Diabetic ketoacidosis: Difference between revisions
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In [[medicine]], '''diabetic ketoacidosis''' ('''DKA''') is a type of metabolic [[acidosis]] that is a "life-threatening complication of diabetes mellitus, primarily of [[Diabetes mellitus type 1|Type 1 Diabetes Mellitus]] with severe [[insulin]] deficiency and [[hyperglycemia]]. It is characterized by excessive [[lipolysis]], oxidation of fatty acids, production of ketone bodies, a sweet smell to the breath ([[ketosis]];) [[dehydration]]; and depressed consciousness leading to [[coma]].<ref>{{MeSH}}</ref> can also occur with [[Diabetes mellitus type 2]]<ref name="pmid16520476">{{cite journal| author=Umpierrez GE, Smiley D, Kitabchi AE| title=Narrative review: ketosis-prone type 2 diabetes mellitus. | journal=Ann Intern Med | year= 2006 | volume= 144 | issue= 5 | pages= 350-7 | pmid=16520476 | In [[medicine]], '''diabetic ketoacidosis''' ('''DKA''') is a type of metabolic [[acidosis]] that is a "life-threatening complication of diabetes mellitus, primarily of [[Diabetes mellitus type 1|Type 1 Diabetes Mellitus]] with severe [[insulin]] deficiency and [[hyperglycemia]]. It is characterized by excessive [[lipolysis]], oxidation of fatty acids, production of ketone bodies, a sweet smell to the breath ([[ketosis]];) [[dehydration]]; and depressed consciousness leading to [[coma]].<ref>{{MeSH}}</ref> can also occur with [[Diabetes mellitus type 2]]<ref name="pmid16520476">{{cite journal| author=Umpierrez GE, Smiley D, Kitabchi AE| title=Narrative review: ketosis-prone type 2 diabetes mellitus. | journal=Ann Intern Med | year= 2006 | volume= 144 | issue= 5 | pages= 350-7 | pmid=16520476 | ||
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=16520476 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref> | | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=16520476 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref> | ||
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==Diagnosis== | ==Diagnosis== | ||
Criteria from the American Diabetic Association state: | |||
* Serum glucose ≥ 250 mg/dL | |||
* Serum anion gap > 10 mEq/L | |||
* Bicarbonate ≤ 18 mEq/L | |||
* Serum pH ≤ 7.30 | |||
* Presence of ketosis | |||
Venous [[blood gas analysis]] may be used in place of arterial [[blood gas analysis]] and serum chemistry.<ref name="pmid21951652">{{cite journal| author=Menchine M, Probst MA, Agy C, Bach D, Arora S| title=Diagnostic accuracy of venous blood gas electrolytes for identifying diabetic ketoacidosis in the emergency department. | journal=Acad Emerg Med | year= 2011 | volume= 18 | issue= 10 | pages= 1105-8 | pmid=21951652 | doi=10.1111/j.1553-2712.2011.01158.x | pmc= | url= }} </ref> | |||
The blood glucose is above 250 mg/dl in over 90% of patients.<ref name="pmid7891491">{{cite journal| author=Lebovitz HE| title=Diabetic ketoacidosis. | journal=Lancet | year= 1995 | volume= 345 | issue= 8952 | pages= 767-72 | pmid=7891491 | The blood glucose is above 250 mg/dl in over 90% of patients.<ref name="pmid7891491">{{cite journal| author=Lebovitz HE| title=Diabetic ketoacidosis. | journal=Lancet | year= 1995 | volume= 345 | issue= 8952 | pages= 767-72 | pmid=7891491 | ||
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=7891491 }} | | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=7891491 }} </ref><ref name="pmid19564476">{{cite journal| author=Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN| title=Hyperglycemic crises in adult patients with diabetes. | journal=Diabetes Care | year= 2009 | volume= 32 | issue= 7 | pages= 1335-43 | pmid=19564476 | ||
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=19564476 | doi=10.2337/dc09-9032 | pmc=PMC2699725 }} | | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=clinical.uthscsa.edu/cite&email=badgett@uthscdsa.edu&retmode=ref&cmd=prlinks&id=19564476 | doi=10.2337/dc09-9032 | pmc=PMC2699725 }}</ref> | ||
Urine test sticks measure [[acetoacetate]] and not [[3-hydroxybutyrate]] (β-hydroxybutyrate) although 3-hydroxybutyrate is the predominant ketone. Acetoacetate may not be elevated until later. | Urine test sticks measure [[acetoacetate]] and not [[3-hydroxybutyrate]] (β-hydroxybutyrate) although 3-hydroxybutyrate is the predominant ketone. Acetoacetate may not be elevated until later. | ||
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==Treatment== | ==Treatment== | ||
Treatment begins with fluid replacement; insulin is not started immediately. As DKA is treated, DKA converts from a high anion gap metabolic [[acidosis]] to a normal anion gap metabolic [[acidosis]] due to "excretion of ketone anions in the urine"<ref name="pmid102229">{{cite journal |author=Oh MS, Carroll HJ, Goldstein DA, Fein IA |title=Hyperchloremic acidosis during the recovery phase of diabetic ketosis |journal=Ann. Intern. Med. |volume=89 |issue=6 |pages=925–7 |year=1978 |month=December |pmid=102229 |doi= |url= |issn=}}</ref>, especially if excreted with sodium or potassium cations. | Treatment begins with fluid replacement; insulin is not started immediately. As DKA is treated, DKA converts from a high anion gap metabolic [[acidosis]] to a normal anion gap metabolic [[acidosis]] due to "excretion of ketone anions in the urine"<ref name="pmid102229">{{cite journal |author=Oh MS, Carroll HJ, Goldstein DA, Fein IA |title=Hyperchloremic acidosis during the recovery phase of diabetic ketosis |journal=Ann. Intern. Med. |volume=89 |issue=6 |pages=925–7 |year=1978 |month=December |pmid=102229 |doi= |url= |issn=}}</ref>, especially if excreted with sodium or potassium cations. | ||
