaction following a vascular injury, whereas HCA is a monoclonal, benign neoplastic lesion. In addition to features that are predominantly found in either FNH or HCA (e.g., dystrophic vessels in FNH and single arteries in HCA), FNH and HCA share morphological vascular abnormalities such as dilated sinusoids. We hypothesized that these anomalous vascular features are associated with altered expression of growth factors involved in vascular remodeling. This was based on reports of morphologically abnormal hepatic vasculature and nodular lesions in transgenic models of hepatocytic overexpression of angiopoietin-1 (Ang-1), a member of the angiopoietin family, which is crucially involved in vascular morphogenesis and homeostasis. We investigated gene and protein expression of members of the angiopoietin system and vascular endothelial growth factor A (VEGF-A) and its receptors in 9 FNH samples, 13 HCA samples, and 9 histologically normal livers. In comparison with normal samples, a significant increase in Ang-1 was found in FNH (P < 0.01) and HCA (P < 0.05), whereas no significant changes in Ang-2, receptor tyrosine kinase with immunoglobulin-like and EGF-like domains 2, VEGF-A, or vascular endothelial growth factor receptor 2 (VEGFR-2) were observed. CONCLUSION: Because of the different etiological contexts of a preceding vascular injury in FNH and a neoplastic growth in HCA, Ang-1 might exert different effects on the vasculature in these lesions. In FNH, it could predominantly stimulate recruitment of myofibroblasts and result in dystrophic vessels, whereas in HCA, it may drive vascular remodeling that produces enlarged vessels and arterial sprouting that generates single arteries.