Hyperosmolar hyperglycemic state historical perspective: Difference between revisions

Jump to navigation Jump to search
No edit summary
 
(25 intermediate revisions by 3 users not shown)
Line 2: Line 2:
{{Hyperosmolar hyperglycemic state}}
{{Hyperosmolar hyperglycemic state}}


{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} {{HS}}


==Overview==
==Overview==
The first cases of the hyperosmolar hyperglycemic state (HHS) were described by Von Frerichs and Dreschfeld in the 1880s in some patients with unusual [[diabetic coma]]. In 1971, Aerieff and Carroll proposed the [[diagnostic criteria]] for patients presenting with [[diabetic coma]] and named it as a [[Hyperosmolar hyperglycemic nonketotic coma|hyperosmolar hyperglycemic nonketotic state]]. In the recent times, the term has been changed to the hyperosmolar hyperglycemic state as most of the patients present without [[coma]] and with minimal [[ketosis]]. Before the discovery of [[insulin]] in 1922, it was rare for the patient of [[diabetes]] with an episode of [[diabetic coma]] to survive for more than a few months. With the discovery of [[insulin]], the development of [[diabetic coma]] in patients with [[diabetes]] became less frequent. The management of hyperosmolar hyperglycemic state has evolved over the years with the use of [[insulin]] and adjustment of doses of [[insulin]] to achieve optimum control of the [[disease]].


==Historical Perspective==
==Historical Perspective==
 
The notable events regarding the history of hyperosmolar hyperglycemic state include:<ref name="pmid820228">{{cite journal |vauthors=Kitabchi AE, Ayyagari V, Guerra SM |title=The efficacy of low-dose versus conventional therapy of insulin for treatment of diabetic ketoacidosis |journal=Ann. Intern. Med. |volume=84 |issue=6 |pages=633–8 |year=1976 |pmid=820228 |doi= |url=}}</ref><ref name="pmid4065612">{{cite journal |vauthors=Fisher JN, Shahshahani MN, Kitabchi AE |title=Diabetic ketoacidosis: low-dose insulin therapy by various routes |journal=N. Engl. J. Med. |volume=297 |issue=5 |pages=238–41 |year=1977 |pmid=406561 |doi=10.1056/NEJM197708042970502 |url=}}</ref><ref name="pmid25342831">{{cite journal| author=Pasquel FJ, Umpierrez GE| title=Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment. | journal=Diabetes Care | year= 2014 | volume= 37 | issue= 11 | pages= 3124-31 | pmid=25342831 | doi=10.2337/dc14-0984 | pmc=4207202 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25342831  }} </ref><ref name="pmid16144505">{{cite journal| author=Milionis HJ, Elisaf MS| title=Therapeutic management of hyperglycaemic hyperosmolar syndrome. | journal=Expert Opin Pharmacother | year= 2005 | volume= 6 | issue= 11 | pages= 1841-9 | pmid=16144505 | doi=10.1517/14656566.6.11.1841 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16144505  }} </ref><ref name="pmid21752485">{{cite journal| author=Fadini GP, de Kreutzenberg SV, Rigato M, Brocco S, Marchesan M, Tiengo A et al.| title=Characteristics and outcomes of the hyperglycemic hyperosmolar non-ketotic syndrome in a cohort of 51 consecutive cases at a single center. | journal=Diabetes Res Clin Pract | year= 2011 | volume= 94 | issue= 2 | pages= 172-9 | pmid=21752485 | doi=10.1016/j.diabres.2011.06.018 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21752485  }} </ref><ref name="pmid16694999">{{cite journal| author=Martin HE, Wick AN| title=QUANTITATIVE RELATIONSHIPS BETWEEN BLOOD AND URINE KETONE LEVELS IN DIABETIC KETOSIS. | journal=J Clin Invest | year= 1943 | volume= 22 | issue= 2 | pages= 235-41 | pmid=16694999 | doi=10.1172/JCI101388 | pmc=435232 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16694999  }} </ref><ref name="pmid14693938">{{cite journal |vauthors=Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI, Wall BM |title=Hyperglycemic crises in diabetes |journal=Diabetes Care |volume=27 Suppl 1 |issue= |pages=S94–102 |year=2004 |pmid=14693938 |doi= |url=}}</ref><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><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>
===Discovery===
* 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.
*[Disease name] was first discovered by [name of scientist], a [nationality + occupation], in [year]/during/following [event].
* 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]].
*The association between [important risk factor/cause] and [disease name] was made in/during [year/event].
* In 1865, Gerhardt discovered [[acetoacetic acid]] in the [[urine]] of patients with [[diabetes]].
*In [year], [scientist] was the first to discover the association between [risk factor] and the development of [disease name].
* In 1874, Kussmaul also described [[diabetic coma]] in detail.
 
