今日の臨床サポート

糖尿病性昏睡

著者: 吉岡成人 NTT東日本札幌病院

監修: 野田光彦 国際医療福祉大学市川病院 糖尿病・代謝・内分泌内科

著者校正/監修レビュー済:2021/08/04

概要・推奨   

  1. 糖尿病ケトアシドーシス(DKA)は、高血糖(≧250mg/dL)、高ケトン血症(β-ヒドロキシ酪酸の増加)、アシドーシス(pH≦7.30、重炭酸塩濃度≦18mEq/L)を来した状態であり、緊急の対応が強く推奨される(推奨度1)。
  1. DKAの治療の基本は脱水の補正とナトリウムの補充であり、生理食塩水を中心とした十分な輸液とインスリンの持続点滴を行うことが推奨される(推奨度1)。
  1. DKAの初期治療としてインスリンの静脈投与(ボーラス投与)をインスリンの持続点滴と併用することは推奨されない(推奨度3)。
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  1. 高血糖(≧600mg/dL)、高浸透圧血症(≧320mOsm/L)をもたらすがアシドーシスは認めない(pH>7.30、HCO3>18~20mEq/L)状態は、高浸透圧高血糖状態(hyperosmolar hyperglycemic syndrome:HHS)と呼ばれ、緊急の対応が推奨される(推奨度1)。
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薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
吉岡成人 : 特に申告事項無し[2021年]
監修:野田光彦 : 特に申告事項無し[2021年]

改訂のポイント:
  1. 定期レビューを行い米国糖尿病学(ADA)、欧州糖尿病学会(EASD)のガイドライン、日本糖尿病学会出版の糖尿病治療ガイドを参考として用語の変更などを行った。

病態・疫学・診察

疾患情報  
  1. インスリンの極端な欠乏とインスリン拮抗ホルモン(グルカゴン、コルチゾール、アドレナリンなど)の増加により、高血糖、高ケトン血症、アシドーシスを来した状態が糖尿病性ケトアシドーシス(DKA)である。
  1. 肝臓におけるグルコースとケトンの過剰産生と、筋肉や中枢神経系でのグルコースやケトンの処理能の低下が認められる。
  1. インスリンの欠乏とインスリン拮抗ホルモンの増加は脂肪組織におけるホルモン感受性リパーゼの活性を亢進し、脂肪分解(lipolysis)を促進して大量の遊離脂肪酸(long-chain non-esterified fatty acids:NEFA)を供給する。遊離脂肪酸は肝臓でcoenzyme A(CoA)の作用を受け、CPT(carnitine palmitoyltransferase)-Ⅰ、CPT-Ⅱにより能動的にミトコンドリア内に取り込まれ、ケトン体の産生に結び付く。
問診・診察のポイント  
  1. インスリン治療中の1型糖尿病患者が感染性胃腸炎などを引き起こし、嘔気・嘔吐などの消化器症状のため十分な摂食ができず、インスリンを減らしたり中止したりしたときに発症することが多い。劇症1型糖尿病の初発症状としても注目されている。

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文献 

著者: Hiroshi Ikegami, Yumiko Kawabata, Shinsuke Noso
雑誌名: Diabetol Int. 2016 Sep;7(3):221-227. doi: 10.1007/s13340-016-0276-9. Epub 2016 Jul 5.
Abstract/Text Type 1 diabetes is caused by destruction of insulin-producing beta cells of the pancreas. The etiology of type 1 diabetes is immune-mediated by either an organ-specific autoimmune mechanism in autoimmune type 1 diabetes or a still unknown but probably immune-mediated mechanism in fulminant type 1 diabetes. Immunomodulation is therefore expected to accelerate or inhibit type 1 diabetes. Recent progress in anti-cancer therapy by immune-checkpoint blockade, such as anti-PD-1 and anti-CTLA4 monoclonal antibodies, has markedly improved the prognosis of patients with advanced cancers. These drugs activate anti-tumor immunity by blocking inhibitory signals of T lymphocytes. Activation of immunological pathways, however, is expected to accelerate immune-mediated diseases. In fact, the development of autoimmune-thyroid diseases and type 1 diabetes, including fulminant type 1 diabetes, has been reported in patients treated with immune checkpoint blockers. The development of fulminant type 1 diabetes is a major concern because of its abrupt onset and very rapid progression, leading to death unless proper treatment is initiated immediately after diagnosis. In this review, the development of type 1 diabetes with immune-checkpoint therapy and its etiological background are discussed.

