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BACKGROUND: Despite their well-recognised shortcomings, haemodialysis catheters (HDCs) remain an important form of haemodialysis access for many patients. There are several HDCs commercially available, each differing considerably in design, which is known to significantly influence performance and survival. We sought to determine which of two tunnelled HDCs, DuraMax® (Angiodynamics, NY, USA) or SplitCath® (MedComp, PA, USA) delivers the best performance, safety and reliability for dialysis patients. METHODS: Eighty-six patients were prospectively randomised to receive either DuraMax® (DM) or SplitCath® (SC). Outcomes included: (i) mean flow rates (mL/min) averaged over the first 10 weeks of dialysis, and urea reduction ratio (URR); and (ii) long-term catheter survival with appraisal of any events leading to catheter dysfunction and early removal. RESULTS: Median flow rates (interquartile range) in the DM and SC groups were 321 (309-343) and 309 (294-322) mL/min, respectively (p = 0.002). URR values for the DM and SC groups were 71 (65-76) and 74 (70-78), respectively, (p = 0.094). There was no significant difference in long-term survival or frequency of incidents that required early HDC removal (9/43 in the DM group, 5/43 patients SC). A slightly higher incidence of HDC dislodgement was noted in the DM group, although this study was not statistically powered to determine its significance. CONCLUSIONS: We conclude that DM yields slightly higher flow rates in the first 10 weeks of dialysis, and a similar low incidence of complications and long-term survival for both DM and SC HDCs.

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We report a case of a 65-year-old female with a recurrent right parotid pleomorphic adenoma (PA) 24 years after initial surgical excision. Positron-emission tomography (PET) and computed tomography (CT) demonstrated an unusual suspicious FDG-avid erosive rim enhancing mass centered in the right supraspinatus muscle. Cytology from CT-guided aspiration of the mass was consistent with a histologically benign PA, and the patient was diagnosed with metastatic pleomorphic adenoma (MPA). The patient later developed diffuse pulmonary metastases and died within 3 months. MPA, although rare, is recognised as a potentially lethal malignant complication of recurrent or longstanding benign PA. As no biochemical or genetic parameters are predictive of malignant change, patients presenting with recurrent PA should be considered for screening for metastatic disease.

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INTRODUCTION: Acute mesenteric ischaemia (AMI) continues to have a high mortality, ranging from 60 to 80%. PRESENTATION OF CASE: A 78-year-old male presented with a 20-hour history of abdominal pain, secondary to a superior mesenteric artery (SMA) thromboembolic occlusion diagnosed on computed tomography (CT) angiography. Following confirmation of bowel viability at laparotomy, endovascular intervention using combined thrombolysis, angioplasty and thromboaspiration was performed. Despite successful recanalisation of the occlusion, his condition continued to deteriorate fatally due to progressive sepsis. DISCUSSION: We discuss the role of biphasic CT in diagnosis of AMI, and review the evidence for endovascular interventions now increasingly used in the emergent management of thromboembolic AMI. CONCLUSION: Early diagnosis using CT angiography is essential, as it is highly sensitive in detecting a visceral arterial occlusion. However, laparotomy is often required to accurately determine bowel viability and the need for resection. Endovascular interventions appear to be effective alternatives to open surgery with appropriate patient selection.

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Corticosteroid joint injections are perceived as being an effective treatment for symptomatic knee osteoarthritis, with a very low risk of complications. While the procedure is often performed in secondary care by orthopaedic surgeons and rheumatologists (and trainees in either specialty), the role of general practitioners (GPs) in chronic disease management has long existed with joint injections also frequently performed in primary care. The perception that serious complications from corticosteroid knee joint injections are rare and that their benefits in treating symptomatic knee osteoarthritis significantly outweigh the risks has not been well addressed. We present a case of a 71-year-old obese female who presented to her general practitioner (GP) with worsening left knee pain and radiographic changes consistent with osteoarthritis. She was administered a corticosteroid joint injection, which gave minimal relief, and over the next few days resulted in worsening severe pain, erythema and swelling. She returned to the GP who commenced oral antibiotics and referred her to casualty. A large knee abscess was diagnosed and intravenous antibiotics were commenced. The patient was admitted under the orthopaedic surgeons with her treatment consisting of multiple surgical procedures over a prolonged duration. Although lengthy, her postoperative recovery was unremarkable. Based on this case report and our review of the literature, we highlight the potential complications associated with corticosteroid knee joint injections and suggest certain patients for whom we would recommend secondary referral before any intervention in primary care.

