糖尿病非酮症高渗性昏迷并横纹肌溶解症一例

患者,男,40岁.2006年11月26日因"多饮、多尿半月,乏力两天,突发神志不清2小时"至急诊,不伴有肢体抽搐、二便失禁.查体:中度昏迷,体温39.4℃,血压66/32 mm Hg,心率105次/分,呼吸22次/分.     

老年糖尿病性非酮症性高渗昏迷合并横纹肌溶解症1例报道

糖尿病性非酮症性高渗昏迷（nonketotic hyperosmolar diabetic coma,NHDC）是糖尿病严重急性并发症之一,病死率较高,可达10%-50%,多见于老年病人。横纹肌溶解综合征（rhabdomyolysis,RM）是指一系列影响横纹肌细胞膜、膜通道及能量供应的多种遗传性或获得性疾病导致的横纹肌损伤,细胞膜完整性遭到破坏,细胞内容物包括肌红蛋白.     

高渗性非糖尿病酮症昏迷合并急性肾功能衰竭及横纹肌溶解1例报告

高渗性非糖尿病酮症昏迷在临床上是糖尿病最常见的危及生命的急性代谢并发症。其合并横纹肌溶解因临床表现不典型,常易漏诊,近年因较高的病死率而引起越来越多的重视。因此,本文通过介绍收治的1例高渗性非糖尿病酮症昏迷合并急性肾功能衰竭并横纹肌溶解患者并进行文献复习,以提高     

高血糖高渗状态和糖尿病酮症酸中毒合并脑水肿、横纹肌溶解综合征1例诊治体会及文献复习

目的：探讨糖尿病高渗性高血糖状态﹙Hyperosmolar Hyperglycemic State,HHS)及糖尿病酮症酸中毒﹙Diabetic ketoacidosis,DKA) 合并横纹肌溶解（Rhabdomyolysis,RM）患者的临床特点及治疗策略。方法：回顾性总结2015年1月在本科的1例HHS及DKA合并RM患者的临床特点、血清学指标、治疗经过及预后。结论：一旦确诊为DKA合并HHS,立即快速扩容、胰岛素降糖,严密监测血糖、尿糖、酮体、电解质、有效血浆渗透压,肾功、激酶,酌情调整输液的种类和速度及胰岛素剂量,纠正离子紊乱。为预防脑水肿和RM的发生,避免补液过量和血浆渗透压下降过快,避免低钾血症的发生。治疗过程中观察患者神志的变化和尿的颜色有无异常。在最短的时间内,做出有效的抢救措施,能够降低DKA-HHS患者的RM和脑水肿的发生,降低患者的致残率及死亡率     

糖尿病高渗性非酮症昏迷并发横纹肌溶解1例报道

糖尿病高渗性非酮症昏迷（HHS）是糖尿病最为常见急性代谢紊乱状态,死亡率10％～50％。而横纹肌溶解症（RM）的发生常伴有威胁生命的代谢紊乱和急性肾功能衰竭等一系列并发症,研究显示,RM的病死率在3％～27％。近年来,有关HHS并发RM的临床病例有一些报道,并因病情凶险,预后差,引起重视,现将我院诊治1例糖尿病高渗性非酮症昏迷并发横纹肌溶解临床资料进行分析。     

糖尿病酮症酸中毒合并高渗高血糖状态致横纹肌溶解1例

该文报道1例糖尿病酮症酸中毒(DKA)合并高渗高血糖状态(HHS)导致横纹肌溶解(RM)的临床诊治过程, 并对DKA、HHS导致RM的发病机制进行探讨。该患者DKA合并高渗状态, 病程中肌酸激酶峰值超过正常上限300倍, 伴茶色尿, 诊断横纹肌溶解, 给予大量补液、胰岛素降糖、纠正电解质紊乱、碱化尿液等治疗, 预后良好。通过整理该病例的诊治过程, 旨在提高临床医师对糖尿病急性并发症导致RM的认识, 加强对肌酶谱的常规筛查, 避免漏诊误诊, 提高患者生存率。     

糖尿病非酮症高渗综合征合并癫痫持续状态15例临床分析

糖尿病性癫痫发作,临床报道日见增多,目前认为是神经系统并发症之一。但糖尿病非酮症高渗综合征合并癫痫持续状态临床不常见,且为内科急症、重症,我科自１９９０年３月～１９９８年１２月共收治糖尿病非酮症高渗综合征７１例,其中本病患者１５例,结合文献进行探讨。临床资料１．一般资料：本组女性１０例,男性５例,年龄５５～６５岁,平均６０．５岁。１５例患者中４例原有糖尿病未坚持常规治疗,１１例就诊前从未被诊断为糖尿病,其中３例患者因乏力、恶心、呕吐,在外院注射葡萄糖出现昏迷,抽搐、转诊我院。２．临床表现：浅昏迷…     