PMID 30603267  Diabetol Int. 2016 Sep;7(3):221-227. doi: 10.1007/s1334・・・
著者: Anne L Peters, Elizabeth O Buschur, John B Buse, Pejman Cohan, Jamie C Diner, Irl B Hirsch
雑誌名: Diabetes Care. 2015 Sep;38(9):1687-93. doi: 10.2337/dc15-0843. Epub 2015 Jun 15.
Abstract/Text OBJECTIVE: Sodium-glucose cotransporter 2 (SGLT-2) inhibitors are the most recently approved antihyperglycemic medications. We sought to describe their association with euglycemic diabetic ketoacidosis (euDKA) in hopes that it will enhance recognition of this potentially life-threatening complication.
RESEARCH DESIGN AND METHODS: Cases identified incidentally are described.
RESULTS: We identified 13 episodes of SGLT-2 inhibitor-associated euDKA or ketosis in nine individuals, seven with type 1 diabetes and two with type 2 diabetes, from various practices across the U.S. The absence of significant hyperglycemia in these patients delayed recognition of the emergent nature of the problem by patients and providers.
CONCLUSIONS: SGLT-2 inhibitors seem to be associated with euglycemic DKA and ketosis, perhaps as a consequence of their noninsulin-dependent glucose clearance, hyperglucagonemia, and volume depletion. Patients with type 1 or type 2 diabetes who experience nausea, vomiting, or malaise or develop a metabolic acidosis in the setting of SGLT-2 inhibitor therapy should be promptly evaluated for the presence of urine and/or serum ketones. SGLT-2 inhibitors should only be used with great caution, extensive counseling, and close monitoring in the setting of type 1 diabetes.

© 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
PMID 26078479  Diabetes Care. 2015 Sep;38(9):1687-93. doi: 10.2337/dc1・・・
著者: David E Trachtenbarg
雑誌名: Am Fam Physician. 2005 May 1;71(9):1705-14.
Abstract/Text A diagnosis of diabetic ketoacidosis requires the patient's plasma glucose concentration to be above 250 mg per dL (although it usually is much higher), the pH level to be less than 7.30, and the bicarbonate level to be 18 mEq per L or less. Beta-hydroxybutyrate is a better measurement of the degree of ketosis than serum ketones. Intravenous insulin and fluid replacement are the mainstays of therapy, with careful monitoring of potassium levels. Phosphorous and magnesium also may need to be replaced. Bicarbonate therapy rarely is needed. Infection, insulin omission, and other problems that may have precipitated ketoacidosis should be treated. Myocardial infarction is a precipitating cause of diabetic ketoacidosis that is especially important to look for in older patients with diabetes. Cerebral edema is a major complication that occurs primarily in children. Education to prevent recurrence should be offered to all patients, including how to manage sick days and when to call a physician.

PMID 15887449  Am Fam Physician. 2005 May 1;71(9):1705-14.
著者: Abbas E Kitabchi, Guillermo E Umpierrez, John M Miles, Joseph N Fisher
雑誌名: Diabetes Care. 2009 Jul;32(7):1335-43. doi: 10.2337/dc09-9032.
Abstract/Text
PMID 19564476  Diabetes Care. 2009 Jul;32(7):1335-43. doi: 10.2337/dc0・・・
著者: A E Kitabchi, G E Umpierrez, M B Murphy, E J Barrett, R A Kreisberg, J I Malone, B M Wall
雑誌名: Diabetes Care. 2001 Jan;24(1):131-53.
Abstract/Text
PMID 11194218  Diabetes Care. 2001 Jan;24(1):131-53.
著者: M I Wiggam, M J O'Kane, R Harper, A B Atkinson, D R Hadden, E R Trimble, P M Bell
雑誌名: Diabetes Care. 1997 Sep;20(9):1347-52.
Abstract/Text OBJECTIVE: To compare the efficacy of an extended insulin regimen using correction of hyperketonemia as endpoint with a more conventional regimen in the treatment of diabetic ketoacidosis.
RESEARCH DESIGN AND METHODS: A total of 22 patients admitted to a Belfast teaching hospital with clinical and biochemical features of diabetic ketoacidosis (pH < 7.25 and/or bicarbonate < 16 mmol/l) were randomized to either conventional or extended insulin regimens. In the conventional regimen, insulin was administered at 5 U/h until near-normoglycemia (blood glucose < or = 10 mmol/l) and then administered at a reduced rate until clinical recovery. In the extended regimen, administration of insulin at 5 U/h was continued beyond attainment of normoglycemia, until resolution of hyperketonemia (3-hydroxybutyrate < 0.5 mmol/l). Main outcome measures were 3-hydroxybutyrate and bicarbonate levels during the 24 h after attainment of near-normoglycemia.
RESULTS: After near-normoglycemia, correction of hyperketonemia was achieved earlier with the extended treatment (5.9 +/- 0.8 vs. 21.8 +/- 3.4 h, P = 0.0004 [mean +/- SD]). The area under the curve of 3-hydroxybutyrate against time for 24 h after near-normoglycemia was reduced with the extended treatment (24.9 +/- 3.8 vs. 55.9 +/- 6.7 mmol.l-1.h-1, P = 0.001). These differences remained statistically significant after adjustment for higher baseline levels of 3-hydroxybutyrate at near-normoglycemia in the extended treatment group. Bicarbonate levels at 6 and 12 h after near-normoglycemia were not significantly different between groups.
CONCLUSIONS: The extended insulin regimen, which was easy to implement at ward level, produced a more rapid resolution of ketosis than the conventional regimen.

