Hyperosmolar hyperglycemic state history and symptoms: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
|||
| (3 intermediate revisions by one other user not shown) | |||
| Line 8: | Line 8: | ||
==History== | ==History== | ||
=== Age of onset === | === Age of onset === | ||
* Older adults especially with | * Older adults especially with a low perception of thirst or low fluid intake, tend to present more likely with hyperosmolar hyperglycemic state (HHS) as the first presentation of [[Diabetes mellitus type 2|type 2 diabetes]].<ref name="pmid23758313">{{cite journal |vauthors=de Vries L, Oren L, Lazar L, Lebenthal Y, Shalitin S, Phillip M |title=Factors associated with diabetic ketoacidosis at onset of Type 1 diabetes in children and adolescents |journal=Diabet. Med. |volume=30 |issue=11 |pages=1360–6 |year=2013 |pmid=23758313 |doi=10.1111/dme.12252 |url=}}</ref><ref name="urlKetoacidosis at first presentation of type 1 diabetes mellitus among children: a study from Kuwait | Scientific Reports">{{cite web |url=https://www.nature.com/articles/srep27519 |title=Ketoacidosis at first presentation of type 1 diabetes mellitus among children: a study from Kuwait | Scientific Reports |format= |work= |accessdate=}}</ref> | ||
* The hyperosmolar hyperglycemic state has also been seen in young adults and children with [[type 1 diabetes]] but less commonly.<ref name="pmid22925225">{{cite journal| author=Bagdure D, Rewers A, Campagna E, Sills MR| title=Epidemiology of hyperglycemic hyperosmolar syndrome in children hospitalized in USA. | journal=Pediatr Diabetes | year= 2013 | volume= 14 | issue= 1 | pages= 18-24 | pmid=22925225 | doi=10.1111/j.1399-5448.2012.00897.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22925225 }} </ref> | * The hyperosmolar hyperglycemic state has also been seen in young adults and children with [[type 1 diabetes]] but less commonly.<ref name="pmid22925225">{{cite journal| author=Bagdure D, Rewers A, Campagna E, Sills MR| title=Epidemiology of hyperglycemic hyperosmolar syndrome in children hospitalized in USA. | journal=Pediatr Diabetes | year= 2013 | volume= 14 | issue= 1 | pages= 18-24 | pmid=22925225 | doi=10.1111/j.1399-5448.2012.00897.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22925225 }} </ref> | ||
=== Initial presentation === | === Initial presentation === | ||
* Patients presents with | * Patients presents with [[nausea]], [[cramps]], and [[fatigue]]. | ||
* Patients may present with a history of poor compliance with [[insulin]] therapy or missed [[insulin]] injections due to [[vomiting]] or [[psychological]] reasons. | * Patients may present with a history of poor compliance with [[insulin]] therapy or missed [[insulin]] injections due to [[vomiting]] or [[psychological]] reasons. | ||
* Hyperosmolar hyperglycemic state has a slower onset, with | * Hyperosmolar hyperglycemic state has a slower onset, with sypmtoms developing over several days to weeks as compared to [[diabetic ketoacidosis]] which presents within hours. | ||
=== Past medical history === | === Past medical history === | ||
* Hyperosmolar hyperglycemic state is associated with a past medical history of [[Diabetes mellitus type 2|type 2 diabetes]]. Type 1 diabetes melitus may also lead to HHS is rare cases.<ref name="pmid15451769">{{cite journal |vauthors=Newton CA, Raskin P |title=Diabetic ketoacidosis in type 1 and type 2 diabetes mellitus: clinical and biochemical differences |journal=Arch. Intern. Med. |volume=164 |issue=17 |pages=1925–31 |year=2004 |pmid=15451769 |doi=10.1001/archinte.164.17.1925 |url=}}</ref><ref name="pmid20119682">{{cite journal |vauthors=Lin MV, Bishop G, Benito-Herrero M |title=Diabetic ketoacidosis in type 2 diabetics: a novel presentation of pancreatic adenocarcinoma |journal=J Gen Intern Med |volume=25 |issue=4 |pages=369–73 |year=2010 |pmid=20119682 |pmc=2842543 |doi=10.1007/s11606-009-1237-9 |url=}}</ref> | * Hyperosmolar hyperglycemic state is associated with a past medical history of [[Diabetes mellitus type 2|type 2 diabetes]]. Type 1 diabetes melitus may also lead to HHS is rare cases.