抢救2型糖尿病非酮症高渗综合征2例的体会

例 1　男性 ,70岁。约 2 0ｄ前进油腻食物后 ,出现持续性腹痛 ,频繁呕吐 ,给予 10 %葡萄糖液 5 0 0ｍｌ加入 6 5 4 2 10ｍｇ。在输液治疗过程中出现频繁的呕吐、烦燥、神志恍惚、三多一少症状 ,急诊入院。既往无高血压、心血管病史 ,有慢性胰腺炎史 2 0年余。入院时患者神志恍惚 ,脉率 10 0次 /ｍｉｎ ,ＢＰ 130 / 80ｍｍＨｇ ,全身皮肤干燥 ,失水明显 ,双眼球凹陷 ,消瘦 ,双瞳孔等大等圆 ,对光反射存在 ,腹部软 ,有压痛 ,四肢活动无异常。血ＷＢＣ 1.79× 10 9/Ｌ ,Ｎ 89.5 % ,血淀粉酶 12 7Ｕ/Ｌ ,尿淀粉酶 2 75Ｕ/Ｌ ,血糖 2 2 .1ｍｍｏ…     

糖尿病急性代谢并发症与非创伤性横纹肌溶解症

糖尿病酮症酸中毒（DKA）与高渗性高血糖状态（HHS）是糖尿病最为严重的急性代谢并发症,在DKA或HHS患者中有50%可合并非创伤性横纹肌溶解症（NRML）,严重者可导致急性肾功能衰竭。DKA或HHS介导NRML的机制可能包括肌肉缺血、缺氧,电解质紊乱及酸碱失衡,感染,应用羟甲戊二酸单酰CoA还原酶抑制剂等。因早期诊断并及时治疗常可逆转病情发展,从而避免发生严重并发症,降低死亡率,因此对NRML及时并准确的诊断很重要。     

A case of psoas abscess due to renal pelvic carcinoma complicated with non-ketotic hyperosmolar diabetic coma]

A 85-year-old man was admitted to our hospital because of semicomatous status. Laboratory data on admission showed elevation of blood sugar (823 mg/dl) and serum osmotic pressure (345 mOsm/l), but ketonuria was not detected. Non-ketotic hyperosmolar diabetic coma was diagnosed. The insulin infusion and physiological saline improved the blood sugar level and consciousness within a day. The abdominal ultrasound examination revealed an abscess in the left kidney and right psoas muscle. The same findings were seen by abdominal computed tomography but the possibility of malignant neoplasm of the left kidney could not be ruled out because of a swelling of the left adrenal gland. Pain associated with psoas abscess and low grade fever were observed. Because of his poor general condition, drainage of the abscess was not performed and conservative therapy using antibiotics was administered. Without any improvement of the abscess, he died due to general deterioration four months later. Autopsy findings showed carcinoma of the left renal pelvis and metastasis to the right psoas muscle, left adrenal gland, liver, bilateral lungs and lymph modes. Psoas abscess is a relatively uncommon disease, especially in elderly patients. The etiology of the disease is divided into primary and secondary causes. Most secondary psoas abscess cases are caused by intestinal diseases, and Crohn's disease has been related to the highest incidence. A few cases of psoas abscess caused by colorectal carcinoma have been reported. Ultrasound and computed tomography are useful in diagnosing this disease and drainage of an abscess is necessary for therapy and proving the cause. Cancer metastasis should considered in differential diagnoses, when psoas abscess is seen in elderly patients.     

Glucose metabolism in a patient with insulinoma complicated by hyperosmolar non-ketotic state

A case of a patient with organic hyperinsulinism complicated by the development of hyperosmolar state is described. The hyperosmolar state was induced by vomiting and dehydration during an acute urinary tract infection. Impairment of glucose metabolism was confirmed by the finding of reduced tissue sensitivity to insulin during a euglycaemic clamp.     

