1例2型糖尿病高渗性昏迷合并脑动脉瘤术后及呼吸道MRSA的护理

正糖尿病高渗性昏迷是糖尿病急性代谢紊乱的一种较少见的、严重的临床并发症,又称糖尿病高渗性非酮症性昏迷,常见于老年2型糖尿病患者。以高血糖、高血钠、严重失水、高血浆渗透压,无酮症或轻微酮症,血尿素、肌酐偏高,伴有不同程度神经精神症状为特征[1]。对于合并脑动脉瘤术后的患者症状易被掩盖和混淆,对于此类患者应提高警惕。本科于2015年4月收治了一例2型糖尿病高渗性昏迷合并脑动脉瘤术后及呼吸道     

非酮症性高血糖性癫痫的护理体会

糖尿病性癫痫是糖尿病神经系统并发症之一,常发生于低血糖昏迷、非酮症高渗性昏迷、糖尿病酮症酸中毒、严重电解质紊乱等情况。但糖尿病非酮症非高渗状态,仅单纯高血糖亦可引起抽搐发作,称为非酮症高血糖（nonketotic hyperglycinemia,NKH）性癫痫,临床较少见。2000年2月～2009年2月我院共收治非酮症性高血糖性癫痫22例,现将护理体会总结如下。     

老年非酮症性高血糖性癫痫1例的急救护理

糖尿病性癫痫是糖尿病神经系统并发症之一,常发生于低血糖昏迷、非酮症高渗性昏迷、糖尿病酮症酸中毒、严重电解质紊乱等情况下,但糖尿病非酮症高渗状态,仅单纯高血糖亦可引起抽搐发作,称为非酮症性高血糖性癫痫,临床较少见[1].既往多无糖尿病病史,以癫痫为首发症状就诊于神经内科,容易误诊.我科在2011-05收治非酮症性高血糖性癫痫1例,现将急救与护理报告如下.     

食管贲门癌合并2型糖尿病41例围术期肠内营养支持临床护理

目的:探讨合并2型糖尿病的食管贲门癌患者围术期肠内营养支持的护理管理.方法:回顾性分析2007年6月~2011年6月手术治疗的食管贲门癌合并Ⅱ型糖尿病41例的临床资料,2例患者术前营养支持,全组术中置鼻肠管,术后肠内营养支持,对肠内营养过程中血糖的护理管理、监测及控制进行分析研究.结果:41例均按计划完成肠内营养,平均输注营养液时间(10.2±3.5)d.术后发生低血糖2例,高血糖5例,其余均控制满意.术后并发颈部吻合口瘘1例、肺部感染5例、切口感染3例、酮症酸中毒2例.均顺利度过围术期,痊愈出院.结论:食管癌合并糖尿病患者围术期需要严格监测和控制血糖,加强术后肠内营养支持,合理应用胰岛素控制血糖是治疗成功的重要因素.     

高渗性高血糖性昏迷1例

高渗性高血糖性非酮症性糖尿病昏迷并不罕见,有报道在2年间即见37例(Medicine 51:73,1972);国内仅见首都医院报告的3例(中华医学杂志53:406,1973)。鉴于有不少患者从无糖尿病史,且以高渗状态及高血糖、循环衰竭、昏迷为突出表现,故认为将命名精简为高渗性高血糖性昏迷更为恰当。兹将最近所见1例并发于结缔组织疾病,长期使用肾上腺皮质激素及随访过程中,突发高渗性高血糖性昏迷致死病例,整理如下:     

糖尿病酮症性和非酮症高渗性昏迷21例临床分析

临床上根据有无酮症把糖尿病昏迷分为糖尿病酮症性和非酮症高渗性昏迷.以下简称前者为酮症组,后者称高渗组.非酮症高渗性糖尿病昏迷的特点是:严重高血糖、高渗血症,脱水征明显,基础糖尿病轻,多发生在年龄较大者.更受到临床工作者重视.国内首次报道是1973年.1978年以后报道增加.我院自1980年以来14年中共收治糖尿病酮症酸中毒53例次(其中伴有神志障碍13例)与同期收治非酮症高渗性糖尿病昏迷8例之比为6.6:1.和国内外材料一致.为了提高对本症的诊治水平,现将21例糖尿病昏迷总结分析.     

高渗性非酮症糖尿病昏迷的救治

高渗性非酮症糖尿病昏迷简称高渗性昏迷，是糖尿病的一种罕见而严重的急性并发症，也是糖尿病昏迷的一种特殊类型。高渗性昏迷是以严重高血糖、高血浆渗透压、严重脱水、无明显酮症伴有进行性意识障碍为主的临床综合征。本病多见于老年糖尿病患者和以往无糖尿病病史的患者，或仅有轻度糖尿病不需要胰岛素治疗者，     

食管癌合并糖尿病患者术后早期肠内营养支持及护理

食管癌患者多数存在营养不良,肠内营养是术后首选的营养支持方法,可改善患者营养状况,降低并发症的发生,提高手术疗效.食管癌合并糖尿病患者术后行常规肠内营养支持容易导致高血糖等并发症,因此寻求适合此类患者的营养支持方式尤为重要.本科对2009年8月至2010年12月的48例食管癌合并糖尿病患者术后早期应用肠内营养,取得良好效果.报告如下.     