<ref name="pmid15451769">{{cite journal |vauthors=Newton CA, Raskin P |title=Diabetic ketoacidosis in type 1 and type 2 diabetes mellitus: clinical and biochemical differences |journal=Arch. Intern. Med. |volume=164 |issue=17 |pages=1925–31 |year=2004 |pmid=15451769 |doi=10.1001/archinte.164.17.1925 |url=}}</ref><ref name="pmid20119682">{{cite journal |vauthors=Lin MV, Bishop G, Benito-Herrero M |title=Diabetic ketoacidosis in type 2 diabetics: a novel presentation of pancreatic adenocarcinoma |journal=J Gen Intern Med |volume=25 |issue=4 |pages=369–73 |year=2010 |pmid=20119682 |pmc=2842543 |doi=10.1007/s11606-009-1237-9 |url=}}</ref> | ||
* History of other | * History of other comorbidities such as cerebrovascular diseases, [[Myocardial infarction|myocardial infarctions]] etc can precipitate hyperosmolar hyperglycemic state by releasing counterregulatory [[hormones]]. | ||
* History of infections (for example, [[Urinary tract infection|urinary tract infections]], [[pneumonia]] in an individual suffering from [[Diabetes mellitus type 2|type 2 diabetes]].<ref name="pmid22701840">{{cite journal |vauthors=Casqueiro J, Casqueiro J, Alves C |title=Infections in patients with diabetes mellitus: A review of pathogenesis |journal=Indian J Endocrinol Metab |volume=16 Suppl 1 |issue= |pages=S27–36 |year=2012 |pmid=22701840 |pmc=3354930 |doi=10.4103/2230-8210.94253 |url=}}</ref> | * History of [[infections]] (for example, [[Urinary tract infection|urinary tract infections]], [[pneumonia]] in an individual suffering from [[Diabetes mellitus type 2|type 2 diabetes]].<ref name="pmid22701840">{{cite journal |vauthors=Casqueiro J, Casqueiro J, Alves C |title=Infections in patients with diabetes mellitus: A review of pathogenesis |journal=Indian J Endocrinol Metab |volume=16 Suppl 1 |issue= |pages=S27–36 |year=2012 |pmid=22701840 |pmc=3354930 |doi=10.4103/2230-8210.94253 |url=}}</ref> | ||
=== Social history === | === Social history === | ||
* Patients may have a history of use of illicit drugs, for example, [[alcohol]] and [[cocaine]].<ref name="pmid9738609">{{cite journal |vauthors=Warner EA, Greene GS, Buchsbaum MS, Cooper DS, Robinson BE |title=Diabetic ketoacidosis associated with cocaine use |journal=Arch. Intern. Med. |volume=158 |issue=16 |pages=1799–802 |year=1998 |pmid=9738609 |doi= |url=}}</ref> | * Patients may have a history of use of illicit drugs, for example, [[alcohol]] and [[cocaine]].<ref name="pmid9738609">{{cite journal |vauthors=Warner EA, Greene GS, Buchsbaum MS, Cooper DS, Robinson BE |title=Diabetic ketoacidosis associated with cocaine use |journal=Arch. Intern. Med. |volume=158 |issue=16 |pages=1799–802 |year=1998 |pmid=9738609 |doi= |url=}}</ref> | ||
* Patients may have poor socioeconomic status, which contributes to poor medication adherence in [[Diabetes mellitus|diabetics]].<ref name="pmid24117508">{{cite journal |vauthors=Lewis KR, Clark C, Velarde MC |title=Socioeconomic factors associated with pediatric diabetic ketoacidosis admissions in Southern West Virginia |journal=Clin. Endocrinol. (Oxf) |volume=81 |issue=2 |pages=218–21 |year=2014 |pmid=24117508 |doi=10.1111/cen.12350 |url=}}</ref> | * Patients may have poor socioeconomic status, which contributes to poor medication adherence in [[Diabetes mellitus|diabetics]].<ref name="pmid24117508">{{cite journal |vauthors=Lewis KR, Clark C, Velarde MC |title=Socioeconomic factors associated with pediatric diabetic ketoacidosis admissions in Southern West Virginia |journal=Clin. Endocrinol. (Oxf) |volume=81 |issue=2 |pages=218–21 |year=2014 |pmid=24117508 |doi=10.1111/cen.12350 |url=}}</ref> | ||
* Elederly patients in instutionalized care may have poor fluid intake. | * Elederly patients in instutionalized care may have poor fluid intake. | ||
