Laparoscopic appendicectomy has been shown to be a safe alternative to open appendicectomy [1] [2] [3] . However some inherent disadvantages of this procedure have prohibited its universal acceptability [4]. We have devised a “two-port modified technique” (Figure [1]) for laparoscopic-assisted appendicectomy (LAA) which we believe addresses these problems.
Abstract Background Intimal angiogenesis is a recognized feature of the atherosclerotic process. It has been described in the context of unstable coronary atherosclerotic lesions. The aims of this study were to assess the association between angiogenesis in atherosclerotic plaques and microscopic features of plaque instability, in particular intraplaque haemorrhage. Methods Consecutive patients undergoing carotid endarterectomy for carotid stenosis were included in the study. Endarterectomy specimens were examined and divided into their constituent atherosclerotic lesions. Histological sections were prepared and stained with haematoxylin and eosin, and immunohistochemically with an endothelial cell marker (CD34). Each lesion was classified according to the American Heart Association classification of atherosclerotic lesions. The size of plaque haemorrhage was measured in transverse histological sections using computerized image analysis. Haemorrhagic lesions were classified according to the size of haemorrhagic area (under 50 per cent of section area; over 50 per cent of section area). Microvessel counts were performed in CD34-stained sections at × 400 magnification and were verified with computerized image analysis. The Kruskal–Wallis test was used to study the differences in microvessel count in different atherosclerotic plaque types. Results A total of 239 atherosclerotic lesions from 73 patients was available for analysis, of which 73 were early lesions, 74 were raised fibroatheromas and 92 were unstable atherosclerotic plaques. One hundred and fifty lesions were not haemorrhagic; 89 exhibited intraplaque haemorrhage, of which 28 involved less than 50 per cent of the plaque section area. In 61 lesions the haemorrhage area was over 50 per cent of the section area. There were higher microvessel counts in plaques containing more than 50 per cent haemorrhage (median 277 (range 43–467)) compared with those containing less than 50 per cent (172 (57–372)) and non-haemorrhagic plaques (81 (7–389)) (P < 0·0001). Higher microvessel counts were observed in unstable atherosclerotic lesions (median 252 (range 43–467)), compared with stable fibroatheromas (106 (14–302)) and early atherosclerotic lesions (55 (7–237)) (P < 0·0001). Conclusion There are strong associations between plaque vascularity and presence and size of haemorrhage within atherosclerotic lesions, as well as features of plaque instability. This finding highlights the likely significance of these new blood vessels in the development of plaque instability and subsequent risk of stroke.
The authors report a 51-year-old female primary care physician who attended the emergency medical department with pleuritic chest pain, shortness of breath and associated tachycardia. She had 6 weeks previously been admitted and treated for similar features with the diagnosis of pulmonary emboli made from a positive ventilation–perfusion scan. CT scanning confirmed the diagnosis of multiple bilateral pulmonary emboli but no abdominal or pelvic pathology and without evidence of deep venous thrombosis. Further clinical assessment found generalised hyperflexibility and swelling of the left popliteal region. Duplex ultrasonography followed by venography confirmed a 5-cm unilateral saccular aneurysm of the above knee popliteal vein containing central thrombus. A temporary IVC filter (Cook, Tulip) was placed and primary aneurysmectomy was performed through a posterior approach. Popliteal venous aneurysms are rare but can present at any age and are associated with wall weakness from many causes. Pulmonary embolism is the most frequent presentation and is not dependant on visualized clot on imaging. As anticoagulation may be ineffective in preventing pulmonary embolism it is recommended all patients should undergo surgical repair.
The aim of our work was to study the relationship between Doppler ultrasound velocity measurements and the presence of histologic features of plaque instability in carotid atherosclerosis, in particular, intraplaque hemorrhage (IPH). Consecutive patients undergoing carotid endarterectomy in a one-year period were included. All patients were examined by duplex ultrasonography and carotid angiography. Endarterectomy specimens were examined histologically for features of plaque instability. The quantity of IPH was measured by digital image analysis. The associations between Peak Systolic Velocity (PSV), end-diastolic velocity (EDV), degree of ICA stenosis, shape and length of the lesion and the features of plaque instability and quantity of IPH were assessed. Seventy-four patients (20 asymptomatic, 54 symptomatic) were included. PSV was independently associated with the presence of significant IPH [p < 0.001, OR = 1.04 (95% CI = 1.01–1.06)], as was the degree of angiographic ICA stenosis [p < 0.05, OR = 0.98 (95% CI = 0.92–1.6)]. Neither EDV nor the shape of the lesion was associated with IPH (p = 0.26 and p = 0.38, respectively). A close correlation was observed between PSV and the quantity of IPH (r 2 = 0.68, p < 0.0001). A significant association was observed between PSV and the presence of plaque ulceration (p < 0.05); however, this was not found to be independent of the quantity of IPH and the degree of ICA stenosis [p = 0.17, OR = 1.28 (95% CI = 0.6–2.44)]. PSV at the site of ICA stenosis appears to be associated with the quantity of intraplaque hemorrhage, independent of the angiographic degree of ICA stenosis. We propose that the role of Doppler velocity measurements extends beyond measurement of the degree of ICA stenosis. Increased ICA peak systolic velocity by itself may be an indicator of atherosclerotic plaque instability.
