Surgical treatment of 50 carotid dissections: indications and results

PURPOSE: This article analyzes the course of 48 patients with 49 chronic carotid dissections (who were treated surgically at our institution after a median anticoagulation period of 9 months because of a persistent high-grade stenosis or an aneurysm) and the course of one additional patient with acute carotid dissection (who underwent early operative reconstruction 12 hours after onset because of fluctuating neurologic symptoms). METHODS: All medical and surgical records and imaging studies were reviewed retrospectively. All histologic specimens were reevaluated by a single pathologist to assess the cause of dissection. Follow-up of 41 patients (85%) after 70 months (range, 1-190 months) consisted of an examination of the extracranial vessels in the neck by Doppler ultrasound scanning and a questionnaire about the patients' medical history and their personal appraisals of cranial nerve function. RESULTS: Seventy percent of the dissections had developed spontaneously; 18% were caused by trauma; 12% of all patients (22% of the women) had a fibromuscular dysplasia. Indication for surgery was a high-grade persisting stenosis and a persisting or newly developed aneurysm. Flow restoration was achieved by resection and vein graft replacement in 40 cases (80%) and thromboendarterectomy and patch angioplasty in three cases (6%). Gradual dilatation was performed and effective in two cases (4%). Five internal carotid arteries (10%) had to be clipped because dissection extended into the skull base. One patient died of intracranial bleeding. Five patients (10%) experienced the development of a recurrent minor stroke (ipsilateral, 4 patients; contralateral, 1 patient). Cranial nerve damage could not be avoided in 29 cases (58%) but were transient in most of the cases. During follow-up, one patient died of unrelated reasons, and only one patient had experienced the development of a neurologic event of unknown cause. CONCLUSION: Chronic carotid dissection can be effectively treated by surgical reconstruction to prevent further ischemic or thromboembolic complications, if medical treatment for 6 months with anticoagulation failed or if carotid aneurysms and/or high-grade carotid stenosis persisted or have newly developed.     

Hispanic health status in Orange County, Florida.

PURPOSE: To assess the health status of the Hispanic population of Orange County, Florida. METHODS: The methodology utilized secondary data for 66 ethnically identified indicators in a comparative framework applied for a 5-year period (1997-2001). FINDINGS: Orange County Hispanics are younger with lower per capita income than their Florida peers, less likely to be White, and much more likely to be of Puerto Rican origin. Relative to the Hispanic populations in the selected peer counties and statewide, Orange County Hispanics have higher age-adjusted death rates for a majority of disease categories and conditions, such as breast, lung, and prostate cancers; chronic liver disease and cirrhosis; diabetes mellitus; pneumonia and influenza; stroke; acquired immunodeficiency syndrome; motor vehicle accidents; and infant, neonatal, and child mortality. Orange County Hispanics did better in comparison to Orange non-Hispanics, with lower age-adjusted death rates for major causes of death such as heart disease, cancer, and stroke. However, for many indicators, the 5-year trends for Orange County Hispanics are moving in an unfavorable direction in contrast to the trends for non-Hispanics, which are either stable or improving. CONCLUSION: Comparative assessments of Hispanic populations using secondary data enable the development of a comprehensive health status profile. However, this approach is currently constrained by the limited number of ethnically identified indicators and, especially for Hispanics, problems in the accuracy and consistency of the assignment to racial categories and subsequent reporting.     

Lesion-associated accumulation of uPAR/CD87- expressing infiltrating granulocytes, activated microglial cells/macrophages and upregulation by endothelial cells following TBI and FCI in humans

Urokinase-type plasminogen activator receptor (uPAR/CD87) together with its ligand, urokinase-type plasminogen activator (uPA), constitutes a proteolytic system associated with tissue remodelling and leucocyte infiltration. uPAR is a member of the glycosyl phosphatidyl inositol (GPI) anchored protein family. The functional role of uPAR comprises fibrinolysis by conversion of plasminogen to plasmin. In addition, uPAR promotes cell adhesion, migration, proliferation, re-organization of the actin cytoskeleton, and angiogenesis. Furthermore, uPAR is involved in prevention of scar formation and is chemoattractant to macrophages and leucocytes. In order to investigate the pathophysiological role of uPAR following human CNS injury we examined necrotic brain lesions resulting from traumatic brain injury (TBI; n = 28) and focal cerebral infarctions (FCI; n = 17) by immunohistochemistry. Numbers of uPAR+ cells and uPAR+ blood vessels were counted. Following brain damage, uPAR+ cells increased significantly within 12 h, reached a maximum after 3-4 days and remained elevated until later stages. uPAR was expressed by infiltrating granulocytes, activated microglia/macrophages and endothelial cells. Numbers of uPAR+ vessels increased in parallel subsiding earlier following FCI than post TBI. The restricted, lesion-associated accumulation of uPAR+ cells in the brain parenchyma and upregulated expression by endothelial cells suggests a crucial role for the influx of inflammatory cells and blood-brain barrier (BBB) disturbance. Through a failure in BBB function, uPAR participates in formation of brain oedema and thus contributes to secondary brain damage. In conclusion, the study defines the localization, kinetic course and cellular source of uPAR as a potential pharmacological target following human TBI and FCI.     