* Patients who have a family history of [[Diabetes mellitus |diabetes]] have less chance of developing diabetic complications, possibly due to increased awareness of [[diabetes]].<ref name="pmid21890652">{{cite journal |vauthors=Hekkala A, Ilonen J, Knip M, Veijola R |title=Family history of diabetes and distribution of class II HLA genotypes in children with newly diagnosed type 1 diabetes: effect on diabetic ketoacidosis |journal=Eur. J. Endocrinol. |volume=165 |issue=5 |pages=813–7 |year=2011 |pmid=21890652 |doi=10.1530/EJE-11-0376 |url=}}</ref> | * Patients who have a family history of [[Diabetes mellitus |diabetes]] have less chance of developing [[diabetic]] complications, possibly due to increased awareness of [[diabetes]].<ref name="pmid21890652">{{cite journal |vauthors=Hekkala A, Ilonen J, Knip M, Veijola R |title=Family history of diabetes and distribution of class II HLA genotypes in children with newly diagnosed type 1 diabetes: effect on diabetic ketoacidosis |journal=Eur. J. Endocrinol. |volume=165 |issue=5 |pages=813–7 |year=2011 |pmid=21890652 |doi=10.1530/EJE-11-0376 |url=}}</ref> | ||
==Symptoms== | ==Symptoms== | ||
===Early Symptoms=== | ===Early Symptoms=== | ||
The early | The early symptoms of hyperosmolar hyperglycemic state are due to hyperglycemia and [[dehydration]] which include:<ref name="pmid23547550">{{cite journal |vauthors=Westerberg DP |title=Diabetic ketoacidosis: evaluation and treatment |journal=Am Fam Physician |volume=87 |issue=5 |pages=337–46 |year=2013 |pmid=23547550 |doi= |url=}}</ref><ref name="pmid15963033">{{cite journal |vauthors=Roche EF, Menon A, Gill D, Hoey H |title=Clinical presentation of type 1 diabetes |journal=Pediatr Diabetes |volume=6 |issue=2 |pages=75–8 |year=2005 |pmid=15963033 |doi=10.1111/j.1399-543X.2005.00110.x |url=}}</ref> | ||
* [[Polyuria]] | * [[Polyuria]] | ||
* [[ | * [[Polydipsia]] | ||
* [[Weakness]] | * [[Weakness]] | ||
* [[Leg cramps]] | * [[Leg cramps]] | ||
| Line 38: | Line 38: | ||
* Symptoms of underlying illness | * Symptoms of underlying illness | ||
===Late Symptoms=== | ===Late Symptoms=== | ||
The following are late symptoms of hyperosmolar hyperglycemic state which are due to plasma | The following are late symptoms of hyperosmolar hyperglycemic state which are due to plasma osmolality:<ref name="pmid26266145">{{cite journal |vauthors=Seth P, Kaur H, Kaur M |title=Clinical Profile of Diabetic Ketoacidosis: A Prospective Study in a Tertiary Care Hospital |journal=J Clin Diagn Res |volume=9 |issue=6 |pages=OC01–4 |year=2015 |pmid=26266145 |pmc=4525534 |doi=10.7860/JCDR/2015/8586.5995 |url=}}</ref><ref name="pmid6419481">{{cite journal |vauthors=Barrett EJ, Sherwin RS |title=Gastrointestinal manifestations of diabetic ketoacidosis |journal=Yale J Biol Med |volume=56 |issue=3 |pages=175–8 |year=1983 |pmid=6419481 |pmc=2589676 |doi= |url=}}</ref><ref name="pmid17308209">{{cite journal |vauthors=Kearney T, Dang C |title=Diabetic and endocrine emergencies |journal=Postgrad Med J |volume=83 |issue=976 |pages=79–86 |year=2007 |pmid=17308209 |pmc=2805944 |doi=10.1136/pgmj.2006.049445 |url=}}</ref><ref name="pmid7808094">{{cite journal |vauthors=Lorber D |title=Nonketotic hypertonicity in diabetes mellitus |journal=Med. Clin. North Am. |volume=79 |issue=1 |pages=39–52 |year=1995 |pmid=7808094 |doi= |url=}}</ref><ref name="pmid5684300">{{cite journal |vauthors=Maccario M |title=Neurological dysfunction associated with nonketotic hyperglycemia |journal=Arch. Neurol. |volume=19 |issue=5 |pages=525–34 |year=1968 |pmid=5684300 |doi= |url=}}</ref><ref name="pmid805337">{{cite journal |vauthors=Guisado R, Arieff AI |title=Neurologic manifestations of diabetic comas: correlation with biochemical alterations in the brain |journal=Metab. Clin. Exp. |volume=24 |issue=5 |pages=665–79 |year=1975 |pmid=805337 |doi= |url=}}</ref> | ||
* [[Confusion]] | * [[Confusion]] | ||
* [[seizure]] | * [[seizure]] | ||
| Line 52: | Line 52: | ||
[[Category:Medicine]] | [[Category:Medicine]] | ||