PMID 9283776  Diabetes Care. 1997 Sep;20(9):1347-52.
著者: G Gamba, J Oseguera, M Castrejón, F J Gómez-Pérez
雑誌名: Rev Invest Clin. 1991 Jul-Sep;43(3):234-8.
Abstract/Text Intravenous sodium bicarbonate has been used for a long time in the treatment of diabetic ketoacidosis. However, there are no clinical studies showing its effectiveness in improving arterial pH in this condition. We therefore designed this study to investigate if bicarbonate therapy improves the rate of increase of arterial pH and to find out its effects on the recovery rate of the other metabolic abnormalities. Twenty patients with severe diabetic ketoacidosis (pH less than 7.15) entered a double-blind, randomized, placebo controlled trial: nine were included in the bicarbonate group and eleven in the placebo group. All patients were studied during the first 24 hours of treatment. Their management was similar, except for the use of sodium bicarbonate in one group and 0.9% saline solution in the placebo group. Heart rate, respiratory rate, arterial pressure, mental status, blood gases, blood glucose, sodium, potassium, and urea were assessed at the beginning of treatment, and then at 2, 6, 12 and 24 hours. No clinical or metabolic differences were found between groups. Two hours after therapy was begun, the arterial pH rose in the bicarbonate group from 7.05 +/- 0.08 to 7.24 +/- 0.04, while it only rose from 7.04 +/- 0.08 to 7.11 +/- 0.09 in the placebo group (p less than 0.02). Simultaneously, arterial bicarbonate increased from 2.87 +/- 1.2 to 6.1 +/- 1.5 mEq/L in the bicarbonate group and from 2.55 +/- 0.81 to 3.6 +/- 2 mEq/L in the placebo group (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

PMID 1667955  Rev Invest Clin. 1991 Jul-Sep;43(3):234-8.
著者: L R Morris, M B Murphy, A E Kitabchi
雑誌名: Ann Intern Med. 1986 Dec;105(6):836-40.
Abstract/Text Twenty-one adult patients with severe diabetic ketoacidosis entered a randomized prospective protocol in which variable doses of sodium bicarbonate, based on initial arterial pH (6.9 to 7.14), were administered to 10 patients (treatment group) and were withheld from 11 patients (control group). During treatment, there were no significant differences in the rate of decline of glucose or ketone levels or in the rate of increase in pH or bicarbonate levels in the blood or cerebrospinal fluid in either group. Similarly, there were no significant differences in the time required for the plasma glucose level to reach 250 mg/dL, blood pH to reach 7.3, or bicarbonate level to reach 15 meq/L. We conclude that in severe diabetic ketoacidosis (arterial pH 6.9 to 7.14), the administration of bicarbonate does not affect recovery outcome variables as compared with those in a control group.

