Evaluation of radial and ulnar blood flow after radial artery cannulation with 20- and 22-gauge cannulae using duplex Doppler ultrasound

This study evaluated ulnar and radial artery blood flow after radial artery cannulation during general anaesthesia using Doppler ultrasound. A total of 80 patients were randomly assigned to receive radial artery cannulation with either a 20‐G or 22‐G cannula. Arterial diameter, peak systolic velocity, end‐diastolic velocity, resistance index and mean volume flow were measured at four time points in both arteries: before anaesthesia; 5 min after intubation; immediately after cannulation; and 5 min after cannulation. After radial artery cannulation, ulnar diameters and blood flow were significantly increased, and persisted until 5 min after cannulation. Radial blood flow was decreased immediately after cannulation and recovered to pre‐cannulation values 5 min after cannulation. There were no statistical differences between groups at each time point. Radial artery cannulation causes compensatory increase in ulnar artery blood flow, and the difference in cannula size has minimal effect on this change.     

Clinical outcomes of autogenous cancellous bone grafts obtained through the portal for tibial nailing

BackgroundThe purpose of this study is to introduce and review the clinical outcomes of a new technique for harvesting autogenous cancellous bone grafts in association with tibial intramedullary (IM) nailing.Materials and methodsWe retrospectively reviewed 21 patients who received autogenous cancellous bone grafts obtained from the entry portal of a tibial IM nail for fracture gaps, malalignment or nonunion in the lower extremities. All patients were scheduled to receive IM nailing or had already received IM nailing for the fixation of an ipsilateral tibia shaft fracture. A total of 33 patients who received only tibial IM nailing were selected as a control group. Through the follow-up, postoperative complications related to the bone harvest were monitored. Further by taking serial X-rays, radiographic changes of the donor site and the knee joint were closely observed. Knee pain (visual analogue scale (VAS)) and function (Lysholm knee score) were compared between the study group and the control group.ResultsAt the last follow-up, the average VAS in the study group was 1.28 (0–5), which was not significantly different from the control group (VAS: 1.36, range 0–7) (P = 0.985). The range of motion of the knee joint was similar in both groups, averaging 130.23° (range: 115–135°) and 131.36° (range: 115–135°), respectively. There was no significant difference in the Lysholm knee score between the study and control groups (P = 0.610). All patients exhibited complete fracture healing at an average of 6 months and no complications associated with the bone donor site were observed.ConclusionsBy using the new technique, autogenous cancellous bone grafting can be performed conveniently and safely to treat fracture gaps, malalignment or nonunion in the lower extremities without additional morbidity at the donor site.     

Use of selective serotonin reuptake inhibitors and risk of fracture: a systematic review and meta-analysis

Previous studies have reported inconsistent findings regarding the association between the use of selective serotonin reuptake inhibitors (SSRIs) and the risk of fracture. We identified relevant studies by searching three electronic databases (MEDLINE, EMBASE, and the Cochrane Library) from their inception to October 20, 2010. Two evaluators independently extracted data. Because of heterogeneity, we used random‐effects meta‐analysis to obtain pooled estimates of effect. We identified 12 studies: seven case‐control studies and five cohort studies. A meta‐analysis of these 12 observational studies showed that the overall risk of fracture was higher among people using SSRIs (adjusted odds ratio [OR] = 1.69, 95% confidence interval [CI] 1.51–1.90, I² = 89.9%). Subgroup analysis by adjusted number of key risk factors for osteoporotic fracture showed a greater increased fracture risk in those adjusted for fewer than four variables (adjusted OR = 1.83, 95% CI 1.57–2.13, I² = 88.0%) than those adjusted for four or more variables (adjusted OR = 1.38, 95% CI 1.27–1.49, I² = 46.1%). The pooled ORs anatomical site of fracture in the hip/femur, spine, and wrist/forearm were 2.06 (95% CI 1.84–2.30, I² = 62.3%), 1.34 (95% CI 1.13–1.59, I² = 48.5%), and 1.51 (95% CI 1.26–1.82, I² = 76.6%), respectively. Subgroup analysis by exposure duration revealed that the strength of the association decreased with a longer window of SSRI administration before the index date. The risk of fracture was greater within 6 weeks before the index date (adjusted OR = 3.83, 95% CI 1.96–7.49, I² = 41.5%) than 6 weeks or more (adjusted OR = 1.60, 95% CI 0.93–2.76, I² = 63.1%). Fracture risk associated with SSRI use may have a significant clinical impact. Clinicians should carefully consider bone mineral density screening before prescribing SSRIs and proper management for high‐risk populations. © 2012 American Society for Bone and Mineral Research.     