Arterial intervention and reduction in amputation for chronic critical leg ischaemia

BACKGROUND: Untreated chronic critical leg ischaemia (CLI) usually leads to an amputation or death of a patient. Surgical and endovascular interventions may improve arterial flow. Long infrainguinal reconstruction may be the most useful method for preventing amputations. The value of different reconstruction methods was assessed by their impact on amputation incidence. METHODS: A nationwide 2-year analysis of the incidence of major amputations and reconstructions for CLI was done in Finland (population 5.1 million). Incidences were compared in hospital regions with more than 150 000 inhabitants. RESULTS: The overall amputation incidence was 216 per million inhabitants per year. The corresponding incidence of arterial reconstructions was 203 per million inhabitants per year. There were large variations in the incidence of amputations and reconstructions; 20-fold differences in infrapopliteal surgical reconstructions and 30-fold differences in endovascular procedures were found. There was a correlation between a high incidence of infrapopliteal surgical reconstructions and a low incidence of amputations. This correlation was found for below-knee amputations only. CONCLUSION: These results suggest that long surgical reconstructions improving perfusion directly to the ischaemic tissue can improve leg salvage.     

One Health surveillance of West Nile and Usutu viruses: a repeated cross-sectional study exploring seroprevalence and endemicity in Southern France, 2016 to 2020

BackgroundWest Nile virus (WNV) and Usutu virus (USUV), two closely related flaviviruses, mainly follow an enzootic cycle involving mosquitoes and birds, but also infect humans and other mammals. Since 2010, their epidemiological situation may have shifted from irregular epidemics to endemicity in several European regions; this requires confirmation, as it could have implications for risk assessment and surveillance strategies.AimTo explore the seroprevalence in animals and humans and potential endemicity of WNV and USUV in Southern France, given a long history of WNV outbreaks and the only severe human USUV case in France in this region.MethodsWe evaluated the prevalence of WNV and USUV in a repeated cross-sectional study by serological and molecular analyses of human, dog, horse, bird and mosquito samples in the Camargue area, including the city of Montpellier, between 2016 and 2020.ResultsWe observed the active transmission of both viruses and higher USUV prevalence in humans, dogs, birds and mosquitoes, while WNV prevalence was higher in horses. In 500 human samples, 15 were positive for USUV and 6 for WNV. Genetic data showed that the same lineages, WNV lineage 1a and USUV lineage Africa 3, were found in mosquitoes in 2015, 2018 and 2020.ConclusionThese findings support existing literature suggesting endemisation in the study region and contribute to a better understanding of USUV and WNV circulation in Southern France. Our study underlines the importance of a One Health approach for the surveillance of these viruses.     

Internal mammary perforators: a cadaver study

Microsurgeons currently employ the internal mammary artery and vein as recipient vessels for microvascular reconstruction of the breast with increasing frequency. Recent reports have demonstrated that the perforating branches of the internal mammary artery and vein can also be used as recipient vessels. The purpose of the following cadaver study was to determine the location and diameter of these internal mammary perforators and whether they are suitable as recipient vessels. Ten fresh cadavers were obtained for this project. Using a micrometer under loupe magnification, bilateral measurements were taken of the perforators from the first five interspaces. The largest arterial perforator averaged 1.74 mm in diameter and the largest venous perforator averaged 1.78 mm in diameter. The largest perforators were most commonly found in the second interspace. Based on the results of this study, the internal mammary perforators appear to have suitable diameter for microvascular anastomosis and should be considered.     

Description of two new ABCB11 mutations responsible for type 2 benign recurrent intrahepatic cholestasis in a French-Canadian family

Benign recurrent intrahepatic cholestasis is a rare clinical entity that is caused by mutations in the canalicular transport genes. The present report describes two individuals from the same family whose symptoms were typical of the clinical characteristics of type 2 benign recurrent intrahepatic cholestasis. Sequencing of the ABCB11 gene revealed two previously unreported mutations that predict the absence of expression of the protein. The clinical presentation of the current cases are discussed, as are the differential diagnosis and genetic characteristics of the hereditary cholestatic disorders, overemphasizing the possibility of making a definite genetic diagnosis.