* In 1878, Foster described some cases of [[diabetic coma]] and [[ketonemia]].
 
* In 1883–1884, Stadelmann, Külz, Minkowski found out that in addition to [[acetone]] patients with [[diabetic coma]] also have [[Hydroxybutyric acid|β-hydroxybutyric acid]].
* 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 1884–1886, Von Frerichs and Dreschfeld described some cases of patients with [[diabetic coma]] but without [[kussmaul breathing]] or [[ketones]].
* In 1828, von Stosch for the first time described [[diabetic coma]] in detail.
* In 1922, [[insulin]] was discovered and isolated by Banting and Best.
* In 1857, Petters discovered [[acetone]] in the urine of patients with [[diabetes]].
* In 1909–1923, Lépine, Revillet, McCaskey and Bock et al also described some cases of patients with [[diabetic coma]] without [[ketonuria]].
* In 1865, Gerhardt discovered [[acetoacetic acid]] in the urine of patients with [[diabetes]].
* In 1930–1935, Lawrence and Joslin described the management of [[diabetic coma]].
1874 Kussmaul (15) First extensive description of diabetic coma
* In 1957, Sament, Schwartz, Graeff, and Lips also described some case reports of [[diabetic coma]] without [[ketones]] and [[hyperosmolality]].
1878 Foster (11) Cases of diabetic coma and acetonemia
* In 1962, Singer et al explained the relationship of [[hyperglycemia]] and [[osmolality]].
1883–1884 Stadelmann (18)/Külz (19)/Minkowski (20) Discovery of β-hydroxybutyric acid in patients with diabetes
* In 1971, Arieff, Carroll and Gerich et al described the modern definition and initial diagnostic criteria of the hyperosmolar hyperglycemic state which they termed as hyperosmolar hyperglycemic non-ketotic state.
1884–1886 von Frerichs (21)/Dreschfeld (14) Description of a nonketotic diabetic coma
* In 1973, Arieff and Kleeman explained the mechanism of [[cerebral edema]] occurring during the treatment of hyperosmolar hyperglycemic state.
1922 Banting et al. (83) Insulin discovery
* In 1976–1977, Alberti, Hockaday and Kitabchi et al described the low-dose [[insulin]] protocols for the treatment of HHS.
1909–1923 Lépine (92)/Revillet (93)/McCaskey (94)/Bock et al. (95) Case series of diabetic coma without ketonuria
* In 2004–2009, [[American Diabetes Association]] published the guidelines for the management of the hyperosmolar hyperglycemic state in adults.
1930–1935 Lawrence (84)/Joslin (17) Initial recommendations for the management of diabetic comas
* In 2011, Pediatric Endocrine Society guidelines for treatment of HHS in children were published.
1957 Sament and Schwartz (30)/de Graeff and Lips (29) Detailed case reports of diabetic coma without ketones and hyperosmolality
1962 Singer et al. (85) Linking osmolality and hyperglycemia
1971 Arieff and Carroll (55)/Gerich et al. (54) Case series of HHS; initial criteria
1973 Arieff and Kleeman (77) Mechanisms leading to cerebral edema
1976–1977 Alberti and Hockaday (60)/Kitabchi et al. (70) Low-dose insulin protocols
2004–2009 Kitabchi et al. (4,86,87) Position Statement, American Diabetes Association: management of hyperglycemic crises
2011 Zeitler et al. (59) Guidelines for the management of HHS in children
 
==Outbreaks==
*There have been several outbreaks of [disease name], which are summarized below:


