小龙虾致横纹肌溶解综合征11例分析

横纹肌溶解综合征（rhabdomyolysis,RM）是一组由于各种原因所引起的骨骼肌损伤,细胞膜完整性改变,细胞内容物（如蛋白、离子、酶）等物质释放入血液中的临床综合征,常伴有代谢紊乱和急性肾衰竭等一系列并发症[1]。其临床表现为肌肉疼痛、肿胀、无力、棕色尿,主要特征有血肌酸激酶、肌红蛋白增高和肌红蛋白尿[2]。若并发急性肾衰竭占     

1例艾滋病并横纹肌溶解症患者的成功救治

正横纹肌溶解症(Rhabdomyolysis,RM)是指由于多种原因引起的横纹肌细胞损伤,进一步引起其细胞膜发生破坏,细胞之内的酶类、肌酐、无机盐离子、肌红蛋白、肌酸激酶等物质被释放到血液中导致的一组临床综合征[1],其可导致多脏器功能障碍甚至衰竭,如发生多脏器功能衰竭则死亡率超过50%[2]。RM常引起肌红蛋白尿,是导致急性肾损伤(AKI)的重要原因之一[3]。艾滋病并横纹肌溶解症病情复杂、危     

横纹肌溶解综合征并急性肾损害43例临床分析

横纹肌溶解综合征（rhabdomyolysis,RM）是指各种原因导致的横纹肌破坏、肌红蛋白等内容物释放引起的代谢紊乱和脏器功能损伤综合征,约15％～40％RM患者合并急性肾功能不全（ARF）,其病死率高达20％,RM病因多样,早期诊断,及时治疗,就有可能改善患者预后。现回顾性分析我院2006年5月至2009年1月资料完整的横纹肌溶解综合征并急性肾功能不全患者（RM—ARF）43例的临床诊断治疗情况,总结经验教训。     

横纹肌溶解症及并发急性肾损伤的研究进展

横纹肌溶解综合征(rhabdomyolysis,RM)是指横纹肌细胞受损后细胞膜破坏,肌细胞内物质释放进入细胞外液和血循环中所引起的一系列临床综合征。此病病因复杂,本文着重对横纹肌溶解症及并发急性肾损伤的病因、诊断及治疗方向进行综述,旨在与各位同仁探讨、交流。     

老年重症肺炎致横纹肌溶解1例临床分析

横纹肌溶解症（rhabdomyolysis,RM）是肌肉受到损伤后,大量肌细胞释放到血液循环,常引起电解质紊乱、酸中毒、急性肾功能衰竭等严重并发症的一组综合征[1]。据报道,RM患者中有10%-50%发生急性肾功能衰竭,其中病死率可＞50%[2]。创伤和非创伤等多种原因都可导致此病发生,该病的早期诊断具有一定难度,而及时诊断和治疗又关系到患者的预后。上海市松江区乐都医院新近收治1例老年重症肺炎并发RM患者,因发现及时,经适当治疗后病情好转,转归明显。查阅中外文献,并无老年重症肺炎并发RM的报道,特报告如下。     

内分泌疾病并发横纹肌溶解综合征12例临床分析

正横纹肌溶解综合征(rhabdomyolysis,RM)是指多种原因导致骨骼肌肌纤维坏死,肌细胞膜破坏,细胞内肌酸激酶和肌红蛋白等多种物质进入血液,并由此产生肌痛、肌无力、肾功能衰竭等一系列症状的临床综合征[1-2]。内分泌疾病导致的横纹肌溶解综合征近年来有增多趋势,了解内分泌疾病相关横纹肌溶解综合征的临床特点及治疗要点,对于早期诊断、及时治疗、改善预后至关重要。1资料与方法     

激肽释放酶-激肽系统对心血管系统的保护作用

1909年Abelous等[1]首次报道静脉注射人尿液可引起狗的血压短暂下降,发现尿中存在降压物质。1930年Kraut等[2]在胰腺发现高浓度此物质,命名为“Kallikrein”,即激肽释放酶(KLK)。近30年来,随着分子生物学和细胞生物学技术的发展和应用,发现激肽释放酶-激肽系统(kallikrein kini     

