一世n this first part of our 2-part podcast on DKA and HHS, DrsMelanie Baile..Bourke Tillmann.Leeor Sommer讨论鉴定鉴定DKA患者的潜在原因或触发的重要性,抑制DKA患者患者正常pH或正常血清葡萄糖,如何有效地缩小差距,为什么停止胰岛素输注几乎从未表明过,如何避免心脏塌陷当DKA患者需要气管插管时,气管中塑料中最好的替代品,为什么使用协议改善患者结果,如何避免低血糖和低钾血症的常见并发症,还有更多...

Podcast voice editing by Raymond Cho. Production, sound design & editing by Anton Helman.

Written Summary and blog post by Lorraine Lau & Winny Li, edited by Anton Helman September, 2020.

引用这个播客是:Helman, A. Baimel, M. Sommer, L. Tillmann, B. Episode 146 – DKA Recognition and ED Management. Emergency Medicine Cases. September, 2020. //www.mp3valve.com/dka-recognition-ed-management访问[日期]。

The Difficulty in Diagnosing Diabetic Ketoacidosis (DKA)

There are no definitive criteria for the diagnosis of DKA according to the 2018 Canadian DKA Guidelines. As such, it is important to have a low threshold to consider the diagnosis in any diabetic patient who presents with polyuria, polydipsia, hyperpnea, abdominal pain/nausea/vomiting or altered level of awareness. While most patients with DKA will have the三合会高血糖,阴离子间隙代谢酸中毒和酮血症那there are important例外

  • DKA.patients can have a没有rmalglucose (euglycemic DKA – see below)
  • DKA.patients can have a没有rmalpH和A.没有rmalbicarbonate (normal VBG) in the context of ketoacidosis plus metabolic alkalosis as a result of vomiting and/or the triggering illness
  • Negative urine ketones should not be used to rule out DKA, as urine tests measure the presence of acetoacetate, but not β-hydroxybutyrate

β-羟基丁酸酯水平> 1.5mmol / L的敏感性为98-100%,特异性为78.6-93.3%,用于患有血清葡萄糖水平升高的糖尿病患者的DKA。

临床珍珠:Many patients with DKA present with some degree of abdominal pain. Severe abdominal pain with only mild ketoacidosis argues一种gainstDKA作为原因。当有疑问,对腹部成像的需要,首先复苏,并进行串行腹部检查。如果酮症中毒改善,则对图像具有低阈值,但患者继续存在症状或临床恶化。

Severity categorization of DKA



dka vs hhs.


Evaluation for precipitating cause of DKA is paramount as it is often the cause of of death in patients with DKA

DKA.can be the initial manifestation of diabetes, but it often occurs in the context of known diabetes plus a trigger. Most often, it is due to medication non-adherence, incorrect dosing or infection. However, any physiologic stress can trigger DKA.


  1. 一世nfection(肺炎,uti,皮肤,腹部)
  2. 一世nfraction(mi,中风,肠梗塞)
  3. 一世nfant on board (pregnancy)
  4. 一世ndiscretion (dietary nonadherence)
  5. 一世nsulin deficiency (insulin pump failure or nonadherence)

一世n addition, common可以触发DKA的药物include glucocorticoids, diuretics and atypical antipsychotics.


DKA.work-up should include CBC, electrolytes, extended electrolytes, creatinine, BUN, albumin, VBG, lactate, serum ketones, as well as consideration for:

  • BhCG (pregnancy may be a trigger of DKA)
  • ECG/Trop (only if ischemia suggested in history)
  • 涉嫌感染触发器的文化,UA等
  • β-hydroxybutyrate if diagnosis unclear


Acid-base disturbances in DKA


在这种情况下,使用Simplified Stewart Approach


[Na−Cl–35] + [1–lactate] + [0.25 x (42−albumin)] + other ions

Other ions =

基础过量 - [Na-C135] + [1乳酸] + [0.25 x(42-白蛋白)]如果酸基的主要决定因素没有解释基础缺陷,则存在未测量的离子。

陷阱:Avoid ruling out DKA based on a normal or near normal VBG. DKA patients can have a normal pH due to the underlying trigger of the DKA contributing to a mixed acid-base picture.