Single-fulcrum laparoscopic cholecystectomy: a single-incision and multi-port technique

Background: Single-incision laparoscopic cholecystectomy (LC) is still technically demanding and usually requires specially designed instruments. This article describes our own technique, a single-fulcrum LC using only standard ports and instruments. Methods: Between March 2009 and December 2010, 130 consecutive patients, all scheduled to undergo elective LC, underwent this single-fulcrum LC for benign gallbladder disease. Perioperative surgical outcomes were retrospectively evaluated. Results: One hundred and ten patients (84.6%) underwent successful single-fulcrum LC, and 20 patients (15.4%) were converted to conventional surgery (n= 18) or required additional trocars (n= 2) during the procedure because of umbilical hernia (n= 3), severe inflammation or adhesion (n= 9), impacted cystic duct stone (n= 3), anatomical anomaly (n= 3) and iatrogenic injury (n= 2). Two intraoperative complications (iatrogenic injury) were securely managed using additional trocars and there was no post-operative morbidity or mortality. This single-fulcrum LC could be performed with comparable cost to conventional LC, and the sequential operative time showed reasonable learning curve. Conclusion: Single-fulcrum LC is feasible, safe and quite reproducible. The surgical wound can be dramatically reduced at a similar cost to conventional LC. It may be an alternative procedure for most uncomplicated benign gallbladder disease.     

Development of flattening and apparent fragmentation following ischemic necrosis of the capital femoral epiphysis in a piglet model

BACKGROUND: The repair response that follows ischemic necrosis of the immature femoral head and the biological processes that are responsible for the development of femoral head deformity and fragmentation have not been clearly defined. A piglet model was used to study the radiographic and histopathologic changes that occur prior to and during the development of femoral head deformity and fragmentation following ischemic necrosis. METHODS: Twenty-five male piglets were studied. A nonabsorbable ligature was placed tightly around the femoral neck to disrupt the blood supply to the capital femoral epiphysis. The animals were killed three days to eight weeks following the induction of ischemia. Radiographs of whole and sectioned femoral heads were made, and the radiographic findings were correlated with the histopathologic changes observed in the specimens. RESULTS: Mild femoral head flattening was observed by four weeks after the induction of ischemia, and severe flattening and fragmentation were observed by eight weeks. The predominant repair response observed following revascularization was osteoclastic bone resorption. Prior to the development of flattening, a large area of osteoclastic bone resorption was observed in the central region of the femoral head. Many osteoclasts were present along the revascularization front, which we believe were responsible for active resorption of the necrotic trabecular bone. Appositional new-bone formation, the hallmark of the repair response in adult ischemic necrosis, was not observed in the area of bone resorption. Instead, the areas of resorbed bone were replaced with a fibrovascular tissue that persisted for up to eight weeks. Appositional new-bone formation was observed, but it was limited to small areas in which revascularization was not followed by osteoclastic bone resorption and in which necrotic trabecular bone was still present. The simultaneous presence of the areas of bone resorption and new-bone formation contributed to the fragmented radiographic appearance of the femoral head. CONCLUSIONS: The predominant repair response observed in the piglet model of ischemic necrosis was osteoclastic bone resorption. The early bone loss, the lack of new-bone formation, and the persistence of fibrovascular tissue in the areas of bone resorption compromised the structural integrity of the femoral head and produced progressive femoral head flattening over time. The repair response was different from that observed in femoral heads removed from adult patients with ischemic necrosis and from that observed in the adult rabbit model of ischemic necrosis. Clinical Relevance: The piglet model of ischemic necrosis may be useful for the investigation of the biological processes that lead to the development of femoral head deformity following ischemic necrosis of the immature femoral head.     

Retropulsion of intervertebral discs associated with traumatic hyperextension of the cervical spine and absence of vertebral fracture: an uncommon mechanism of spinal cord injury

STUDY DESIGN: Case report of a 68-year-old male who sustained cervical trauma following a bodysurfing accident. OBJECTIVE: To describe the pathology of a relatively uncommon mechanism of injury involving extradural cord compression associated with traumatic disc protrusion and herniation, following a cervical hyperextension injury in which there was no vertebral fracture or residual subluxation. SETTING: Department of Neuropathology, Royal Perth Hospital, West Australia. METHOD: Postmortem pathology report. RESULTS: Evidence of multiple ruptures of anterior longitudinal ligament with posterior intervertebral disc herniation and three discrete foci of central cord hemorrhage. CONCLUSION: Observations are consistent with cervical extension injury and an injury vector that involves intense axial loading sufficient to cause multiple disc failures, disc herniation and retropulsion leading to extradural disc compression and cord hemorrhage.     