糖尿病非酮症性高渗性昏迷、酮症酸中毒或乳酸性酸中毒时血浆氨基酸的改变

糖尿病性昏迷包括非酮症性高渗性昏迷、酮症酸中毒及乳酸性酸中毒昏迷。这些都是糖尿病患者常见的并发症。作者分析了这几种患者血浆中的游离氨基酸,并同时与7例正常人对照,对所得结果作了分析、比较和讨论。非酮症性高渗性昏迷患者(4例)的血浆总氨基酸值为2448μM,与正常者(2744μM)比较则偏低。特别是精氨酸、牛磺酸、丝氨酸的浓度及克分子比值(MR)明显低于正常,鸟氨酸的浓度亦降低。但苯丙氨酸的浓度及MR高于正常;谷氨酸的浓度升高:酪氨酸MR升高。糖尿病酮症酸中毒患者(6例)与非酮症性高渗性昏迷患者情况不同,其血浆总氨基酸值为     

糖尿病高渗性非酮症性昏迷的抢救与护理

高渗性非酮症昏迷(HONK)为糖尿病严重的急性并发症之一,其临床特征主要为严重的高血糖、脱水,血浆渗透压升高而无明显的酮症酸中毒,患者常有意识障碍或昏迷。HONK预后不佳,死亡率高达40%以上,因此及时合理、准确的抢救至关重要,现将我科2000～2003年收住抢救10例糖尿病非酮症高渗性昏迷患者抢救护理体会报告如下。     

Complications of diabetes: acute and chronic.

The acute and chronic complications of diabetes account for the morbidity and mortality associated with this disease. Acute complications include diabetic ketoacidosis, hyperosmolar hyperglycemic nonketotic coma, and hypoglycemia. Chronic hyperglycemia is central to the pathophysiology of chronic complications such as cardiovascular and peripheral vascular disease, retinopathy, nephropathy, and neuropathy. Pathophysiology and assessment of, and interventions for these complications are discussed.     

Diabetic ketoacidosis and hyperosmolar hyperglycemic nonketotic coma

Diabetic ketoacidosis and hyperosmolar hyperglycemic nonketotic coma are two of the most common acute complications of diabetes. The pathophysiologic changes that occur in both disease states represent an extreme example of the super-fasted state. The physiology of the fed and fasted state, evaluation, therapeutic issues, recommendations for therapy, immediate follow up care, and complications of therapy are reviewed for both syndromes.     

高渗性非酮症糖尿病昏迷23例的

目的探讨高渗性非酮症糖尿病昏迷的临床特点和诊治体会。方法采用回顾性调查研究,对23例高渗性非酮症糖尿病昏迷病人的临床资料进行分析。结果高渗性非酮症糖尿病昏迷病人老年人占69.6%,临床好转13例,死亡8例自动放弃2例,病死率34.8%,首诊误诊率47.9%,感染占诱因的60.9%。结论高渗性非酮症糖尿病昏迷好发于老年人,极易误诊,病死率高,早期诊断,及早纠正脱水及水电解质紊乱,积极治疗诱因和并发症是抢救成功的关键。     

合并糖尿病消化道肿瘤患者术后早期肠内营养支持的护理研究

目的:探讨消化道肿瘤合并糖尿病患者在术后早期肠内营养过程中的护理方法。方法:37例消化道肿瘤合并糖尿病患者术后24h经鼻空肠营养管重力滴入肠内营养糖尿病专用制剂,检测治疗前后各项营养、生化及免疫指标变化。通过一系列相关护理措施,监测和控制血糖,预防并发症的发生。结果:在输注肠内营养过程中患者无1例发生严重并发症,仅有5例出现腹胀腹泻症状,2例出现咽喉炎,均对症治疗后缓解。81.08%患者血糖稳定,控制在(7.8±1.1)mmol/L范围内。治疗后血清白蛋白、前清蛋白、转铁蛋白等营养指标水平显著增高(P0.05),体重、血红蛋白、丙氨酸氨基转移酶、总胆红素无明显改变,IgG、IgA、IgM免疫指标水平比术前有明显升高(P0.01)。结论:对消化道肿瘤合并糖尿病患者术后早期应用糖尿病专用制剂是营养支持的有效手段。治疗期间应采取科学有效的护理方法,加强基础护理,监测血糖变化,预防糖尿病和手术相关并发症的发生。     

Diabetes emergencies in the patient with type 2 diabetes

Type 2 diabetes has traditionally been associated with the development of hyperglycemic hyperosmolar nonketotic syndrome (HHNKS), yet evidence suggests that diabetic ketoacidosis (DKA) is increasing among this population. Patients with type 2 diabetes may develop DKA or HHNKS and require hospitalization. In addition, patients with type 2 diabetes, hospitalized for other medical or surgical conditions, are clearly at risk for the development of metabolic decompensation during hospitalization. This article explores the acute complications of type 2 diabetes and some of the issues associated with managing these patients in the hospital setting.     

