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Diabetic Ketoacidosis and Hyperosmolar BMJ: First Published As 10.1136/Bmj.L1114 on 29 May 2019 STATE OF THE ART REVIEW Diabetic ketoacidosis and hyperosmolar BMJ: first published as 10.1136/bmj.l1114 on 29 May 2019. Downloaded from hyperglycemic syndrome: review of acute decompensated diabetes in adult patients Esra Karslioglu French,1 Amy C Donihi,2 Mary T Korytkowski1 1Division of Endocrinology and Metabolism, Department of ABSTRACT Medicine, University of Pittsburgh, Pittsburgh, PA, USA Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome (HHS) are life threatening 2University of Pittsburgh School of complications that occur in patients with diabetes. In addition to timely identification of the Pharmacy, Pittsburgh, PA, USA Correspondence to: M Korytkowski precipitating cause, the first step in acute management of these disorders includes aggressive [email protected] administration of intravenous fluids with appropriate replacement of electrolytes (primarily Cite this as: BMJ 2019;365:l1114 doi: 10.1136/bmj.l1114 potassium). In patients with diabetic ketoacidosis, this is always followed by administration Series explanation: State of the of insulin, usually via an intravenous insulin infusion that is continued until resolution of Art Reviews are commissioned on the basis of their relevance to ketonemia, but potentially via the subcutaneous route in mild cases. Careful monitoring academics and specialists in the US and internationally. For this reason by experienced physicians is needed during treatment for diabetic ketoacidosis and HHS. they are written predominantly by Common pitfalls in management include premature termination of intravenous insulin US authors therapy and insufficient timing or dosing of subcutaneous insulin before discontinuation of intravenous insulin. This review covers recommendations for acute management of diabetic ketoacidosis and HHS, the complications associated with these disorders, and methods for http://www.bmj.com/ preventing recurrence. It also discusses why many patients who present with these disorders are at high risk for hospital readmissions, early morbidity, and mortality well beyond the acute presentation. Introduction Sources and section criteria on 29 September 2021 by guest. Protected copyright. Diabetic ketoacidosis and hyperosmolar hyperglycemic We searched PubMed from May 1975 through January syndrome (HHS) are life threatening emergencies that 2019 to identify English language articles published in occur in patients with type 1 diabetes and type 2 diabe- peer reviewed journals by using the following search tes.1-4 Diabetic ketoacidosis is defined by a triad of hyper- terms: diabetic ketoacidosis, euglycemic diabetic ketoac- glycemia (or a diagnosis of diabetes), metabolic acidosis, idosis, hyperosmolar hyperglycemic syndrome, hyper- and ketonemia (table 1).1 2 5-7 HHS is defined by severe glycemic crisis, sodium glucose cotransporter 2 (SGLT2) hyperglycemia, high serum osmolality, and dehydra- inhibitors, protocols, cerebral edema, and hyperchlo- tion (table 2).4 8 The presentation of each of these dia- remic metabolic acidosis. We also identified references betic emergencies often overlaps.3 8 Early diagnosis and from relevant review articles, as well as from the similar management with attention to prevention strategies are items section of PubMed. We screened and reviewed more essential to improve patients’ outcomes.1 2 This is particu- than 200 articles in the preparation of this manuscript. larly important for patients presenting with “euglycemic” We reviewed only articles including humans. We consid- diabetic ketoacidosis, which is a term used to describe ered inclusion of studies with smaller numbers of par- diabetic ketoacidosis accompanied by lower than antici- ticipants to be important, as these make up the majority pated blood glucose.1 5 7 9 10 of prospective studies for both diabetic ketoacidosis and The target audience for this review is endocrinolo- HHS. Retrospective database reviews are also included, gists, hospital based physicians, and other physicians or as is one case report illustrating the rare development of healthcare providers involved in the care of adult patients cerebral edema in an adult patient.11 We excluded articles with or at risk for diabetic ketoacidosis and HHS. We pre- published in non-peer reviewed journals or those that sent the epidemiology, pathophysiology, precipitating were not available in PubMed. We prioritized publica- causes, clinical presentation, acute management, com- tions within the past decade covering the epidemiology plications, and prevention of these disorders. In addition, and treatment of diabetic ketoacidosis and HHS in adult we review some of the controversies and observed pitfalls patients. We also prioritized inclusion of manuscripts that in