慢性乙型肝炎肝衰竭并发急性横纹肌溶解综合征患者1例护理体会

正横纹肌溶解综合征(rhabdomyolysis,RM)是指由多种原因导致广泛横纹肌肌纤维坏死,细胞膜受损,短时间内释放大量的肌酸激酶(CK)、肌红蛋白(Mb)和乳酸脱氢酶(LDH)等代谢产物进入血循环的一组临床综合征~([1~3])。我科于2016年6月收治1例慢性乙型肝炎肝衰竭并发RM患者,虽经122天的内科综合治疗和护理,患者仍因ARF而死亡。现将对该患者的治疗和护理要点分析、报告如下。     

Hoffmann综合征1例临床及病理分析

<正>甲状腺激素为人体细胞及组织器官代谢所必需,各种原因导致的低甲状腺激素血症或甲状腺激素抵抗可以引起隐秘起病的全身系统肌强直的肥大性肌病(发生于成人称为Hoffmann综合征、儿童称为DebreKocker-Semelaigne综合征)、多发性肌炎样综合征、不伴肌强直的肥大性肌病、不伴肌肥大的肌强直以及肌萎缩~[1]。同时存在肌肉痛性痉挛、肌肥大和肌强直的病人称为Hoffmann综合征,临床较为少见。本研究报     

红细胞分布宽度和血小板相关参数与脑梗死关系的临床研究

<正>脑梗死具有高发病率、高病死率和高复发率等特点,严重威胁人类的健康和生命^[1-2]。脑梗死是各种原因导致的脑部血液供应障碍,供血区脑组织缺血、缺氧性坏死,进而出现相应神经功能缺损的一类临床综合征,多在动脉粥样硬化(AS)基础上发生^[3]。AS是一种缓慢进展的炎性反应病理过程。细胞分布宽度(RDW)参与AS炎症反应的病理过程,RDW升高反映机体存在炎症状态^[4];PLT在AS病变部位的聚集及活性物质的释放是脑梗死形成的关键^[5]。     

Rhabdomyolysis

Rhabdomyolysis is a syndrome involving the breakdown of skeletal muscle causing myoglobin and other intracellular proteins and electrolytes to leak into the circulation. The development of rhabdomyolysis is associated with a wide variety of diseases, injuries, medications and toxins. While the exact mechanisms responsible for all the causes are not fully understood, it is clear that muscle damage can occur from direct injury or by metabolic inequalities between energy consumption and energy production. Rhabdomyolysis is diagnosed by elevations in serum creatine phosphokinase (CPK), and while there is no established serum level cut-off, many clinicians use five times the upper limit of normal (∼1000 U/l). Rhabdomyolysis can be complicated by acute renal failure (occurring in 4–33% of patients), compartment syndrome, cardiac dysrhythmias via electrolyte abnormalities, and disseminated intravascular coagulopathy. The mainstay of treatment is hospitalisation with aggressive intravenous fluid (IVF) resuscitation with the correction/prevention of electrolyte abnormalities. There are additional adjunctive therapies to IVF, such as alkalinisation of the urine with sodium bicarbonate, diuretic therapy or combinations of both; however the lack of large randomised control studies concerning the benefits of these treatments makes it difficult to make strong recommendations for or against their use in the treatment of rhabdomyolysis. Regardless of these controversies, the overall prognosis for rhabdomyolysis is favourable when treated with early and aggressive IVF resuscitation, and full recovery of renal function is common. Irrespective of the cause of rhabdomyolysis the mortality rate may still be as high as 8%. This is a comprehensive review of the pathophysiology, diagnosis, complications and treatment options for rhabdomyolysis.     

Muscular involvement in Legionnaires' disease. Review of the literature apropos of 2 cases

Two cases of Legionnaires' disease proven by seroconversion in indirect immunofluorescence are reported. Creatine phosphokinase (CPK) was increased in both patients, and one had rhabdomyolysis with acute renal failure and acute respiratory distress. A review of the literature brought out 9 other cases of rhabdomyolysis associated with Legionnaires' disease. Myalgias are an inconstant warning symptom; renal impairment is present in more than one half of the cases, and although pulmonary lesions are moderate, respiratory muscle involvement may require mechanical ventilation. In view of the severe complications of rhabdomyolysis, CPK should be systematically assayed in patients with Legionnaires' disease; 57 p. 100 of whom, according to published reports, have high CPK levels. In a retrospective study of bacterial pneumonia caused by common pathogens, we found that CPK was elevated in 31 p. 100 of the cases. The mechanism of muscular involvement is discussed.     

