Rosenbloom Arlan L
Division of Endocrinology, Department of Pediatrics, University of Florida College of Medicine, Children's Medical Services Center, 1701 SW 16th Avenue, Gainesville 32608, USA.
J Pediatr Endocrinol Metab. 2007 Jan;20(1):5-18. doi: 10.1515/jpem.2007.20.1.5.
The object of this review is to provide the definitions and criteria for diabetic ketoacidosis (DKA) and the hyperglycemic hyperosmolar state (HHS), and convey current knowledge of the causes of permanent disability or mortality from complications of these conditions, of the risk factors for DKA and HHS, and of early indicators and contemporary treatment of suspected cerebral edema. The frequency of DKA at onset of type 1 diabetes mellitus (DM1) varies from 10-70%, depending on availability of health care and frequency of diabetes. At the onset of type 2 diabetes (DM2), DKA occurs in 5-52%. One study reported HHS in approximately 4% of new patients with DM2. Recurrent DKA rates are equally dependent on variability in medical services and socio-economic circumstances, and are estimated to be eight episodes per 100 patient years, with 20% of patients accounting for 80% of the episodes. Mortality for each episode of DKA internationally varies from 0.15-0.31%, with idiopathic cerebral edema accounting for two-thirds or more of this mortality. Other causes of death or disability include untreated DKA or HHS, hypokalemia, hypophosphatemia, hypoglycemia, other intracerebral complications, peripheral venous thrombosis, mucormycosis, rhabdomyolysis, acute pancreatitis, acute renal failure, sepsis, aspiration pneumonia, and other pulmonary complications. Population-based studies from the UK, Australia, the USA, and Canada report cerebral edema incidence in DKA of 0.5-2.0%. Published information does not support the notion that treatment factors are causal in cerebral edema. Younger age, greater severity of acidosis, degree of hypocapnia, and severity of dehydration have been suggested as risk factors in several studies. Bimodal distribution of the time of onset of cerebral edema and wide variation in brain imaging findings suggest the variability and likely multiple causation of the clinical picture. Functional brain scanning has indicated that DKA is accompanied by increased cerebral blood flow suggesting that the predominant mechanism of edema formation is a vasogenic process. A method of monitoring for diagnostic and major and minor signs of cerebral edema has been proposed and tested which indicates that intervention will be required in five individuals to provide early intervention for a single case of cerebral edema. The preferred intervention of mannitol infusion has typically been accompanied by intubation and hyperventilation, but recent evidence indicates outcome is adversely affected by aggressive hyperventilation. The prevention of DKA and HHS at the onset of diabetes mellitus requires a high degree of awareness and suspicion by primary care providers; prevention of recurrent DKA necessitates a diligent team effort.
本综述的目的是提供糖尿病酮症酸中毒（DKA）和高血糖高渗状态（HHS）的定义及标准，并传达有关这些病症并发症导致永久性残疾或死亡的原因、DKA和HHS的危险因素，以及疑似脑水肿的早期指标和当代治疗方法的当前知识。1型糖尿病（DM1）发病时DKA的发生率在10%至70%之间，具体取决于医疗保健的可及性和糖尿病的发病频率。2型糖尿病（DM2）发病时，DKA的发生率为5%至52%。一项研究报告称，在新诊断的DM2患者中，HHS的发生率约为4%。DKA的复发率同样取决于医疗服务和社会经济状况的差异，估计为每100患者年8次发作，其中20%的患者发作次数占总发作次数的80%。国际上，每次DKA发作的死亡率在0.15%至0.31%之间，其中特发性脑水肿占该死亡率的三分之二或更多。其他死亡或残疾原因包括未治疗的DKA或HHS、低钾血症、低磷血症、低血糖、其他脑内并发症、外周静脉血栓形成、毛霉菌病、横纹肌溶解、急性胰腺炎、急性肾衰竭、败血症、吸入性肺炎和其他肺部并发症。来自英国、澳大利亚、美国和加拿大的基于人群的研究报告称，DKA患者中脑水肿的发生率为0.5%至2.0%。已发表的信息不支持治疗因素是脑水肿病因的观点。几项研究表明，年龄较小、酸中毒更严重、低碳酸血症程度和脱水严重程度是危险因素。脑水肿发病时间的双峰分布以及脑成像结果的广泛差异表明了临床表现的变异性和可能的多种病因。功能性脑扫描表明，DKA伴有脑血流量增加，这表明水肿形成的主要机制是血管源性过程。已提出并测试了一种监测脑水肿诊断及主要和次要体征的方法，该方法表明，每5名患者中就需要进行干预，以便为1例脑水肿患者提供早期干预。甘露醇输注的首选干预措施通常伴有插管和过度通气，但最近的证据表明，积极的过度通气会对预后产生不利影响。在糖尿病发病时预防DKA和HHS需要初级保健提供者高度警惕和怀疑；预防DKA复发需要团队的不懈努力。