the management of these patients. provided elegant examinations of the pathophysiology of For personal use only 1 of 15 STATE OF THE ART REVIEW 10 Table 1 | Diagnostic criteria for diabetic ketoacidosis in adults iture of $2.4bn (£1.9bn; €2.1bn) per year in the US. In the BMJ: first published as 10.1136/bmj.l1114 on 29 May 2019. Downloaded from 1 2 5 UK, the average cost for an episode of diabetic ketoacidosis Criteria ADA UK AACE/ACE 18 Year of publication 2009 2013 2016 is estimated to be £2064 ($2682; €2384) per patient. Plasma glucose concentration, >13.9 (250 mg/dL)* >11 (>200 mg/dL)or NA Diabetic ketoacidosis was a fatal disease before the dis- mmol/L known diabetes covery of insulin in 1921. Nearing 100 years of insulin pH Mild: 7.25-7.30; moderate: <7.3 (severe: <7.0) <7.3 availability, mortality related to diabetic ketoacidosis in 7.00-7.24; severe: <7.00 the adult population has progressively declined to less Bicarbonate concentration, Mild: 15-18; moderate: <15 (severe: <5) NA than 1%.13 Certain groups of patients have mortality rates mmol/L or mEq/L 10-14.9; severe: <10 Anion gap: Na+–(Cl–+HCO –) Mild: >10; moderate: >12; NA (severe: >16) >10 of up to 5%, including patients with significant comor- 3 19 severe: >12 bid conditions and those of advanced age. HHS, which Urine acetoacetate Positive Positive Positive occurs more commonly in older adults with underlying (nitroprusside reaction) comorbidities, has a 10-20% mortality rate.8 20 † Blood β-hydroxybutyrate, NA ≥3 (31 mg/dL) (severe: >6) ≥3.8 (40 mg/dL) Interest has been renewed in euglyemic diabetic mmol/L ketoacidosis, which was first described as a case series Mental status Mild: alert; moderate: alert or NA Drowsy, stupor, or drowsy; severe: stupor or coma coma of 37 patients presenting with blood glucose below 300 9 AACE/ACE=American Association of Clinical Endocrinologists/American College of Endocrinology; ADA=American Diabetes mg/dL. Euglycemic diabetic ketoacidosis can result in Association; NA=not included in guideline document. delayed diagnosis and treatment, as well as potential *2019 ADA guideline provides update to this 2009 guideline and now states “There is considerable variability… ranging from 17 euglycemia or mild hyperglycemia and acidosis to severe hyperglycemia, dehydration, and coma.”6 for adverse metabolic consequences. Since the recent †β-hydroxybutyrate updated to >3 mmol/L in 2016 updated review cited in 2019 ADA guideline.6 7 introduction of the SGLT2 inhibitors, several case reports and series describing euglycemic diabetic ketoacidosis Table 2 | Diagnostic criteria for hyperglycemic hyperosmolar state in adults in patients treated with these agents have been pub- 21-23 Criteria ADA1 UK4 lished. The entity of euglycemic diabetic ketoacidosis Year of publication 2009 2015 is not limited to patients using SGLT2 inhibitors, however, Plasma glucose concentration, mmol/L >33.3 ≥30 as it has also been described in the setting of alcohol use 9 24 pH >7.30 >7.30 disorders, pregnancy, and chronic liver disease. Bicarbonate concentration, mmol/L >18* >15 + – – Anion gap: Na –(Cl +HCO3 ) NA NA Pathophysiology Urine acetoacetate (nitroprusside reaction) Negative or low positive NA Both diabetic ketoacidosis and HHS result from relative or Blood β-hydroxybutyrate, mmol/L NA <3 absolute insulin deficiency together with an increase in Osmolality, mmol/kg >320† ≥320‡ circulating concentrations of counterregulatory hormones http://www.bmj.com/ Presentation Stupor or coma Severe dehydration and feeling unwell (figure).1 25 ADA=American Diabetes Association; NA=not included in guideline document. *Updated to >15 mmol/L in 2016 updated review cited in 2019 ADA guideline.6 7 †ADA guideline calculates effective plasma osmolality using equation 2×Na+glucose (mmol/L) or 2×Na+glucose (mg/ Pathophysiology of diabetic ketoacidosis dL)/18. In the usual clinical situation, a rise in counterregula- ‡UK guideline calculates osmolality using equation 2×Na+glucose (mmol/L)+(blood urea nitrogen (mmol/L) or 2×Na+glucose (mg/dL)/18+blood urea nitrogen (mg/dL))/2.8. tory hormones contributes to accelerated gluconeogen- esis, glycogenolysis, and impaired glucose utilization by peripheral tissues and leads to diabetic ketoacidosis.25 on 29 September 2021 by guest. Protected copyright. both diabetic ketoacidosis and HHS that were published Glucagon is the primary counterregulatory hormone between 1980 and 1987, as it is unlikely that these stud- responsible for development of diabetic ketoacidosis, ies will be repeated. We included randomized controlled as increases in other counterregulatory hormones (cat- trials (RCTs) and original articles published in the past echolamines, cortisol, and growth hormone) are not 40 years, as well as consensus statements, guidelines, necessarily observed.1 However, even
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