PMID 3096181  Ann Intern Med. 1986 Dec;105(6):836-40.
著者: Abbas E Kitabchi, Mary Beth Murphy, Judy Spencer, Robert Matteri, Jim Karas
雑誌名: Diabetes Care. 2008 Nov;31(11):2081-5. doi: 10.2337/dc08-0509. Epub 2008 Aug 11.
Abstract/Text OBJECTIVE: The purpose of this study was to assess the efficacy of an insulin priming dose with a continuous insulin infusion versus two continuous infusions without a priming dose.
RESEARCH DESIGN AND METHODS: This prospective randomized protocol used three insulin therapy methods: 1) load group using a priming dose of 0.07 units of regular insulin per kg body weight followed by a dose of 0.07 unit x kg(-1) x h(-1) i.v. in 12 patients with diabetic ketoacidosis (DKA); 2) no load group using an infusion of regular insulin of 0.07 unit . kg body weight(-1) x h(-1) without a loading dose in 12 patients with DKA, and 3) twice no load group using an infusion of regular insulin of 0.14 x kg(-1) x h(-1) without a loading dose in 13 patients with DKA. Outcome was based on the effects of insulin therapy on biochemical and hormonal changes during treatment and recovery of DKA.
RESULTS: The load group reached a peak in free insulin value (460 microU/ml) within 5 min and plateaued at 88 microU/ml in 60 min. The twice no load group reached a peak (200 microU/ml) at 45 min. The no load group reached a peak (60 microU/ml) in 60-120 min. Five patients in the no load group required supplemental insulin doses to decrease initial glucose levels by 10%; patients in the twice no load and load groups did not. Except for these differences, times to reach glucose or=7.3, and HCO(3)(-) >or=15 mEq/l did not differ significantly among the three groups.
CONCLUSIONS: A priming dose in low-dose insulin therapy in patients with DKA is unnecessary if an adequate dose of regular insulin of 0.14 unit x kg body weight(-1) x h(-1) (about 10 units/h in a 70-kg patient) is given.

PMID 18694978  Diabetes Care. 2008 Nov;31(11):2081-5. doi: 10.2337/dc0・・・
著者: Gregg D Stoner
雑誌名: Am Fam Physician. 2005 May 1;71(9):1723-30.
Abstract/Text Hyperosmolar hyperglycemic state is a life-threatening emergency manifested by marked elevation of blood glucose, hyperosmolarity, and little or no ketosis. With the dramatic increase in the prevalence of type 2 diabetes and the aging population, this condition may be encountered more frequently by family physicians in the future. Although the precipitating causes are numerous, underlying infections are the most common. Other causes include certain medications, non-compliance, undiagnosed diabetes, substance abuse, and coexisting disease. Physical findings of hyperosmolar hyperglycemic state include those associated with profound dehydration and various neurologic symptoms such as coma. The first step of treatment involves careful monitoring of the patient and laboratory values. Vigorous correction of dehydration with the use of normal saline is critical, requiring an average of 9 L in 48 hours. After urine output has been established, potassium replacement should begin. Once fluid replacement has been initiated, insulin should be given as an initial bolus of 0.15 U per kg intravenously, followed by a drip of 0.1 U per kg per hour until the blood glucose level falls to between 250 and 300 mg per dL. Identification and treatment of the underlying and precipitating causes are necessary. It is important to monitor the patient for complications such as vascular occlusions (e.g., mesenteric artery occlusion, myocardial infarction, low-flow syndrome, and disseminated intravascular coagulopathy) and rhabdomyolysis. Finally, physicians should focus on preventing future episodes using patient education and instruction in self-monitoring.

PMID 15887451  Am Fam Physician. 2005 May 1;71(9):1723-30.
著者: Maryann Mazer, Esther Chen
雑誌名: Ann Emerg Med. 2009 Feb;53(2):259-63.
Abstract/Text To determine whether intermittent subcutaneous administration of rapid-acting insulin is as effective as intravenous infusion of regular insulin for treating uncomplicated diabetic ketoacidosis, we performed a MEDLINE, EMBASE, and Cochrane Library search, using the key words "subcutaneous insulin AND intravenous insulin AND diabetic ketoacidosis; LIMIT humans and English." We also searched the references in these articles for additional studies. This search yielded a total of 35 articles, 4 of which directly addressed the question at hand. According to this review of the available evidence; subcutaneous administration of rapid-acting insulin analogs such as lispro is as effective and safe as intravenous infusion of regular insulin for the management of uncomplicated diabetic ketoacidosis. In addition, use of insulin analogs may confer an overall cost savings, obviating the need for infusion pumps and ICU admissions in certain institutions. Therefore, it would be safe and effective to use subcutaneously administered rapid-acting insulin analogues instead of intravenous regular insulin infusions for patients with uncomplicated diabetic ketoacidosis.