The differential diagnosis for ketoacidosis包括:

  • DKA.
  • 酒精酮症化
  • 饥饿刺激
  • 异丙醇摄入


Euglycemic DKA

Euglycemic DKA涉及相对碳水化合物缺乏状态/血清葡萄糖的标准化,并伴随着对抗调节胁迫激素的升高,导致游离脂肪酸分解代谢和酮生产。

Maintain a high index of suspicion for DKA in the following patients who present with nausea, vomiting, shortness of breath and/or metabolic acidosis, and evaluate for DKA with serum ketones and/or β-hydroxybutyrate:

  • T1/T2DM Patients taking SGLT-2 inhibitors (the “zins”)
  • Pregnant patients – due to transplacental glucose transport, will have relative euglycemia (more common in second or third trimester)
  • 慢性胰腺炎
  • 畜牧手术患者 - 由于吸收问题

对于Egglycex DKA的管理,您可能需要在治疗过程中早期用葡萄糖开始流体。

沃尔特HIMMEL在eGlycex DKA上的最佳案例


Goals of treatment in DKA

The initial goals of treatment in patients with DKA include:

  • 纠正流体缺陷
  • Replacement of potassium
  • Stopping ketone production by closing the anion gap with insulin
  • 治疗潜在的沉淀剂



使用standardized DKA order setsfor the management of DKA has been shown to decrease the time to anion gap closure, reduce length of stay in hospital, and minimize complications during treatment.




渗透Diuresis.来自高血糖导致显着的结果volume depletion。流体复苏将有助于恢复血管内体积,实现正常张力,改善器官灌注,降低乳酸形成,改善肾功能。

  • 使用NS或RL进行初始流体更换(美国糖尿病协会-ADA):1000-1500ml,超过1小时),然后调整患者的血液动力学和电解质状态,并保持在250到500毫升/小时之间
  • ADA:在液体置换的第一小时后,可以在液态溶液中的正常或高溶液浓度切换至0.45%氯化钠
  • Add dextrose (D5W) to the IV fluid if/when blood glucose approaches normal to allow continued insulin infusion at a rate sufficient to resolve DKA while avoiding hypoglycemia OR when glucose <15 (250-300mg/DL) switch to D5-1/2NS NS at an initial rate of 150 to 250 mL/h
  • Our experts recommend starting with NS or RL and consider ongoing fluid resuscitation with RL to avoid the hyperchloremic acidosis associated with large volumes of NS

关键点:Volume resuscitationmustprecede insulin therapyin order to adequately restore intravascular volume and tonicity. Early insulin therapy has the added risk of hypoglycemia and hypokalemia.


两袋半ns在每小时血糖监测的基础上调整一个没有10%葡萄糖(D10W)的一个,保持250ml / h的IV流体速率。两种以上患者的回顾性研究发现,与常规递送IV液体相比,2袋方法与酸中毒的早期校正和较短的IV胰岛素校正相关。在ED中使用HE 2袋法可能会降低医院入院的需求,与常规治疗相比,它可能与较少的低血糖相关联。

DKA.一世nsulin Therapy: Closing the Gap


  • 以固定的基于重量的0.1u / kg / hr的给药开始短作用胰岛素
  • 目标血糖为12-14mmol / L和阴离子间隙的标准化
  • 当血糖<14mmol / L时,加入右旋糖D5输注,以防止低血糖在继续胰岛素输注时
  • 如果葡萄糖落下<4mmol / L,请勿终止胰岛素输注,但减少50%(不小于0.5u / kg / hr),提供1放大的D50,从D5到D10切换右侧输注



What about insulin bolus?There is没有引发胰岛素的作用,除了可能在围困情况下。推注胰岛素增加降血糖事件的风险,长期间隙闭合,较长的医院住宿。


患有DKA的患者具有大量的身体钾缺陷。然而,由于次要体积收缩和代谢酸中毒的细胞内变化,初始钾读数通常是正常的或高。Potassium must be replaced prior to initiation of insulin therapy由于胰岛素进一步促进钾的细胞内偏移。


一世f the patient can tolerateoral potassium replacement那it is preferred over the IV route as it thought to have better systemic absorption.



患者通常可以用他们的家用胰岛素方案治疗(理想的是每日狼吞虎咽的每日剂量)。对于胰岛胰岛素的耐心,可以给出0.25单位/ kg每天的狼原体(锰料)的起始剂量。

Role of Bicarbonate in Severe DKA

The literature does not support replacing bicarb in adult DKA patients with pH ≥6.9. There is retrospective evidence of transient paradoxical worsening of ketosis and an increased need for potassium supplementation in patients who received bicarb. Our experts caution against the routine use of bicarbonate therapy in DKA. The decision to give bicarb should be tailored to the individual patient, their hemodynamics and their acid/base status.

emergency management of pediatric seizures




  • 一世nadequate fluid resuscitation
  • 胰岛素剂量不足
  • Malfunction of insulin infusion
  • 潜在的诊断有助于未解决的阴离子差距

一世nterventions if the anion gap is not closing:

  • Evaluate fluid status (e.g. with ultrasonography), provide additional crystalloid if necessary
  • 考虑增加胰岛素输注率(见下一部分)
  • 重新评估错过的潜在诊断
  • 考虑检查β-羟基丁酸酯和乳酸水平,以排除神秘/恶化乳酸一种cidosis