Nonketotic hyperosmolar coma in a patient with type 1 diabetes-related diabetic nephropathy: Case report

Nonketotic hyperosmolar coma (NHC) is characterized by severe hyperglycemia; absence of, or only slight ketosis; nonketotic acidosis; severe dehydration; depressed sensorium or frank coma; and various neurologic signs. This condition is uncommon in type 1 diabetes. Because of little or no osmotic diuresis in patients with diabetic nephropathy, increases in plasma osmolality and therefore the likelihood of neurologic symptoms are limited. A 20-year-old male patient with type 1 diabetes with chronic kidney disease on conservative treatment (glomerular filtration rate [GFR], 18 mL/dk) presented with acute nonketotic hyperosmolar syndrome. The patient was admitted presenting with thirst, fatigue, and drowsiness. Blood biochemistry levels were urea 87 mg/dL, creatinine 5.09 mg/dL, glucose 830 mg/dL, glycosylated hemoglobin (HbA_1c) 8%, C peptide < 0.3 ng/mL, sodium 131 mmol/L, chloride 93 mmol/L, potassium 5.2 mmol/L, and calculated serum osmolality 385 mOsm/kg. The presumptive diagnosis on admission was nonketotic hyperosmolar syndrome precipitated by urinary infection. This is the first case report of hyperosmolar coma in a patient with type 1 diabetes with chronic kidney disease.     

子宫肌瘤合并糖尿病患者的围术期护理

目的评价有效的护理措施在子宫肌瘤合并糖尿病患者围术期的应用价值。方法回顾性分析78例子宫肌瘤合并糖尿病患者的临床资料及护理体会。结果 78例患者中,腹部切口Ⅰ期愈合76例,Ⅱ期愈合2例;3例患者出现轻度泌尿系感染症状;所有患者均未出现糖尿病酮症酸中毒、非酮症高渗性昏迷、糖尿病足等严重并发症。结论心理护理、血糖监测、控制饮食、足部护理等综合护理干预可明显减少子宫肌瘤合并糖尿病患者围术期并发症的发生。     

2型糖尿病并发高渗性昏迷3例分析

目的：探讨糖尿病高渗性非酮症性昏迷抢救的方法，以提高抢救成功率。方法：对经治3例确诊病例进行回顾性分析。结果：3例糖尿病高渗性非酮症性昏迷患者在治疗过程中由于偶然原因病情加重，结果发现是血糖与脊液糖不平衡所致。结论：糖尿病高渗性非酮症性昏迷在治疗过程中病情加重可能与血糖与脑脊液糖不平衡有关。     

Olanzapine-lnduced hyperglycemic nonketonic coma

OBJECTIVE: To report a case of olanzapine-induced hyperglycemia leading to a hyperosmolar, hyperglycemic, nonketonic coma. CASE SUMMARY: A 51-year-old, 85.5-kg (ideal body weight 79.9 kg), white man presented to a Veterans Affairs hospital with a serum glucose concentration of 1596 mg/dL. Soon thereafter, he went into a hyperosmolar, hyperglycemic, nonketonic coma. Olanzapine therapy had been instituted less than six months prior to this event; approximately two months before this event, his blood glucose was 108 mg/dL. Eight days after stopping olanzapine, the glucose concentration returned to normal, and the patient no longer required insulin nor any other glucose-lowering agents. DISCUSSION: The insulin resistance caused by olanzapine is normally attributed to the weight gain associated with the drug. In this patient, it appears that olanzapine caused hyperglycemia by a mechanism other than weight gain. CONCLUSIONS: This case report and others from the literature suggest that olanzapine therapy may induce hyperglycemia in some patients.     

Prognostic factors in hyperglycemic hyperosmolar nonketotic syndrome

Twenty-four patients suffering hyperglycemic hyperosmolar nonketotic syndrome were studied retrospectively to define initial prognostic factors. Twenty percent of these elderly patients (mean age 76 +/- 4.6 yr) had no history of diabetes, and only 54% experienced coma, which was not related to the level of plasma osmolality or to final outcome. The overall mortality was 46%, but death was directly related to nonmetabolic disorders in 64% of cases. Age; sex; acute precipitating factors (except precipitating drugs); admission levels of serum sodium, serum potassium, blood glucose, plasma osmolality, and serum creatinine; and insulin, macromolecular, and total fluid volumes infused during the first 24 h in the ICU were not related to death. The simplified acute physiology score was approximately the same for both survivors and nonsurvivors.