Spontaneous dissection of the carotid artery is an important differential diagnosis to consider in cases of early onset stroke. Its natural history is variable, ranging from a benign course to permanent disability or death. Dissection usually occurs in the cervical portion of the artery, rendering it amenable to surgical therapy. These issues are compounded if there is intrapetral extension, with associated mortality rates up to 75%. The authors describe such a case of spontaneous dissection and discuss imaging and therapy issues that result.
Objective: The aim of this study was to develop a new international classification of acute pancreatitis severity on the basis of a sound conceptual framework, comprehensive review of published evidence, and worldwide consultation.
Background: The Atlanta definitions of acute pancreatitis severity are ingrained in the lexicon of pancreatologists but suboptimal because these definitions are based on empiric descriptions of occurrences that are merely associated with severity.
Methods: A personal invitation to contribute to the development of a new international classification of acute pancreatitis severity was sent to all surgeons, gastroenterologists, internists, intensive medicine specialists, and radiologists who are currently active in clinical research on acute pancreatitis. The invitation was not limited to members of certain associations or residents of certain countries. A global Web-based survey was conducted and a dedicated international symposium was organised to bring contributors from different disciplines together and discuss the concept and definitions.
Result: The new international classification is based on the actual local and systemic determinants of severity, rather than descriptions of events that are correlated with severity. The local determinant relates to whether there is (peri)-pancreatic necrosis or not, and if present, whether it is sterile or infected. The systemic determinant relates to whether there is organ failure or not, and if present, whether it is transient or persistent. The presence of one determinant can modify the effect of another such that the presence of both infected (peri) pancreatic necrosis and persistent organ failure have a greater effect on severity than either determinant alone. The derivation of a classification based on the above principles results in 4 categories of severity - mild, moderate, severe, and critical.
Conclusions: This classification is the result of a consultative process amongst pancreatologists from 49 countries spanning North America, South America, Europe, Asia, Oceania, and Africa. It provides a set of concise up-to-date definitions of all the main entities pertinent to classifying the severity of acute pancreatitis in clinical practice and research. This ensures that the determinant-based classification can be used in a uniform manner throughout the world.
New blood vessels in atherosclerotic lesions are postulated to be responsible for plaque instability by acting as conduits for inflammatory cells. This study assessed the association between macrophage content of plaque caps of carotid atherosclerotic lesions, plaque vascularity, and endothelial-cell activation within these blood vessels. Carotid endarterectomy specimens from patients who underwent endarterectomy for carotid occlusive disease (ten symptomatic, six asymptomatic) were examined. Sequential transverse sections were obtained and were stained conventionally and immunohistochemically with CD 34 (an endothelial-cell marker) and CD 68 (a macrophage marker), as well as VCAM-1 and ICAM-1 (markers of endothelial-cell activation). Microvessel and macrophage counts were performed for the whole plaque and the plaque cap respectively. The differences in microvessel density, macrophage content, and ICAM-1 and VCAM-1 expression, between symptomatic and asymptomatic patients and in different plaque types were examined, as was the association between microvessel density and microvessel content of atherosclerotic lesions. Higher microvessel counts were observed in patients with symptomatic carotid occlusive disease (p < 0.01). Higher ICAM-1 and VCAM-1 expression was noted in new blood vessels in plaques obtained from patients with symptomatic carotid occlusive disease, compared with asymptomatic patients (p < 0.001 and p < 0.01 respectively). A close association was observed between macrophage content of the plaque cap and microvessel counts in atherosclerotic lesions (p < 0.0001), as well as ICAM-1 (p < 0.001) and VCAM-1 (p < 0.001) expression, in these microvessels. This study highlights the significance of neovascularity and endothelial-cell activation in the evolution of symptomatic carotid occlusive disease. Furthermore, it points to a relationship between the inflammatory process and angiogenesis within the plaque, which may be mediated through endothelial-cell activation.
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