Editing Diabetic ketoacidosis (section)

==History==
The first full description of diabetic ketoacidosis is attributed to [[Julius Dreschfeld]], a German-British pathologist working in [[Manchester]], United Kingdom. In his description, which he gave in an 1886 lecture at the [[Royal College of Physicians]] in London, he drew on reports by [[Adolph Kussmaul|Adolf Kussmaul]] as well as describing the main ketones, acetoacetate and β-hydroxybutyrate, and their chemical determination.<ref>{{cite journal |vauthors=Dreschfeld J |date=August 1886 |title=The Bradshawe Lecture on Diabetic Coma |journal=British Medical Journal |volume=2 |issue=1338 |pages=358–363 |doi=10.1136/bmj.2.1338.358 |pmc=2256374 |pmid=20751675}}</ref> The condition remained almost universally fatal until the [[Insulin#Discovery and characterization|discovery of insulin]] in the 1920s; by the 1930s, mortality had fallen to 29 percent,<ref name="Eledrisi" /> and by the 1950s it had become less than 10 percent.<ref name="Kitabchi2008">{{cite journal |vauthors=Kitabchi AE, Umpierrez GE, Fisher JN, Murphy MB, Stentz FB |date=May 2008 |title=Thirty years of personal experience in hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state |journal=The Journal of Clinical Endocrinology and Metabolism |volume=93 |issue=5 |pages=1541–1552 |doi=10.1210/jc.2007-2577 |pmc=2386681 |pmid=18270259}}</ref> The entity of cerebral edema due to DKA was described in 1936 by a team of doctors from Philadelphia.<ref name="Brown2004" /><ref>{{cite journal |vauthors=Dillon ES, Riggs HE, Dyer WW |year=1936 |title=Cerebral lesions in uncomplicated fatal diabetic acidosis |journal=American Journal of the Medical Sciences |volume=192 |issue=3 |pages=360–365 |doi=10.1097/00000441-193609000-00007 |s2cid=72917358}}</ref>

Numerous research studies since the 1950s have focused on the ideal treatment for diabetic ketoacidosis. A significant proportion of these studies have been conducted at the [[University of Tennessee Health Science Center]] and [[Emory University School of Medicine]].<ref name="Kitabchi2008" /> Treatment options studied have included high- or low-dose intravenous, subcutaneous or intramuscular (e.g. the "[[George Alberti|Alberti]] regime"<ref>{{cite journal | vauthors = Page MM, Alberti KG, Greenwood R, Gumaa KA, Hockaday TD, Lowy C, Nabarro JD, Pyke DA, Sönksen PH, Watkins PJ, West TE | display-authors = 6 | title = Treatment of diabetic coma with continuous low-dose infusion of insulin | journal = British Medical Journal | volume = 2 | issue = 5921 | pages = 687–690 | date = June 1974 | pmid = 4855253 | pmc = 1611148 | doi = 10.1136/bmj.2.5921.687 }}</ref>) insulin, potassium supplementation, need for a loading dose of insulin, and the appropriateness of using bicarbonate therapy in moderate DKA.<ref name="Kitabchi2008" /> Various questions remain unanswered, such as whether bicarbonate administration in severe DKA makes any real difference to the clinical course, and whether an insulin loading dose is needed in adults.<ref name="Kitabchi2008" />