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PURPOSE: Corticosteroid knee injections are being increasingly used in the conservative management of knee osteoarthritis. The procedure is usually performed in secondary care by orthopaedic surgeons and rheumatologists, but as the role of general practitioners in chronic disease management expands, joint injections are now frequently being performed in primary care. It is commonly perceived amongst clinicians that the benefits of corticosteroid knee joint injections in treating symptomatic knee osteoarthritis significantly outweigh the risks of complications. METHODS: The evidence in the literature for the benefits, accuracy, safety and complications of corticosteroid knee injections in osteoarthritis is reviewed. The perception that serious complications are rare is addressed, and the incidence of infectious complications is estimated. RESULTS AND CONCLUSIONS: Short-term symptomatic relief is the only evidence-based benefit of corticosteroid injection of an osteoarthritic knee. Accurate intra-articular placement is not achieved in up to 20% of injections and varies considerably with the anatomical approach used. There is no evidence that a medial approach is more accurate. The incidence of serious infectious complications following knee joint injections ranges widely, and may be as high as 1 in 3,000 and potentially far higher in high-risk patients for whom specialist management is advised.

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Nitric oxide (NO) released from mechanosensitive bone cells plays a key role in the adaptation of bone structure to its mechanical usage. Despite its importance in bone, the mechanisms involved in NO mechanotransduction at the cellular level remain unknown. Using combined atomic force microscopy and fluorescence microscopy, we report both stimulation and real-time monitoring of NO responses in single osteoblasts induced by application of quantified periodic indenting forces to the osteoblast membrane. Peak forces ranging from 17 to 50 nN stimulated three distinct NO responses in the indented osteoblasts: (1) a rapid and sustained diffusion of NO from the perinuclear region, (2) diffusion of NO from localized pools throughout the osteoblast, and (3) an initial increase and subsequent drop in intracellular NO. Force-indentation characteristics showed considerable interosteoblast variation in elasticity. NO responses were associated with application of force to more rigid membrane sites, suggesting cytoskeletal involvement in mechanotransduction.

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Fluid flowing through the bone porosity might be a primary stimulus for functional adaptation of bone. Osteoblasts, and osteocytes in particular, respond to fluid flow in vitro with enhanced nitric oxide (NO) and prostaglandin E(2) (PGE(2)) release; both of these signaling molecules mediate mechanically-induced bone formation. Because the cell cytoskeleton is involved in signal transduction, we hypothesized that the pulsatile fluid flow-induced release of NO and PGE(2) in both osteoblastic and osteocytic cells involves the actin and microtubule cytoskeleton. In testing this hypothesis we found that fluid flow-induced NO response in osteoblasts was accompanied by parallel alignment of stress fibers, whereas PGE(2) response was related to fluid flow stimulation of focal adhesions formed after cytoskeletal disruption. Fluid flow-induced PGE(2) response in osteocytes was inhibited by cytoskeletal disruption, whereas in osteoblasts it was enhanced. These opposite PGE(2) responses are likely related to differences in cytoskeletal composition (osteocyte structure was more dependent on actin), but may occur via cytoskeletal modulation of shear/stretch-sensitive ion channels that are known to be dominant in osteocyte (and not osteoblast) response to mechanical loading.

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Bone undergoes continuous remodeling in response to mechanical loading. However, the underlying mechanisms by which bone cells respond to their changing mechanical environment, that is, strain in the load-bearing matrix or fluid flow through the canalicular network, are not well understood. It has been established in vitro that bone cells respond differently to substrate strain and fluid shear stress treatments. Uncovering the mechanical basis of these differences represents a significant challenge to our understanding of cellular mechanotransduction and bone remodeling. To investigate this problem, we developed a biomechanical model of an adherent cell, to test the hypothesis that bone cells respond differently to 0.6 Pa fluid shear stress and 1,000 mu(epsilon) substrate strain stimulation because of qualitative and quantitative differences in the cellular deformation caused. Fluid shear stress loading conditions resulted in maximum displacements at the apical surface of the cell approximately 8 times higher than those due to strain at the cell-substrate interface and also caused higher stressing of all parts of the cell. Significantly, this shows that the deforming effects of fluid shear stress and strain on a cellular level are qualitatively different, which may provide a basis for explaining differences in bone cell responses to both stimuli as reported in several studies. Although our approach to modeling the morphology and complex physical environment of an adherent cell is certainly simplified, our results do show independent roles for fluid flow and strain as mechanical stimuli and highlight the importance of deformation on a cellular level in bone physiology.

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