嗜血细胞综合征12例临床分析

目的 分析嗜血细胞综合征(HPS)的临床特点,探讨发病原因、诊断及治疗,提高临床医疗水平.方法 对江苏省人民医院2000年1月至2007年7月收治的12例HPS患者进行回顾性分析,并复习相关文献.结果 12例患者均为继发性HPS,多继发于病毒和细菌感染,亦有系统性红斑狼疮和坏死性淋巴结炎.均出现高热,在短时间内三系细胞减少,肝功能异常,经抗病毒、抗感染等原发病的积极治疗和对症支持治疗后,11例患者好转出院,1例死亡.结论 HPS发病率低,预后较差.故对于不明原因的发热、三系细胞减少患者需多次多部位进行骨髓检查,以求尽早诊断,合理有效治疗,改善预后.     

An adolescent girl with Meyer-Betz syndrome

Idiopathic paroxysmal rhabdomyolysis indicating a classical triad of symptoms consisting of muscle pain, weakness, and discolored urine is known as “Meyer-Betz syndrome”. It may result in acute renal failure due to precipitation of the myoglobin casts in the tubuli or to the direct toxic effects of myoglobin to the tubular epithelium. On the other hand, outcome may be uneventful. In this study, we reported the case of a 16-year-old girl who was admitted with red-colored urine after a slight exertion. She had tenderness and weakness in upper parts of her legs and bilateral flank pain. She had a positive urine dipstick test for heme despite absent red cells on microscopic examination. White cell count, liver function tests, serum creatine kinase (CK), lactate dehydrogenase (LDH), and urine myoglobin levels were raised. All metabolic tests were in normal ranges and EMG was normal. A muscle biopsy performed after recurrent exertional rhabdomyolysis attacks demonstrated normal findings and ruled out metabolic disorders. At the time of attacks, hydration along with alkalinization was applied and she did not experience renal failure. She was advised to avoid strenuous physical exertion and had an uneventful outcome for the last 5 months. We reported the clinical course and follow-up of an adolescent girl with Meyer-Betz syndrome.     

Rhabdomyolysis, renal failure, pericardial effusion, and acquired von Willebrand disease resulting from hypothyroidism in a 10-year-old girl.

A 10-year-old girl manifested unexplained muscle aches and high creatine phosphokinase (CPK) concentrations attributed to rhabdomyolysis in association with severe hypothyroidism due to autoimmune thyroiditis. The response to therapy strongly suggested that hypothyroidism was the cause of rhabdomyolysis. Hypothyroidism is a rare cause of rhabdomyolysis. It should always be considered in a patient with muscular symptoms and elevated CPK concentrations. In addition, the patient developed other uncommon manifestations of hypothyroidism such as pericardial effusion, acute renal failure, and acquired von Willebrand disease. After thyroxine replacement, the symptoms and abnormal findings disappeared. The patient was also diagnosed as having celiac disease, which is often associated with autoimmune thyroiditis. Conditions accompanying autoimmune thyroid disease may result from altered thyroid function and from the presence of other autoimmune diseases. The butterfly-shaped thyroid gland has a tremendous impact on metabolism, which may be compared to a phenomenon termed the "Butterfly Effect".     

Serum hepatic enzyme manifestations in patients with severe acute respiratory syndrome： Retrospective analysis

AIM: To evaluate the hepatic function in patients with severe acute respiratory syndrome (SARS) and possible causes of hepatic disorder in these patients. METHODS: One hundred and eighty-two patients with SARS were employed in a retrospective study that investigated hepatic dysfunction. Liver alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactic dehydrogenase (LDH) were analyzed in these patients. Patients with different hospital treatments were further investigated. RESULTS: Of the 182 patients, 128(70.3%) had abnormal ALT activity, 57(31.3%) had abnormal AST activity and 87(47.8%) had abnormal LDH activity. The peak of elevated hepatic enzyme activities occurred between the sixth day and the tenth day after the first day of reported fever. Of the 182 patients, 160(87.9%) had been treated with antibiotics, 137(75.2%) with Ribavirin, and 115(63.2%) with methylpredisolone. There was no statistically significant correlation between the duration of Ribavirin treatment and hepatic dysfunction. CONCLUSION: Abnormal liver functions were common in patients with SARS and could be associated with virus replication in the liver.     