乙型肝炎肝硬化合并横纹肌溶解症1例报告

<正>1病例资料患者男性,49岁,因"发现HBs Ag阳性20年,腹胀、乏力2月余"于2013年1月25日于本院住院治疗。患者1993年查体发现HBs Ag阳性,2012年11月于外院就诊化验肝功能:ALT 36U/L,AST 47 U/L,TBil 18.4μmol/L;乙型肝炎抗原抗体五项:HBs Ag、抗-HBc阳性,HBV DNA 1.27×105IU/ml;腹部B超提示"肝     

C-peptide blood levels in keto-acidosis and in hyperosmolar non-ketotic diabetic coma

Summary For further evaluation of B-cell secretion in diabetic keto-acidosis (KA) and in non-ketotic hyperosmolar coma (NKHC), basal and post-i.v. tolbutamide blood CPR and IRI values were measured in 34 patients (22 KA and 12 NKHC). FFA, cortisol and HGH measurements were also performed. IRI was low in both KA and NKHC (0.07±0.01 and 0.082±0.01 nmol/l) as opposed to CPR which was significantly higher in NKHC (1.14±0.1 nmol/l) than in KA (0.21±0.03 nmol/l). After tolbutamide injection, CPR and IRI levels did not change in any of the KA cases, whereas they significantly increased in half of the NKHC cases. Cortisol and FFA values were similarly increased in both situations, as opposed to HGH which was significantly higher (6.1±1.2 ng/ml) in KA than in NKHC (1.9±0.2 ng/ml). These results suggest that B-cell function is less deficient in NKHC than in KA. Residual insulin amounts reaching the liver via the portal vein could partly account for the absence of ketosis in NKHC.     

复杂性嵌合体Klinefelter综合征合并代谢综合征一例

报道一例染色体类型为46,XY/47,XXY/48,XXXY嵌合体同时合并代谢综合征的Klinefelter综合征患者。     

糖尿病急症并发横纹肌溶解综合征的实验研究

目的:研究不同的代谢紊乱状态与骨骼肌细胞损伤的关系,探讨糖尿病急症并发横纹肌溶解综合征(RM)的可能机制。方法:40只大鼠随机分成5组,每组8只。糖尿病组(DM)给予腹腔注射STZ(链脲佐菌素)60 mg/Kg;急性高钠模型组给予腹腔注射4M Na Cl 0.8 m L/100 g;糖尿病高渗组(HHS)给予氢化可的松局部肌肉注射4~6 d,并于注射第3天开始禁水,不禁食,禁水持续1~3 d,直到大鼠出现神经症状;正常对照组腹腔注射等量生理盐水;激素对照组单纯给予局部肌肉注射氢化可的松5 mg,5 d。检测5组大鼠血清肌酸激酶(CK)、血糖、血钠等生化指标;并同期取大鼠骨骼肌、心肌组织标本,行HE染色,光镜下(40×)观察形态学改变。结果:与其他组相比,DM组及HHS组血糖明显升高(P0.05),HHS组及高钠组血渗透压明显增高(P0.05),且血清CK值也明显高于其他组(P0.05);RM大鼠中,血钠、血渗透压与CK呈正相关(r=0.32,P=0.03;r=0.42,P=0.01)。HE染色,光镜下可见糖尿病高渗组与急性高钠组有明显骨骼肌细胞溶解征象,对照组无明显异常。结论:高血钠和高血渗透压是糖尿病状态下RM发生的主要危险因素。     

Plasma angiotensin II concentrations in diabetic ketoacidosis and in hyperosmolar non-ketotic hyperglycemia

Summary Plasma angiotensin II concentrations were measured in 14 patients in diabetic ketoacidosis and in two patients with hyperosmolar non-ketotic hyperglycemia, before treatment and again when blood glucose control was restored. In the ketoacidosis group plasma angiotensin II before treatment was markedly raised in all patients with otherwise uncomplicated diabetes, but was within the normal range in some patients with long-term complications such as neuropathy, retinopathy and nephropathy. Mean angiotensin II before treatment was significantly higher in otherwise uncomplicated patients than in those with long-term complications. However, plasma angiotensin II decreased with improved control in all. Angiotensin II levels did not correlate with indices of rehydration such as changes in blood urea, packed cell volume and calculated changes in plasma volume. There was, however, a significant negative association between pretreatment angiotensin II and pH. Two patients with hyperosmolar non-ketotic hyperglycemia were more dehydrated but less acidotic. Pre-treatment angiotensin II in each was well below the mean of the ketoacidosis group. These data are further evidence that the renin-angiotensin system may be impaired in diabetics with long-term complications. In addition, they suggest that factors other than fluid depletion are also important in activating the renin-angiotensin system in uncontrolled diabetes.