==Landmark Events in the Development of Treatment Strategies==
==Landmark Events in the Development of Treatment Strategies==
*In [year], [diagnostic test/therapy] was developed by [scientist] to treat/diagnose [disease name].
The landmark events in the treatment of hyperosmolar hyperglycemic state are:<ref name="pmid820228">{{cite journal |vauthors=Kitabchi AE, Ayyagari V, Guerra SM |title=The efficacy of low-dose versus conventional therapy of insulin for treatment of diabetic ketoacidosis |journal=Ann. Intern. Med. |volume=84 |issue=6 |pages=633–8 |year=1976 |pmid=820228 |doi= |url=}}</ref><ref name="pmid4065612">{{cite journal |vauthors=Fisher JN, Shahshahani MN, Kitabchi AE |title=Diabetic ketoacidosis: low-dose insulin therapy by various routes |journal=N. Engl. J. Med. |volume=297 |issue=5 |pages=238–41 |year=1977 |pmid=406561 |doi=10.1056/NEJM197708042970502 |url=}}</ref><ref name="pmid25342831">{{cite journal| author=Pasquel FJ, Umpierrez GE| title=Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment. | journal=Diabetes Care | year= 2014 | volume= 37 | issue= 11 | pages= 3124-31 | pmid=25342831 | doi=10.2337/dc14-0984 | pmc=4207202 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25342831  }} </ref><ref name="pmid16144505">{{cite journal| author=Milionis HJ, Elisaf MS| title=Therapeutic management of hyperglycaemic hyperosmolar syndrome. | journal=Expert Opin Pharmacother | year= 2005 | volume= 6 | issue= 11 | pages= 1841-9 | pmid=16144505 | doi=10.1517/14656566.6.11.1841 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16144505  }} </ref><ref name="pmid21752485">{{cite journal| author=Fadini GP, de Kreutzenberg SV, Rigato M, Brocco S, Marchesan M, Tiengo A et al.| title=Characteristics and outcomes of the hyperglycemic hyperosmolar non-ketotic syndrome in a cohort of 51 consecutive cases at a single center. | journal=Diabetes Res Clin Pract | year= 2011 | volume= 94 | issue= 2 | pages= 172-9 | pmid=21752485 | doi=10.1016/j.diabres.2011.06.018 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21752485  }} </ref><ref name="pmid16694999">{{cite journal| author=Martin HE, Wick AN| title=QUANTITATIVE RELATIONSHIPS BETWEEN BLOOD AND URINE KETONE LEVELS IN DIABETIC KETOSIS. | journal=J Clin Invest | year= 1943 | volume= 22 | issue= 2 | pages= 235-41 | pmid=16694999 | doi=10.1172/JCI101388 | pmc=435232 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16694999  }} </ref><ref name="pmid14693938">{{cite journal |vauthors=Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI, Wall BM |title=Hyperglycemic crises in diabetes |journal=Diabetes Care |volume=27 Suppl 1 |issue= |pages=S94–102 |year=2004 |pmid=14693938 |doi= |url=}}</ref>
 
{{Family tree/start}}
==Impact on Cultural History==
{{familytree | boxstyle= text-align: Center; | | | |B01| | | | |B01='''''Preinsulin era'''''<br> •The treatment modalities used for [[diabetic coma]] include [[blood transfusion]], castor oil with potassium citrate, and saline solutions with sodium carbonate among other therapies.
| boxstyle_B02= text-align: Center;
| boxstyle_B03= text-align: left;
}}
{{Family tree | | | | |!| | | | | }}
{{familytree | boxstyle= text-align: Center; | | | |B01| | | | |B01= '''''1930–1950'''''<br> •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]].
| boxstyle_B02= text-align: Center;
| boxstyle_B03= text-align: left;
}}
{{Family tree | | | | |!| | | | | }}
{{familytree | boxstyle= text-align: Center; | | | |B01| | | | |B01= '''''1950–1970s'''''<br> • In that period, the [[insulin]] was given as 2 units/kg bolus of crystalline [[insulin]]; up to 920 units in the first 7 h.
| boxstyle_B02= text-align: Center;
| boxstyle_B03= text-align: left;
}}
{{Family tree | | | | |!| | | | | }}
{{familytree | boxstyle= text-align: Center; | | | |B01| | | | |B01= '''''Early 1970s'''''<br> • [[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.
}}
{{Family tree | | | | |!| | | | | }}
{{familytree | boxstyle= text-align: Center; | | | |B01| | | | |B01= '''''1990s'''''<br> • [[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)
}}
{{Family tree | | | | |!| | | | | }}
{{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}}


==Famous Cases==
*The following are a few famous cases of [[disease name]]:
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
Line 50: Line 62:
{{WH}}
{{WH}}
{{WS}}
{{WS}}
[[Category:Medicine]]
[[Category:Endocrinology]]
[[Category:Up-To-Date]]​
[[Category:Emergency medicine]]

Latest revision as of 14:45, 17 October 2017

Hyperosmolar hyperglycemic state Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Hyperosmolar hyperglycemic state from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic study of choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Hyperosmolar hyperglycemic state historical perspective On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Hyperosmolar hyperglycemic state historical perspective