Acute pancreatitis and rhabdomyolysis: a new association

Abstract Fourteen cases of acute severe pancreatitis complicated by non-traumatic rhabdomyolysis are described and compared to case controls. Pancreatitis of various aetiologies was confirmed by surgical diagnosis, laparotomy, abdominal paracentesis, CAT scan and post mortem. Pancreatitis was severe with a high Ranson prognostic score (7.4 ± 0.5 vs controls 1.9 ± 0.4, p< 0.001), longer ICU admission and a mortality of 79%. Rhabdomyolysis occurred two to 19 days after the onset of pancreatitis (with a median CPK peak at 6.5 days) and was accompanied by multiple organ failure in 93% of cases. Severe rhabdomyolysis and myoglobinuric renal failure occurred in three patients out of 12 with acute renal failure. Hypocalcaemia was common (93%), severe (with a mean minimum value of 1.79 ± 0.07 vs 2.34 ± 0.04mmol/L, p<0.01) and prolonged (remaining abnormal for 5.2 ± 0.8 vs 0.07 ± 0.07 days, p < 0.001). Intravenous calcium supplements were required in 50% of patients. Plasma phosphate, potassium, urate and anion gap were elevated (all p<0.05) and accompanying clinical features included fever, ascites, leuco-cytosis, hypoalbuminaemia and abnormal liver function tests. Rhabdomyolysis is associated with acute severe pancreatitis, appearing as a late phenomenon in the context of severe prolonged hypocalcaemia, multiple organ failure and a poor outcome. (Aust NZ J Med 1991; 21: 414–417.)     

非外伤性横纹肌溶解症39例临床分析

目的总结非外伤性横纹肌溶解症的病因、临床特点、治疗及预后。方法回顾性分析1999年1月至2006年11月北京协和医院收治的39例非外伤性横纹肌溶解症患者的病因、临床特点、治疗及预后。结果非外伤性横纹肌溶解症的主要表现为发热、乏力、受累肌肉疼痛和(或)压痛、肌肉肿胀、尿色改变及少尿或无尿,均有血清肌酶和血肌红蛋白明显升高。非外伤性横纹肌溶解症的并发症或合并症有急性肾衰竭、电解质和代谢紊乱、肌间隙综合征和多器官功能衰竭(MOSF)等。感染(33.3%)和药物(25.6%)是本组非外伤性横纹肌溶解症最常见的病因,其次为代谢紊乱(10.3%)、酒精中毒(7.7%)。治疗包括减少肌肉损伤、补液、碱化尿液及并发症的处理,必要时行肾脏替代治疗。总体病死率为15.4%,合并急性肾衰竭(ARF)者病死率为20.7%。MOSF是死亡的预测因素。存活者若无慢性肾功能异常,其肾功能均可恢复或维持正常。结论非外伤性横纹肌溶解症是一种病因、临床表现、并发症及合并症多样的综合征,早期诊断有一定困难。但只要治疗正确、及时,存活者肾功能多有望恢复或维持正常。     

Rhabdomyolysis-Associated Acute Kidney Injury With Normal Creatine Phosphokinase

Rhabdomyolysis is a syndrome characterized by the breakdown of skeletal muscle and leakage of intracellular myocyte contents, such as creatine phosphokinase (CPK) and myoglobin, into the interstitial space and plasma resulting in acute kidney injury (AKI). Elevated CPK of at least 5 times the upper limit of normal is an important diagnostic marker of Rhabdomyolysis. We present a case of rhabdomyolysis with severe AKI with a normal CPK at presentation. A 32-year-old man presented with acute respiratory failure and AKI after an overdose of recreational drugs. Urinalysis at presentation showed trace amounts of blood, identified as rare red blood cells under microscopy. CPK was 156 U/L at presentation. Workup for glomerulonephritis and vasculitis was negative. He was initiated on renal replacement therapy, and a kidney biopsy showed severe acute tubular injury with positive myoglobin casts. Supportive management and renal replacement therapy was provided, and renal function spontaneously improved after a few weeks. This is an uncommon clinical presentation of severe rhabdomyolysis complicated by AKI. This suggests that CPK alone may not be a sensitive marker for rhabdomyolysis-induced AKI in some cases.