Efficacy of 3-dimensional endorectal ultrasonography compared with conventional ultrasonography and computed tomography in preoperative rectal cancer staging

BACKGROUND: This study was performed to verify reports of the decreased accuracy of endorectal ultrasonography (EUS) in preoperative staging of rectal cancer, and to compare the efficacy of 3-dimensional (3D) EUS with that of 2-dimensional (2D) EUS and computed tomography (CT). METHODS: Eighty-six consecutive rectal cancer patients undergoing curative surgery were evaluated by 2D EUS, 3D EUS, and CT scan. RESULTS: The accuracy in T-staging was 78% for 3D EUS, 69% for 2D EUS, and 57% for CT (P < .001-.002), whereas the accuracy in evaluating lymph node metastases was 65%, 56%, and 53%, respectively (P < .001-.006). Examiner errors were the most frequent cause of misinterpretation, occurring in 47% of 2D EUS examinations and in 65% of 3D EUS examinations. By eliminating examiner errors, the accuracy rates in T-staging and lymph node evaluation could be improved to 88% and 76%, respectively, for 2D EUS, and to 91% and 90%, respectively, for 3D EUS. Conical protrusions along the deep tumor border on 3D images were correlated closely with infiltration grade, advanced T-stage, and lymph node metastasis. CONCLUSIONS: We found that 3D EUS showed greater accuracy than 2D EUS or CT in rectal cancer staging and lymph node metastases. Concrete 3D images based on tumor biology appear to provide more accurate information on tumor progression.     

Risk Factors and Clinical Outcome for Anastomotic Leakage After Total Mesorectal Excision for Rectal Cancer

BACKGROUND: Anastomosis leakage is a major complication of rectal surgery. The aim of this study was to identify risk factors for anastomotic leakage after low anterior resection (LAR) in rectal cancer patients and study its impact on long-term prognosis and disease-free survival and overall survival in rectal cancer patients. METHODS: Consecutive patients who underwent rectal resection with primary anastomosis below the pelvic peritoneal reflexion for rectal cancer between October 1996 to February 2006 were included. RESULTS: Anastomosis leakage after LAR occurred in 51 patients (4.0%). The median time to leakage was 4 days (range = 2-30 days). In univariate analysis, gender, level of anastomosis less than 4 cm, preoperative concomitant chemoradiation (CCRT), and length of operation greater than 120 min were significantly associated with anastomosis leakage. In a multivariate analysis, gender (p = 0.041; relative risk = 2.007; 95% CI = 1.030-3.912) and preoperative CCRT (p = 0.003; relative risk = 2.861; 95% CI = 1.417-5.778) were identified as independent prognostic factors. The overall survival of the nonleakage group and the leakage group was 80.2% and 64.9%, respectively (p = 0.170). The 5-year disease-free survival rates were not significantly different between the nonleakage and leakage groups (78.1% vs. 65.9%, p = 0.166). CONCLUSIONS: The incidence of anastomotic leakage after low anterior resection is relatively low. Male gender and preoperative CCRT were associated with increased risk for anastomotic leakage after rectal cancer surgery. No effect of anastomosis leakage on local recurrence was found in this series.     

Protective role of programmed death 1 ligand 1 (PD-L1)in nonobese diabetic mice: the paradox in transgenic models