PMID 19177639  Ann Emerg Med. 2009 Feb;53(2):259-63.
著者: Guillermo E Umpierrez, Sidney Jones, Dawn Smiley, Patrick Mulligan, Trevor Keyler, Angel Temponi, Crispin Semakula, Denise Umpierrez, Limin Peng, Miguel Cerón, Gonzalo Robalino
雑誌名: Diabetes Care. 2009 Jul;32(7):1164-9. doi: 10.2337/dc09-0169. Epub 2009 Apr 14.
Abstract/Text OBJECTIVE: To compare the safety and efficacy of insulin analogs and human insulins both during acute intravenous treatment and during the transition to subcutaneous insulin in patients with diabetic ketoacidosis (DKA).
RESEARCH DESIGN AND METHODS: In a controlled multicenter and open-label trial, we randomly assigned patients with DKA to receive intravenous treatment with regular or glulisine insulin until resolution of DKA. After resolution of ketoacidosis, patients treated with intravenous regular insulin were transitioned to subcutaneous NPH and regular insulin twice daily (n = 34). Patients treated with intravenous glulisine insulin were transitioned to subcutaneous glargine once daily and glulisine before meals (n = 34).
RESULTS: There were no differences in the mean duration of treatment or in the amount of insulin infusion until resolution of DKA between intravenous treatment with regular and glulisine insulin. After transition to subcutaneous insulin, there were no differences in mean daily blood glucose levels, but patients treated with NPH and regular insulin had a higher rate of hypoglycemia (blood glucose <70 mg/dl). Fourteen patients (41%) treated with NPH and regular insulin had 26 episodes of hypoglycemia and 5 patients (15%) in the glargine and glulisine group had 8 episodes of hypoglycemia (P = 0.03).
CONCLUSIONS: Regular and glulisine insulin are equally effective during the acute treatment of DKA. A transition to subcutaneous glargine and glulisine after resolution of DKA resulted in similar glycemic control but in a lower rate of hypoglycemia than with NPH and regular insulin. Thus, a basal bolus regimen with glargine and glulisine is safer and should be preferred over NPH and regular insulin after the resolution of DKA.

PMID 19366972  Diabetes Care. 2009 Jul;32(7):1164-9. doi: 10.2337/dc09・・・
著者: J N Fisher, A E Kitabchi
雑誌名: J Clin Endocrinol Metab. 1983 Jul;57(1):177-80. doi: 10.1210/jcem-57-1-177.
Abstract/Text The use of phosphate therapy in the management of diabetic ketoacidosis (DKA) has been controversial, particularly with respect to the effect of phosphate intermediates on tissue oxygenation. In a prospective randomized study we evaluated the effect of phosphate (8.5 mmol/h or approximately 6 g phosphate/24 h) (experimental group) vs. no phosphate therapy (control group) in 30 DKA patients, 15 in each group. Various determinations including erythrocyte 2,3-diphosphoglycerate (2,3-DPG), oxyhemoglobin dissociation (p50), serum phosphate, calcium, lactate, pyruvate, electrolytes, and response time to reach predetermined values for glucose, bicarbonate, and pH were measured at frequent intervals during the first 24 h of therapy and daily for 5 days after metabolic control. Initial electrolytes, glucose, pH, erythrocyte 2,3-DPG, lactate, and p50 were not different in either group. Whereas the experimental group had a greater level of 2,3-DPG than the control group by 48 h, the difference was not statistically significant. Recovery indices, including hours to reach glucose of 250 mg/dl, bicarbonate greater than 15 meq/liter, pH greater than 7.3, and mental alertness, were not different in the two groups nor were the p50 or lactate measurements. The experimental group exhibited significantly lower plasma ionized calcium values during therapy. We conclude that phosphate therapy may accelerate regeneration of erythrocyte 2,3-DPG but in the relatively small number of patients studied it had no demonstrable influence on tissue oxygenation or clinical response to low dose insulin therapy of DKA. Furthermore, the exaggeration of hypocalcemia seen in phosphate-treated patients may be reason for caution in the use of such therapy.

PMID 6406531  J Clin Endocrinol Metab. 1983 Jul;57(1):177-80. doi: 10・・・

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ご契約の場合はご招待された方だけのご優待特典があります。

以下の優待コードを入力いただくと、

契約期間が通常12ヵ月のところ、14ヵ月ご利用いただけます。

優待コード: (利用期限:まで)

ご契約はこちらから