DKA is resolved when:<ref name="pmid20048266"/> | |||
* glucose level less than 11.1 mmol/L (200 mg/dL) | |||
** two of | |||
** serum bicarbonate level ≥ 15 mmol/L | |||
** venous pH greater than 7.3 | |||
** anion gap < 12 | |||
When resolved and the patient is adequately eating, the patient should resume their usual insulin, or if the patient is a new diabetic, they should take a total of 0.5 to | |||
0.8 U/kg per day.<ref name="pmid20048266"/> | |||
===Hospitalization=== | |||
Criteria for hospitalization, according to the American Diabetic Association, are:<ref name="pmid14693939">{{cite journal| author=American Diabetes Association| title=Hospital admission guidelines for diabetes. | journal=Diabetes Care | year= 2004 | volume= 27 Suppl 1 | issue= | pages= S103 | pmid=14693939 | doi= | pmc= | url= }} </ref> | |||
* Plasma glucose >250 mg/dl (>13.9 mmol/l) with | |||
# arterial pH <7.30 and | |||
# serum bicarbonate level <15 mEq/l | |||
# moderate ketonuria and/or ketonemia | |||
==References== | ==References== | ||
<references/> | <small> | ||
<references> | |||
</references> | |||
</small> | |||
[[Category:Suggestion Bot Tag]] | |||
Latest revision as of 12:37, 1 November 2024
In medicine, diabetic ketoacidosis (DKA) is a type of metabolic acidosis that is a "life-threatening complication of diabetes mellitus, primarily of Type 1 Diabetes Mellitus with severe insulin deficiency and hyperglycemia. It is characterized by excessive lipolysis, oxidation of fatty acids, production of ketone bodies, a sweet smell to the breath (ketosis;) dehydration; and depressed consciousness leading to coma.[1] can also occur with Diabetes mellitus type 2[2]
DKA is often secondary to infection or other comorbidity, which must be diagnosed and treated.[3][4]
Diagnosis
Criteria from the American Diabetic Association state:
- Serum glucose ≥ 250 mg/dL
- Serum anion gap > 10 mEq/L
- Bicarbonate ≤ 18 mEq/L
- Serum pH ≤ 7.30
- Presence of ketosis
Venous blood gas analysis may be used in place of arterial blood gas analysis and serum chemistry.[5]
The blood glucose is above 250 mg/dl in over 90% of patients.[6][7]
Urine test sticks measure acetoacetate and not 3-hydroxybutyrate (β-hydroxybutyrate) although 3-hydroxybutyrate is the predominant ketone. Acetoacetate may not be elevated until later.
The anion gap and serum osmolality must be measured.
Treatment
Treatment begins with fluid replacement; insulin is not started immediately. As DKA is treated, DKA converts from a high anion gap metabolic acidosis to a normal anion gap metabolic acidosis due to "excretion of ketone anions in the urine"[8], especially if excreted with sodium or potassium cations.
DKA is resolved when:[3]
- glucose level less than 11.1 mmol/L (200 mg/dL)
- two of
- serum bicarbonate level ≥ 15 mmol/L
- venous pH greater than 7.3
- anion gap < 12
When resolved and the patient is adequately eating, the patient should resume their usual insulin, or if the patient is a new diabetic, they should take a total of 0.5 to 0.8 U/kg per day.[3]
Hospitalization
Criteria for hospitalization, according to the American Diabetic Association, are:[9]
- Plasma glucose >250 mg/dl (>13.9 mmol/l) with
- arterial pH <7.30 and
- serum bicarbonate level <15 mEq/l
- moderate ketonuria and/or ketonemia
References
- ↑ Anonymous (2024), Diabetic ketoacidosis (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Umpierrez GE, Smiley D, Kitabchi AE (2006). "Narrative review: ketosis-prone type 2 diabetes mellitus.". Ann Intern Med 144 (5): 350-7. PMID 16520476.
- ↑ 3.0 3.1 3.2 Wilson JF (2010). "In clinic. Diabetic ketoacidosis.". Ann Intern Med 152 (1): ITC1. DOI:10.1059/0003-4819-152-1-201001050-01001. PMID 20048266. Research Blogging.
- ↑ Rucker DW (February 12, 2008), "Diabetic ketoacidosis", eMedicine
- ↑ Menchine M, Probst MA, Agy C, Bach D, Arora S (2011). "Diagnostic accuracy of venous blood gas electrolytes for identifying diabetic ketoacidosis in the emergency department.". Acad Emerg Med 18 (10): 1105-8. DOI:10.1111/j.1553-2712.2011.01158.x. PMID 21951652. Research Blogging.
- ↑ Lebovitz HE (1995). "Diabetic ketoacidosis.". Lancet 345 (8952): 767-72. PMID 7891491.
- ↑ Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN (2009). "Hyperglycemic crises in adult patients with diabetes.". Diabetes Care 32 (7): 1335-43. DOI:10.2337/dc09-9032. PMID 19564476. PMC PMC2699725. Research Blogging.
- ↑ Oh MS, Carroll HJ, Goldstein DA, Fein IA (December 1978). "Hyperchloremic acidosis during the recovery phase of diabetic ketosis". Ann. Intern. Med. 89 (6): 925–7. PMID 102229. [e]
- ↑ American Diabetes Association (2004). "Hospital admission guidelines for diabetes.". Diabetes Care 27 Suppl 1: S103. PMID 14693939. [e]