OBJECTIVE—Coinhibitory signals mediated via programmed death 1 (PD-1) receptor play a critical role in downregulating immune responses and in maintaining peripheral tolerance. Programmed death 1 ligand 1 (PD-L1), the interacting ligand for PD-1, widely expressed in many cell types, acts as a tissue-specific negative regulator of pathogenic T-cell responses. We investigated the protective potential of PD-L1 on autoimmune diabetes by transgenically overexpressing PD-L1 in pancreatic β-cells in nonobese diabetic (NOD) mice.RESEARCH DESIGN AND METHODS—We established an insulin promoter–driven murine PD-L1 transgenic NOD mouse model to directly evaluate the protective effect of an organ-specific PD-L1 transgene against autoimmune diabetes. Transgene expression, insulitis, and diabetic incidence were characterized in these transgenic NOD mice. Lymphocyte development, Th1 cells, and regulatory T-cells were analyzed in these transgenic mice; and T-cell proliferation, adoptive transfer, and islet transplantation were performed to evaluate the PD-L1 transgene–mediated immune-protective mechanisms.RESULTS—The severity of insulitis in these transgenic mice is significantly decreased, disease onset is delayed, and the incidence of diabetes is markedly decreased compared with littermate controls. NOD/SCID mice that received lymphocytes from transgenic mice became diabetic at a slower rate than mice receiving control lymphocytes. Moreover, lymphocytes collected from recipients transferred by lymphocytes from transgenic mice revealed less proliferative potential than lymphocytes obtained from control recipients. Transgenic islets transplanted in diabetic recipients survived moderately longer than control islets.CONCLUSIONS—Our results demonstrate the protective potential of transgenic PD-L1 in autoimmune diabetes and illustrate its role in downregulating diabetogenic T-cells in NOD mice.Programmed death 1 (PD-1) is an immunoreceptor of the CD28/CTLA-4 family whose expression is induced in activated T- and B-cells and in macrophages (1,2). PD-1 has two cytoplasmic tyrosine motifs: one an immunoreceptor tyrosine-based inhibition motif and the other an immunoreceptor tyrosine-based switch motif (ITSM). On interaction of PD-1 with its ligands PD-L1 (B7-H1) or PD-L2 (B7-DC), the tyrosine-phosphorylated ITSM of PD-1 recruits a src homology 2 domain–containing tyrosine phosphatase 2, which mediates the dephosphorylation signaling and reduces lymphocyte activation (3). PD-1^−/− mice on different genetic backgrounds develop distinct autoimmune phenotypes, such as lupus-like glomerulonephritis/arthritis in C57Bl/6 (B6) mice or anticardiac troponin I–mediated dilated cardiomyopathy in Balb/c mice (4,5). These observations indicate that PD-1 is a critical negative regulator of lymphocyte activation and that the phenotype of PD-1 deficiency–induced autoimmunity is highly influenced by other genetic factors.Murine PD-L1 is expressed on many cell types, including stromal cells within many organs, but PD-L2 expression is much more restricted, occurring mainly in dendritic cells, activated monocytes, and macrophages (6,7). Although accumulating data indicate that both PD-L1/PD-1 and PD-L2/PD-1 signals can suppress T-cell proliferation and effector function by blocking cell cycle progression and cytokine production, signaling through PD-L1 interaction is more potent than that through PD-L2 (8). This is consistent with the observations that cytokine production, cytotoxic activity, and clonal expansion were significantly enhanced in T-cells and antigen-presenting cells from PD-L1^−/− mice, compared with cells from wild-type or PD-L2^−/− mice (9,10). Moreover, the PD-L1^−/− mice revealed an increased susceptibility to the induction of autoimmune diseases, such as experimental allergic encephalomyelitis (9), strongly suggesting a protective role of tissue PD-L1 in the maintenance of immune tolerance. Furthermore, treatment of nonobese diabetic (NOD) mice with a combination of agonistic PD-L1.Ig fusion protein and monoclonal antibodies (mAbs) to CD154 induced long-term islet allograft survival, whereas the inhibition of PD-L1–mediated signals by blocking antibody exacerbated autoimmune diabetes (11). Based on these findings, we hypothesize that transgenic expression of PD-L1 in an islet-specific manner may help in preventing T-cell–mediated islet destruction in NOD mice.To investigate the preventive and/or therapeutic potential of PD-L1 in autoimmune diabetes, we generated transgenic NOD mice overexpressing PD-L1 under control of an insulin promoter. Although a recent report demonstrated that local expression of transgenic PD-L1 on β-cells of B6 mice unexpectedly promotes organ-specific autoimmunity and transplant rejection (12), we hypothesized that overexpression of PD-L1 on islet cells in NOD mice would enhance inhibitory signaling through the PD-1–PD-L1 interaction and protect islet cells from lymphocyte attack. Our results demonstrate that transgenic PD-L1 on islet cells significantly ameliorates the severity of insulitis and incidence of diabetes in NOD mice. Interestingly, our results also indicate that local transgene expression not only protects islets in situ but also mediates a peripheral tolerance. Moreover, transgenic islets transplanted in diabetic recipients survived moderately longer than control islets. Overall, we demonstrate for the first time the preventive potential of transgenic PD-L1 in autoimmune diabetes and provide a theoretical basis for organ-specific genetic manipulation for disease prevention.     

主动脉支架植入术后少见并发症及其治疗

目的探讨主动脉腔内支架治疗后少见井发症及其治疗方法。方法 回顾性分析5例主动脉疾病患者的特点和行主动脉支架治疗后所出现的并发症。结果4例患者在支架植入后出现的并发症经手术或再次支架治疗均获缓解,1例患者死亡。结论主动脉腔内支架植入的并发症与传统手术并发症截然不同．术者应具备良好的手术技巧和介入治疗水平,以及时治疗可能出现的并发症。