Definition/Zh

• Original, v.1.1: English
• Translations, v.1.1: العربية • български • català • čeština • Deutsch • Ελληνικά • Esperanto • español • فارسی • français • galego • hrvatski • italiano • 한국어 • македонски • मराठी • norsk bokmål • Nederlands • norsk nynorsk • polski • português • română • русский • slovenčina • slovenščina • svenska • Tiếng Việt
• Translations, v.1.0 (update/review pending): suomi
• More in progress

Stable versionThis is stable version 1.0 of the definition. The version number will be updated as the definition develops. The editable version of the definition can be found at Definition/Unstable. See authoring process for more information, and see translations if you want to contribute a version in another language.

摘要

这份文件所定义的“自由文化作品”（Free Cultural Works）是指可以被任何人自由地研究、使用、复制和/或修改，并且用于任何目的的作品或表现形式。它还阐述了某些可以被接受的限制，以尊重或保护这些基本的自由。该定义还区分了与“自由作品”（free works）之间的差别，以及自由许可协议在一个处于法律保护状态的自由作品上的使用。这个定义本身并不是一个许可协议；它是一个工具，用以确定一个作品或协议是否可以被视为是“自由”的。

前言

社会与技术的进步，使得越来越多的人可以“获取、创建、修改、出版和分发”各类作品：艺术作品、科教资料、软件、文章，总之就是“任何可以通过数字形式呈现的作品”。Many communities have formed to exercise those new possibilities and create a wealth of collectively re-usable works.

大多数的作者，无论活跃于哪个领域，无论是业余还是专业，都对这样一种生态系统很感兴趣：在其中作品可以被传播、重制和创造性的衍生。这有利于作品的重制和衍生，从而丰富我们的文化。

为了保证这个生态系统的优秀机能，原创作品应该是自由的。我们所说的“自由”是指：

• 自由的使用作品并从使用中获益
• 自由的学习作品并从中获得知识
• 自由的制作和分发全部或部分的资料或表达方式
• 自由的修改和改进并分发衍生作品

这种自由应该对任何人，在任何地点、任何时间都有效。作品在这方面的使用不应该受到限制。创意是利用现有资源的行为方式，以前在某种程度上还未设想过。

但是在很多国家这种自由都被一种称为“著作权法”的法律所打压。他们视作者为神圣的创作者，并且给与他们对“内容”如何被重制的独家垄断权。这种垄断阻碍了文化的繁荣，他并未对作者的经济状况有所帮助，反而恰恰保障了强大的出版社的商业模式。

法律虽然这样，但是作者可以为他们的作品自由选择一种称之为自由许可的法律文件。对作者而言，选择将作品在自由许可下授权并不意味着丧失一切权利，但是它提供了上面列出的任何一种自由。

这是非常重要的。任何作品声明自由提供（上述的自由）不会有任何风险。这也是我们为今后的原创作品和许可提供一个确切的自由定义的原因。

译文

Ascites due to right atrial myxoma in a haemodialysis patient

                    Anindya Banerjee1 and Andrew Davenport1

Abstract

Background Persistent fluid overload in patients on renal replacement therapy despite good dialysis adequacy or obvious cardiac dysfunction should prompt a search for rarer causes.

Case presentation We report here a rare cause of persistent peripheral oedema and ascites in a well-dialysed patient. CT scanning revealed a right atrial myxoma that was later confirmed on an echocardiogram.

Conclusion Fluid overload states are common in patients on dialysis. Common causes are inadequacy of dialysis and non-compliance. Where aetiology is not easily apparent further investigations into rarer causes should be sought. Background Cardiovascular disease is responsible for about 50% of deaths in patients with end stage renal disease on dialysis. Such patients often show evidence of fluid overload. This is usually attributable to poor fluid removal, often associated with inadequate dialysis, and/or congestive cardiac failure. This can often be managed by a period of intensive dialysis with appropriate ultrafiltration [1]. Where a cause for fluid overload is not readily identifiable however, and fails to respond to increased dialysis, it is important to look for other contributory factors. We report here a case of right atrial myxoma in a patient on haemodialysis who presented with features of congestive cardiac failure, in particular, ascites that failed to respond to increased dialysis therapy.