[[Category:Endocrinology]] | [[Category:Endocrinology]] | ||
[[Category:Up-To-Date]] | [[Category:Up-To-Date]] | ||
| |||
[[Category:Emergency medicine]] | [[Category:Emergency medicine]] | ||
Latest revision as of 18:05, 23 October 2017
|
Hyperosmolar hyperglycemic state Microchapters |
|
Differentiating Hyperosmolar hyperglycemic state from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Hyperosmolar hyperglycemic state history and symptoms On the Web |
|
American Roentgen Ray Society Images of Hyperosmolar hyperglycemic state history and symptoms |
|
FDA on Hyperosmolar hyperglycemic state history and symptoms |
|
CDC on Hyperosmolar hyperglycemic state history and symptoms |
|
Hyperosmolar hyperglycemic state history and symptoms in the news |
|
Blogs on Hyperosmolar hyperglycemic state history and symptoms |
|
Risk calculators and risk factors for Hyperosmolar hyperglycemic state history and symptoms |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Husnain Shaukat, M.D [2]
Overview
The majority of patients with the hyperosmolar hyperglycemic state are elderly, type 2 diabetics and having underlying other comorbidities as well as a limited fluid intake. However, some cases of a hyperosmolar hyperglycemic state have also been seen in children and young adults with type 1 diabetes. The initial symptoms are due to hyperglycemia and dehydration which include lethargy, extreme fatigue, polyuria, excessive thirst and leg cramps. The neurological symptoms develop with increase plasma osmolality greater than 320 mOsm/kg and include confusion, seizures and eventually coma.
History
Age of onset
- Older adults especially with a low perception of thirst or low fluid intake, tend to present more likely with hyperosmolar hyperglycemic state (HHS) as the first presentation of type 2 diabetes.[1][2]
- The hyperosmolar hyperglycemic state has also been seen in young adults and children with type 1 diabetes but less commonly.[3]
Initial presentation
- Patients presents with nausea, cramps, and fatigue.
- Patients may present with a history of poor compliance with insulin therapy or missed insulin injections due to vomiting or psychological reasons.
- Hyperosmolar hyperglycemic state has a slower onset, with sypmtoms developing over several days to weeks as compared to diabetic ketoacidosis which presents within hours.
Past medical history
- Hyperosmolar hyperglycemic state is associated with a past medical history of type 2 diabetes. Type 1 diabetes melitus may also lead to HHS is rare cases.[4][5]
- History of other comorbidities such as cerebrovascular diseases, myocardial infarctions etc can precipitate hyperosmolar hyperglycemic state by releasing counterregulatory hormones.
- History of infections (for example, urinary tract infections, pneumonia in an individual suffering from type 2 diabetes.[6]
Social history
- Patients may have a history of use of illicit drugs, for example, alcohol and cocaine.[7]
- Patients may have poor socioeconomic status, which contributes to poor medication adherence in diabetics.[8]
- Elederly patients in instutionalized care may have poor fluid intake.
- Patients who have a family history of diabetes have less chance of developing diabetic complications, possibly due to increased awareness of diabetes.[9]
Symptoms
Early Symptoms
The early symptoms of hyperosmolar hyperglycemic state are due to hyperglycemia and dehydration which include:[10][11]
- Polyuria
- Polydipsia
- Weakness
- Leg cramps
- Nausea and vomiting
- Sluggish, extreme tiredness
- Lethargy and apathy
- Symptoms of underlying illness
Late Symptoms
The following are late symptoms of hyperosmolar hyperglycemic state which are due to plasma osmolality:[12][13][14][15][16][17]
References
- ↑ de Vries L, Oren L, Lazar L, Lebenthal Y, Shalitin S, Phillip M (2013). "Factors associated with diabetic ketoacidosis at onset of Type 1 diabetes in children and adolescents". Diabet. Med. 30 (11): 1360–6. doi:10.1111/dme.12252. PMID 23758313.