分析了患者生理上的挑战patients to intubate for several reasons. Their respiratory dynamics of hyperpnea to correct their underlying metabolic acidosis means the ventilator must equally match their large tidal volume and respiratory rate. This intrinsically puts the patient at risk for ventilator induced lung injury and subsequent development of ARDS. Furthermore, these patients with profound metabolic acidosis are at risk of circulatory collapse peri-intubation as periods of apnea during intubation will cause their pCO2水平迅速上升,恶化酸中毒。

一世f you must intubate:

  1. Resuscitate before you intubate
  2. Consider ketamine +/- paralytic; continue to bag if paralytic used to avoid any period of apnea
  3. Consider an antiemetic
  4. 考虑给予IV BOLUS BICARB,特别是如果血清BICARB <10
  5. 高潮量(8CC / kg)和RR(24-28)过度通气
  6. Consider asking for additional help from your anesthesiology colleagues

The Role of NIPPV in DKA

Oxygenation is rarely an issue in DKA, but rather work of breathing and respiratory fatigue may occur. Our experts do没有trecommend the routine use of BiPAP in DKA patients given the risk of aspiration and emesis in these patients, as they often concurrently have gastroparesis. Only consider NIPPV if the patient is in a highly monitored setting with one-to-one nursing care.


Avoiding Cerebral Edema in DKA

The key to avoiding cerebral edema in the management of DKA is togo slowwith resuscitation.

  • 避免过度激进的液体给药
  • 不要太快放下葡萄糖;避免在<200mg / dl(<11.1mmol)以下的葡萄糖
  • 逐渐更换液体
    • 考虑等渗流体(例如,D5 R1可以用作含葡萄糖的IV液体的源,而不是低渗流体,例如D10W或D5 1/2 NS)。
    • 避免将血清渗透压降低超过3mmol / kg /小时或通过> 10 mmol / 24小时降低钠
  • 请注意,钠通常最初increaseduring resuscitation due to glucose entering the cells. This does没有t反映血清渗透压的增加,并确实如此没有t需要用自由水进行治疗


葡萄糖<11.1mmol(<200mg / dl)+ 2:

  1. Normalization of AG
  2. 静脉pH> 7.3
  3. 血清碳酸氢盐≥15meq/ l


  1. 一世dentify the underlying cause/trigger which is often the cause of death in DKA and HHS patients – use the mnemonic5“我”加药物if that helps you remember the triggers
  2. 做没有t rule out DKA based on a normal serum pH or a normal serum glucose – measure beta-hydroxybutyrate when in doubt
  3. DKA中的主要目标是缩小间隙,不正常化葡萄糖水平
  4. 当血清葡萄糖变得正常或低时,请勿停止胰岛素;相反,给葡萄糖
  5. Allow patient to eat as soon as there is no aspiration risk
  6. Avoid intubation and BiPAP whenever possible in severe DKA – HFNC is your go-to if they are not doing well on a non-rebreather
  7. 知道如何区分酮症中的所有原因 - 有微妙的线索
  8. Use a protocol – there is good evidence that protocols for DKA management improve patient outcomes
  9. Monitor carefully for complications of DKA: hypoglycemia, hypokalemia, ARDS


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  3. Wolfsdorf JI, Glaser N, Agus M, et al. ISPAD Clinical Practice Consensus Guidelines 2018: diabetic ketoacidosis and the hyperglycemic hyperosmolar state. Pediatr Diabetes. 2018;19 Suppl 27:155-177.Fayfman M, Pasquel F, Umpierrez G. Management of Hyperglycemic Crises: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State. Med Clin North Am. 2017;101(3):587-606.
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  5. Goyal N,Miller JB,Sankey SS等。初始推注胰岛素治疗糖尿病酮症病的效用。j excremed。2010; 38(4):422-427。
  6. Ma Oj,Rush Md,Godfrey MM,等。动脉血气结果很少影响疑似糖尿病酮症病患者的患者应急医师管理。Acad Embered Med。2003; 10(8):836-841。
  7. AdroguéHJ,Barrero J,Eknoyan G.适度流体置换在糖尿病酮症中成人治疗的良好影响。在没有极端亏损的患者中使用。贾马。1989; 262(15):210.8-2113
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Euglycemic DKA

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  2. Jazi M, Porfiris G. Euglycemic diabetic ketoacidosis in type 2 diabetes treated with a sodium-glucose cotransporter-2 inhibitor. Can Fam Physician. 2016;62(9):722-4.
  3. Munro JF, Campbell IW, McCuish AC, Duncan LJP. Euglycaemic diabetic ketoacidosis. BMJ 1973;2:578–580.
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  5. Rosenstock J等人。可染糖尿病酮症症:具有SGLT2抑制剂的可预测,可检测和可预防的安全性问题。糖尿病护理。2015年9月38日(9):1638-42。

Drs。蒂尔曼大木船Baimel和大梁没有有限公司nflicts of interest to declare