Metal implant removal: benefits and drawbacks--a patient survey.

BACKGROUND: Hardware removals are among the most commonly performed surgical procedures worldwide. Current literature offers little data concerning postoperative patient satisfaction. The purpose of our study was to evaluate the patients' point of view on implant removal. METHODS: We surveyed patients of a German level one trauma center, who underwent hardware removal in 2009 and 2010, with regard to their personal experiences on implant removal. Exclusively, data obtained out of the survey were analyzed. RESULTS: In 332 patients surveyed, most hardware removals were performed at the ankle joint (21%) followed by the wrist (15%). The most frequent indication was a doctor's recommendation (68%), followed by pain (31%) and impaired function (31%). Patient reported complication rate of implant removal was 10%. Importantly, after implant removal because of pain or impaired function patients reported an improvement in function (72%) as well as decreased pain (96%). 96% of all responding patients and 66% of the patients who suffered from subsequent complications would opt for surgical implant removal again. CONCLUSION: In summary, despite the challenging and frequently troublesome nature of surgical hardware removal our data contradicts the widely held view that implant removal is often without a positive effect on the patients. These findings may influence the surgeons' attitude towards implant removal and their day-to-day routine in patient counseling.

Massive cerebral air embolism after blunt chest trauma with full neurological recovery.

Cerebral air embolism (CAE) is a common, often lethal, complication in blunt and penetrating chest trauma. The factors affecting the outcome of CAE patients are poorly understood, and there is no generally accepted treatment algorithm. In this report, we present the case of a 28-year-old male motorcyclist with a massive CAE, including bilateral internal carotid artery air on computed tomographic examination following blunt chest trauma. With prehospital intubation, oxygen, transfusion, and open laparotomy but without any specific treatment regarding the CAE, a follow-up computed tomography (CT) scan approximately 6 hours later showed resolution of the cerebrovascular air. Recovery was unremarkable, and the patient was discharged neurologically intact after 22 days.

Injury pattern, outcome and characteristics of severely injured pedestrian.

BACKGROUND: Pedestrians who are involved in motor vehicle collisions present with a unique trauma situation. The aim of this study was to demonstrate the specific clinical characteristics of this patient population in comparison to injured motor vehicle occupants in the medical emergency setting. METHODS: A total of 4435 pedestrian traffic collision victims admitted to hospitals participating at TraumaRegister DGU® between 2002 and 2012 (primary admission, Injury Severity Score, ISS ≥ 9; age ≥ 2 years) was assessed and compared to 16,042 severely injured motor vehicle occupants. Analyses included features such as demographic distribution, injury patterns, treatment course, subsequent complications and overall clinical outcome. RESULTS: Severely injured pedestrians more commonly were female (42 % vs. 34 % of motor vehicle occupants) and children below 16 years (12 % vs. 2 %) or seniors above 60 years of age (39 % vs. 17 %). Pedestrians were injured more severely (ISS: 26 vs. 25; NISS 32 vs. 30) with higher rates of head injuries (64 % vs. 47 %), pelvic injuries (32 % vs. 23 %) and lower extremity injuries (52 % vs. 43 %). Accordingly, pedestrians more commonly presented with Glasgow Coma Scale <9 (36 % vs. 28 %) and a systolic blood pressure below 90 mmHg (18 % vs. 13 %) accumulating in a worse prognosis (RISC-Score 24 % vs. 15 %) despite of a shorter on-scene treatment time (26 min vs. 38 min) and a shorter period from the collision until hospital admission (61 min vs. 78 min). Finally, pedestrians showed a higher mortality (22 % vs. 12 %). CONCLUSION: Severely injured pedestrians represent a challenging patient population with unique injury patterns and high subsequent mortality. Emergency team members should be sensitized to the trigger term "pedestrian" in order to improve the initial emergency management and thus the overall clinical outcome.

Fusion of CCL21 non-migratory active breast epithelial and breast cancer cells give rise to CCL21 migratory active tumor hybrid cell lines.