Case report A 75 year old patient with end stage renal failure secondary to diabetes and hypertension who had been regularly dialyzed for 11 years presented with several weeks history of reduced appetite, weight loss, tiredness and nausea. He had also noted abdominal distension, and more recently ankle swelling.

On examination he was apyrexial, blood pressure 135/69 mmHg, an indeterminate jugular venous pressure (due to numerous previous central venous dialysis catheters), normal heart and chest sounds. He had signs of congestive cardiac failure with bilateral oedema to the mid calf and a 3 cm smooth hepatomegaly with moderate ascites.

Blood tests showed a haemoglobin of 13.8 g/dl, an albumin of 36 g/dl, elevated alkaline phosphatase of 418 iu/L (normal < 120 iu/l), gamma glutamyl-transferase 383 u/l (normal < 55 u/l) and C reactive protein of 62 mg/L (normal < 5 mg/l). Transaminases were normal with aspartate transaminase of 43 u/l and alanine transaminase 32 (normal < 45 u/l). Hepatitis B core antibody had been positive for many years.

He was well dialysed through a transposed native brachio-basilic fistula with a urea reduction ratio of 70% and Kt/v > 1.2. We attempted to reduce his dry weight over a few dialysis sessions without any success in reducing ascites.

The persistent ascites prompted further tests. Ascitic fluid tap revealed a sterile transudate with protein concentration of 29 g/dl (serum albumin 34 g/dl). Abdominal ultrasound scan showed moderate ascites with normal liver architecture without biliary dilatation or parenchymal lesions.

A diagnostic computed tomogram of the chest was obtained (fig 1). This showed a soft tissue mass, 5 cm × 4 cm within the right atrium which was confirmed on a repeat echocardiogram to be a right atrial myxoma. There was no evidence of a mass from an earlier echocardiogram in 2002, which reported an ejection fraction of 63% with mild tricuspid regurgitation and moderate left ventricular hypertrophy.

Figure 1 

CT scan showing soft tissue mass within atrium which is isodense with myocardium and appearing to arise from the atrial wall by a stalk.

Although open-heart surgery was planned, he had a sudden cardiac death from an electrical-mechanical dissociation with no detectable cardiac output, probably related to occlusion of the tricuspid valve.

Discussion Right atrial myxomas constitute 25% of the exceedingly rare group of patients with primary tumours of the heart (incidence 0.001–0.33%) [2,3]. Symptoms vary from constitutional to thrombo-embolic and obstructive, the most common being congestive cardiac failure [4]. de novo primary cardiac tumours in patients on chronic haemodialysis as in our case however are rare and have not been reported before. There are reports though of right atrial masses from organised clots or thrombus in longstanding haemodialysis patients dialysing via internal jugular semi-permanent catheters [5]. Persistent ascites that does not respond to aggressive fluid removal by daily haemodialysis and ultrafiltration [1] could be a clue to such rarer causal factors.

Pericardial effusion could be another cause of fluid retention with ascites particularly in an inadequately dialysed patient, but also following an intercurrent illness or as part of a connective tissue disease in a well-dialysed patient. Uraemic pericarditis describes pericarditis before renal replacement therapy or within 8 weeks of initiation, whereas dialysis pericarditis occurs usually after ≥ 8 weeks of dialysis. The reported incidence of dialysis pericarditis ranges from 2 to 21% [6].

Our patient had been well dialyzed prior to admission and did not respond to a planned reduction in dry weight. He did have a generalized inflammatory state, characterized by weight loss and elevated C-reactive protein. Constitutional features such as fever and weight loss are related to cytokines, including interleukin-6 released from atrial myxomas [7].

Transthoracic echocardiography is usually the initial diagnostic test in patients with a suspected cardiac mass. However, its small field of views and insufficient acoustic window in some patients restricts this technique. Magnetic resonance imaging (MRI) and multislice spiral computed tomography allow for detailed delineation of intra and pericardiac tumors, their extent, and their influence on cardiac function [8]. Although an echocardiogram and a CT scan were requested for our patient the CT was available earlier and the findings were corroborated on a later echocardiogram.

Conclusion Features of nephrogenic ascites or congestive cardiac failure in a patient on renal replacement treatment who is adequately dialysed, and in whom the fluid overload state does not respond to intensification of dialysis and fluid removal including daily dialysis, should prompt further search for another underlying aetiology, as treatment options may vary.