Hyperosmolar hyperglycemic state historical perspective: Difference between revisions
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* In 1878, Foster described some cases of [[diabetic coma]] and [[acetonemia]]. | * In 1878, Foster described some cases of [[diabetic coma]] and [[acetonemia]]. | ||
* In 1883–1884, Stadelmann, Külz, Minkowski found out that in addition to [[acetone]] patients with [[diabetic coma]] also have [[β-hydroxybutyric acid]]. | * In 1883–1884, Stadelmann, Külz, Minkowski found out that in addition to [[acetone]] patients with [[diabetic coma]] also have [[β-hydroxybutyric acid]]. | ||
* In 1884–1886, von Frerichs and Dreschfeld described some cases of patients with [[diabetic coma]] but without [[kussmaul breathing]] or [[ketones]]. | * In 1884–1886, von Frerichs and Dreschfeld described some cases of patients with [[diabetic coma]] but without [[kussmaul breathing]] or [[ketones]].<ref name="pmid20751675">{{cite journal |vauthors=Dreschfeld J |title=The Bradshawe Lecture on Diabetic Coma |journal=Br Med J |volume=2 |issue=1338 |pages=358–63 |year=1886 |pmid=20751675 |pmc=2256374 |doi= |url=}}</ref> | ||
* In 1922, [[insulin]] was discovered and isolated by Banting and Best. | * In 1922, [[insulin]] was discovered and isolated by Banting and Best. | ||
* In 1909–1923, Lépine, Revillet, McCaskey and Bock et al also described some cases of patients with [[diabetic coma]] without [[ketonuria]]. | * In 1909–1923, Lépine, Revillet, McCaskey and Bock et al also described some cases of patients with [[diabetic coma]] without [[ketonuria]]. | ||
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* In 1971, Arieff, Carroll and Gerich et al described the modern definition and initial criteria of the hyperosmolar hyperglycemic state which they called hyperosmolar hyperglycemic non-ketotic state. | * In 1971, Arieff, Carroll and Gerich et al described the modern definition and initial criteria of the hyperosmolar hyperglycemic state which they called hyperosmolar hyperglycemic non-ketotic state. | ||
* In 1973, Arieff and Kleeman explained the mechanism of [[cerebral edema]] in the treatment of hyperosmolar hyperglycemic state. | * In 1973, Arieff and Kleeman explained the mechanism of [[cerebral edema]] in the treatment of hyperosmolar hyperglycemic state. | ||
* In 1976–1977, Alberti, Hockaday and Kitabchi et al described the low-dose [[insulin]] protocols. | * In 1976–1977, Alberti, Hockaday and Kitabchi et al described the low-dose [[insulin]] protocols.<ref name="pmid8325282">{{cite journal |vauthors=Fleckman AM |title=Diabetic ketoacidosis |journal=Endocrinol. Metab. Clin. North Am. |volume=22 |issue=2 |pages=181–207 |year=1993 |pmid=8325282 |doi= |url=}}</ref> | ||
* In 2004–2009, [[American Diabetes Association]] has consensus for the management of the hyperosmolar hyperglycemic state in adults. | * In 2004–2009, [[American Diabetes Association]] has consensus for the management of the hyperosmolar hyperglycemic state in adults. | ||
* In 2011, Pediatric Endocrine Society guidelines for treatment of HHS in children were published. | * In 2011, Pediatric Endocrine Society guidelines for treatment of HHS in children were published. | ||
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{{familytree | boxstyle= text-align: Center; | | | |B01| | | | |B01= '''''2004–2009'''''<br> • ADA consensus for treatment of DKA and HHS in adult patients according to which Initial bolus (0.1 units/kg i.v.), followed by 0.1 units/kg/h until glucose <250 mg/dL, then reduce insulin by 50% | {{familytree | boxstyle= text-align: Center; | | | |B01| | | | |B01= '''''2004–2009'''''<br> • ADA consensus for treatment of DKA and HHS in adult patients according to which Initial bolus (0.1 units/kg i.v.), followed by 0.1 units/kg/h until glucose <250 mg/dL, then reduce insulin by 50% | ||
}} | }} | ||
{{Family tree/end}} | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 22:28, 20 September 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Historical Perspective
- The known history of diabetes dates back to the Egyptian era, and the first documented evidence was found in an Egyptian papyrus dating back to 1552 BC.
- In 1828, von Stosch for the first time described diabetic coma in detail.
- In 1857, Petters discovered acetone in the urine of patients with diabetes.
- In 1865, Gerhardt discovered acetoacetic acid in the urine of patients with diabetes.
- In 1874, Kussmaul also described diabetic coma in detail.
- In 1878, Foster described some cases of diabetic coma and acetonemia.
- In 1883–1884, Stadelmann, Külz, Minkowski found out that in addition to acetone patients with diabetic coma also have β-hydroxybutyric acid.
- In 1884–1886, von Frerichs and Dreschfeld described some cases of patients with diabetic coma but without kussmaul breathing or ketones.[1]
- In 1922, insulin was discovered and isolated by Banting and Best.
- In 1909–1923, Lépine, Revillet, McCaskey and Bock et al also described some cases of patients with diabetic coma without ketonuria.
- In 1930–1935, Lawrence and Joslin described the management of diabetic coma.
- In 1957, Sament, Schwartz, Graeff, and Lips also described some case reports of diabetic coma without ketones and hyperosmolality.
- In 1962, Singer et al explained the relationship of hyperglycemia and osmolality.
- In 1971, Arieff, Carroll and Gerich et al described the modern definition and initial criteria of the hyperosmolar hyperglycemic state which they called hyperosmolar hyperglycemic non-ketotic state.
- In 1973, Arieff and Kleeman explained the mechanism of cerebral edema in the treatment of hyperosmolar hyperglycemic state.
- In 1976–1977, Alberti, Hockaday and Kitabchi et al described the low-dose insulin protocols.[2]
- In 2004–2009, American Diabetes Association has consensus for the management of the hyperosmolar hyperglycemic state in adults.
- In 2011, Pediatric Endocrine Society guidelines for treatment of HHS in children were published.
Landmark Events in the Development of Treatment Strategies
| Preinsulin era •The treatment modalities used for diabetic coma include blood transfusion, castor oil with potassium citrate, and saline solutions with sodium carbonate among other therapies. | |||||||||||||||||||
| 1930–1950 •The usual practice was to use insulin in 20–100 units i.v. or s.c. bolus followed by 20 units s.c. every 30–60 min depending on glucosuria. | |||||||||||||||||||
| 1950–1970s • In that period, the insulin was given as 2 units/kg bolus of crystalline insulin; up to 920 units in the first 7 h. | |||||||||||||||||||
| Early 1970s • Insulin was given as low-dose insulin regimens with Regular insulin 0.1 units/kg i.v. followed by 0.1–0.3 units/h i.v., s.c., or i.m. | |||||||||||||||||||
| 1990s • Insulin was administered as 0.1 units/kg i.v. bolus, then 0.1 units/kg/h as continuous infusion until glucose level <13.8 mmol/L (250 mg/dL) | |||||||||||||||||||
| 2004–2009 • ADA consensus for treatment of DKA and HHS in adult patients according to which Initial bolus (0.1 units/kg i.v.), followed by 0.1 units/kg/h until glucose <250 mg/dL, then reduce insulin by 50% | |||||||||||||||||||