The biological phenomenon of cell fusion has been linked to tumor progression because several data provided evidence that fusion of tumor cells and normal cells gave rise to hybrid cell lines exhibiting novel properties, such as increased metastatogenic capacity and an enhanced drug resistance. Here we investigated M13HS hybrid cell lines, derived from spontaneous fusion events between M13SV1-EGFP-Neo breast epithelial cells exhibiting stem cell characteristics and HS578T-Hyg breast cancer cells, concerning CCL21/CCR7 signaling. Western Blot analysis showed that all cell lines varied in their CCR7 expression levels as well as differed in the induction and kinetics of CCR7 specific signal transduction cascades. Flow cytometry-based calcium measurements revealed that a CCL21 induced calcium influx was solely detected in M13HS hybrid cell lines. Cell migration demonstrated that only M13HS hybrid cell lines, but not parental derivatives, responded to CCL21 stimulation with an increased migratory activity. Knockdown of CCR7 expression by siRNA completely abrogated the CCL21 induced migration of hybrid cell lines indicating the necessity of CCL21/CCR7 signaling. Because the CCL21/CCR7 axis has been linked to metastatic spreading of breast cancer to lymph nodes we conclude from our data that cell fusion could be a mechanism explaining the origin of metastatic cancer (hybrid) cells.

Characterization of hybrid cells derived from spontaneous fusion events between breast epithelial cells exhibiting stem-like characteristics and breast cancer cells.

Several data of the past years clearly indicated that the fusion of tumor cells and tumor cells or tumor cells and normal cells can give rise to hybrids cells exhibited novel properties such as an increased malignancy, drug resistance, or resistance to apoptosis. In the present study we characterized hybrid cells derived from spontaneous fusion events between the breast epithelial cell line M13SV1-EGFP-Neo and two breast cancer cell lines: HS578T-Hyg and MDA-MB-435-Hyg. Short-tandem-repeat analysis revealed an overlap of parental alleles in all hybrid cells indicating that hybrid cells originated from real cell fusion events. RealTime-PCR-array gene expression data provided evidence that each hybrid cell clone exhibited a unique gene expression pattern, resulting in a specific resistance of hybrid clones towards chemotherapeutic drugs, such as doxorubicin and paclitaxel, as well as a specific migratory behavior of hybrid clones towards EGF. For instance, M13MDA435-4 hybrids showed a marked resistance towards etoposide, doxorubicin and paclitaxel, whereas hybrid clones M13MDA-435-1 and -2 were only resistant towards etoposide. Likewise, all investigated M13MDA435 hybrids responded to EGF with an increased migratory activity, whereas the migration of parental MDA-MB-435-Hyg cells was blocked by EGF, suggesting that M13MDA435 hybrids may have acquired a new motility pathway. Similar findings have been obtained for M13HS hybrids. We conclude from our data that they further support the hypothesis that cell fusion could give rise to drug resistant and migratory active tumor (hybrid) cells in cancer.

Recurrence cancer stem cells--made by cell fusion?

Within the past 10-15 years our knowledge about cancer and how cancer cells might originate has changed dramatically. It is now generally believed that a tumor has its origin in cancer stem cells (CSCs), which originated either from transformed tissue stem cells or transformed progenitor cells that have regained self-renewal activity. CSCs share several characteristics of normal stem cells, such as self-renewal capacity, slow cell cycle activity, differentiation capacity, possessing an enhanced resistance towards cytotoxic agents and radiation, as well as tissue restoration capacity. Due to the increased drug and radiation resistance and slow cell cycle activity concomitant with tumor initiation capacity it is generally assumed that recurrent cancers originate from first line therapy surviving CSCs. But how does the CSC hypothesis explain "oncogenic resistance", which describes the phenomenon that most recurrent cancers are characterized by both an increased malignancy as well as resistance towards first line cancer therapy. To us, "oncogenic resistance" can not be simply attributed to the resistance properties of normal CSCs. If so, the recurring tumor should be treatable by first line therapy, which is mostly not the case. Thus, we conclude that "oncogenic resistance" demands a new type of tumor initiating cells, the so-called recurrence CSCs (rCSCs). This type of tumor initiating cell originates during first line therapy and is characterized by giving rise to first line therapy resistant and highly malignant progenies. Because several characteristics of "oncogenic resistance", such as increased drug resistance, increased resistance to apoptosis and an enhanced malignancy have been linked to cell fusion we further conclude that rCSCs might originate from this cellular event. However, which cell types have to fuse with each other to ultimately give rise to rCSCs is not clear. In any case, tumor tissues, particularly those being destructed by first line therapy comprise of a variety of fusogenic cells including tumor cells and CSCs as well as recruited monocytes/macrophages and bone marrow-derived stem cells. The fusogenic properties of these cells concomitant with phenotypic heterogeneity, which is also a property of cell fusion, will then lead to the origin of rCSCs. In accordance with Darwinian evolution only those cells will survive that can resist best to the selection pressure first line therapy.