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Hyperosmolar hyperglycemic state historical perspective

CDC on Hyperosmolar hyperglycemic state historical perspective

Hyperosmolar hyperglycemic state historical perspective in the news

Blogs on Hyperosmolar hyperglycemic state historical perspective

Directions to Hospitals Treating Psoriasis

Risk calculators and risk factors for Hyperosmolar hyperglycemic state historical perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Husnain Shaukat, M.D [2]

Overview

The first cases of the hyperosmolar hyperglycemic state (HHS) were described by Von Frerichs and Dreschfeld in the 1880s in some patients with unusual diabetic coma. In 1971, Aerieff and Carroll proposed the diagnostic criteria for patients presenting with diabetic coma and named it as a hyperosmolar hyperglycemic nonketotic state. In the recent times, the term has been changed to the hyperosmolar hyperglycemic state as most of the patients present without coma and with minimal ketosis. Before the discovery of insulin in 1922, it was rare for the patient of diabetes with an episode of diabetic coma to survive for more than a few months. With the discovery of insulin, the development of diabetic coma in patients with diabetes became less frequent. The management of hyperosmolar hyperglycemic state has evolved over the years with the use of insulin and adjustment of doses of insulin to achieve optimum control of the disease.

Historical Perspective

The notable events regarding the history of hyperosmolar hyperglycemic state include:[1][2][3][4][5][6][7][8][9]

  • 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 ketonemia.
  • 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 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 diagnostic criteria of the hyperosmolar hyperglycemic state which they termed as hyperosmolar hyperglycemic non-ketotic state.
  • In 1973, Arieff and Kleeman explained the mechanism of cerebral edema occurring during the treatment of hyperosmolar hyperglycemic state.
  • In 1976–1977, Alberti, Hockaday and Kitabchi et al described the low-dose insulin protocols for the treatment of HHS.
  • In 2004–2009, American Diabetes Association published the guidelines 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

The landmark events in the treatment of hyperosmolar hyperglycemic state are:[1][2][3][4][5][6][7]

 
 
 
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%
 
 
 
 

References

  1. 1.0 1.1 Kitabchi AE, Ayyagari V, Guerra SM (1976). "The efficacy of low-dose versus conventional therapy of insulin for treatment of diabetic ketoacidosis". Ann. Intern. Med. 84 (6): 633–8. PMID 820228.
  2. 2.0 2.1 Fisher JN, Shahshahani MN, Kitabchi AE (1977). "Diabetic ketoacidosis: low-dose insulin therapy by various routes". N. Engl. J. Med. 297 (5): 238–41. doi:10.1056/NEJM197708042970502. PMID 406561.
  3. 3.0 3.1 Pasquel FJ, Umpierrez GE (2014). "Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment". Diabetes Care. 37 (11): 3124–31. doi:10.2337/dc14-0984. PMC 4207202. PMID 25342831.
  4. 4.0 4.1 Milionis HJ, Elisaf MS (2005). "Therapeutic management of hyperglycaemic hyperosmolar syndrome". Expert Opin Pharmacother. 6 (11): 1841–9. doi:10.1517/14656566.6.11.1841. PMID 16144505.
  5. 5.0 5.1 Fadini GP, de Kreutzenberg SV, Rigato M, Brocco S, Marchesan M, Tiengo A; et al. (2011). "Characteristics and outcomes of the hyperglycemic hyperosmolar non-ketotic syndrome in a cohort of 51 consecutive cases at a single center". Diabetes Res Clin Pract. 94 (2): 172–9. doi:10.1016/j.diabres.2011.06.018. PMID 21752485.
  6. 6.0 6.1 Martin HE, Wick AN (1943). "QUANTITATIVE RELATIONSHIPS BETWEEN BLOOD AND URINE KETONE LEVELS IN DIABETIC KETOSIS". J Clin Invest. 22 (2): 235–41. doi:10.1172/JCI101388. PMC 435232. PMID 16694999.
  7. 7.0 7.1 Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI, Wall BM (2004). "Hyperglycemic crises in diabetes". Diabetes Care. 27 Suppl 1: S94–102. PMID 14693938.
  8. Dreschfeld J (1886). "The Bradshawe Lecture on Diabetic Coma". Br Med J. 2 (1338): 358–63. PMC 2256374. PMID 20751675.
  9. Fleckman AM (1993). "Diabetic ketoacidosis". Endocrinol. Metab. Clin. North Am. 22 (2): 181–207. PMID 8325282.

Template:WH Template:WS