- ↑ "Ketoacidosis at first presentation of type 1 diabetes mellitus among children: a study from Kuwait | Scientific Reports".
- ↑ Bagdure D, Rewers A, Campagna E, Sills MR (2013). "Epidemiology of hyperglycemic hyperosmolar syndrome in children hospitalized in USA". Pediatr Diabetes. 14 (1): 18–24. doi:10.1111/j.1399-5448.2012.00897.x. PMID 22925225.
- ↑ Newton CA, Raskin P (2004). "Diabetic ketoacidosis in type 1 and type 2 diabetes mellitus: clinical and biochemical differences". Arch. Intern. Med. 164 (17): 1925–31. doi:10.1001/archinte.164.17.1925. PMID 15451769.
- ↑ Lin MV, Bishop G, Benito-Herrero M (2010). "Diabetic ketoacidosis in type 2 diabetics: a novel presentation of pancreatic adenocarcinoma". J Gen Intern Med. 25 (4): 369–73. doi:10.1007/s11606-009-1237-9. PMC 2842543. PMID 20119682.
- ↑ Casqueiro J, Casqueiro J, Alves C (2012). "Infections in patients with diabetes mellitus: A review of pathogenesis". Indian J Endocrinol Metab. 16 Suppl 1: S27–36. doi:10.4103/2230-8210.94253. PMC 3354930. PMID 22701840.
- ↑ Warner EA, Greene GS, Buchsbaum MS, Cooper DS, Robinson BE (1998). "Diabetic ketoacidosis associated with cocaine use". Arch. Intern. Med. 158 (16): 1799–802. PMID 9738609.
- ↑ Lewis KR, Clark C, Velarde MC (2014). "Socioeconomic factors associated with pediatric diabetic ketoacidosis admissions in Southern West Virginia". Clin. Endocrinol. (Oxf). 81 (2): 218–21. doi:10.1111/cen.12350. PMID 24117508.
- ↑ Hekkala A, Ilonen J, Knip M, Veijola R (2011). "Family history of diabetes and distribution of class II HLA genotypes in children with newly diagnosed type 1 diabetes: effect on diabetic ketoacidosis". Eur. J. Endocrinol. 165 (5): 813–7. doi:10.1530/EJE-11-0376. PMID 21890652.
- ↑ Westerberg DP (2013). "Diabetic ketoacidosis: evaluation and treatment". Am Fam Physician. 87 (5): 337–46. PMID 23547550.
- ↑ Roche EF, Menon A, Gill D, Hoey H (2005). "Clinical presentation of type 1 diabetes". Pediatr Diabetes. 6 (2): 75–8. doi:10.1111/j.1399-543X.2005.00110.x. PMID 15963033.
- ↑ Seth P, Kaur H, Kaur M (2015). "Clinical Profile of Diabetic Ketoacidosis: A Prospective Study in a Tertiary Care Hospital". J Clin Diagn Res. 9 (6): OC01–4. doi:10.7860/JCDR/2015/8586.5995. PMC 4525534. PMID 26266145.
- ↑ Barrett EJ, Sherwin RS (1983). "Gastrointestinal manifestations of diabetic ketoacidosis". Yale J Biol Med. 56 (3): 175–8. PMC 2589676. PMID 6419481.
- ↑ Kearney T, Dang C (2007). "Diabetic and endocrine emergencies". Postgrad Med J. 83 (976): 79–86. doi:10.1136/pgmj.2006.049445. PMC 2805944. PMID 17308209.
- ↑ Lorber D (1995). "Nonketotic hypertonicity in diabetes mellitus". Med. Clin. North Am. 79 (1): 39–52. PMID 7808094.
- ↑ Maccario M (1968). "Neurological dysfunction associated with nonketotic hyperglycemia". Arch. Neurol. 19 (5): 525–34. PMID 5684300.
- ↑ Guisado R, Arieff AI (1975). "Neurologic manifestations of diabetic comas: correlation with biochemical alterations in the brain". Metab. Clin. Exp. 24 (5): 665–79. PMID 805337.