Hyperglycemic crises resident survival guide: Difference between revisions
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'''For more information about DKA, click [[DKA|here]].''' | |||
Diabetic ketoacidosis | {{CMG}}; {{AE}} {{HK}}, {{HS}} | ||
{| class="infobox" style="margin: 0 0 0 0; border: 0; float: right; width: 100px; background: #A8A8A8; position: fixed; top: 250px; right: 21px; border-radius: 10px 10px 10px 10px;" cellpadding="0" cellspacing="0" ; | |||
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! style="padding: 0 5px; font-size: 85%; background: #A8A8A8" align="center" | {{fontcolor|#2B3B44|Hyperglycemic crises Resident Survival Guide Microchapters}} | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" | [[{{PAGENAME}}#Overview|Overview]] | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" | [[{{PAGENAME}}#Classification|Classification]] | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" | [[{{PAGENAME}}#Causes|Causes]] | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" | [[{{PAGENAME}}#FIRE: Focused Initial Rapid Evaluation|FIRE]] | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" | [[{{PAGENAME}}#Diagnosis|Diagnosis]] | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" | [[{{PAGENAME}}#Treatment|Treatment]] | |||
|- | |||
! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" | [[{{PAGENAME}}#Do's|Do's]] | |||
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! style="font-size: 80%; padding: 0 5px; background: #DCDCDC" align="left" | [[{{PAGENAME}}#Don'ts|Don'ts]] | |||
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==Overview== | |||
[[Diabetic ketoacidosis]] (DKA) and [[hyperosmolar hyperglycemic state]] (HHS) are life threatening complications of untreated or inadequately treated [[diabetes mellitus]]. [[HHS]] is characterized by [[hyperglycemia]], [[hyperosmolarity]] and [[dehydration]]; whereas DKA is characterized by [[hyperglycemia]], [[acidosis]], and [[ketosis]].<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 | doi=10.2337/dc09-9032 | pmc=PMC2699725 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19564476 }} </ref> | |||
==Causes== | ==Causes== | ||
==Life Threatening Causes== | ===Life Threatening Causes=== | ||
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. Hyperosmolar hyperglycemic state is a life-threatening condition and must be treated as such irrespective of the causes. | |||
===Common Causes=== | |||
Common causes of hyperosmolar hyperglycemic state (HHS) include: | |||
* [[Infections]]: | |||
** [[Pneumonia]]<ref name="pmid1906798">{{cite journal |vauthors=Bouter KP, Diepersloot RJ, van Romunde LK, Uitslager R, Masurel N, Hoekstra JB, Erkelens DW |title=Effect of epidemic influenza on ketoacidosis, pneumonia and death in diabetes mellitus: a hospital register survey of 1976-1979 in The Netherlands |journal=Diabetes Res. Clin. Pract. |volume=12 |issue=1 |pages=61–8 |year=1991 |pmid=1906798 |doi= |url=}}</ref> | |||
** [[Sepsis]]<ref name="pmid24827487">{{cite journal |vauthors=Nakamura K, Inokuchi R, Doi K, Fukuda T, Tokunaga K, Nakajima S, Noiri E, Yahagi N |title=Septic ketoacidosis |journal=Intern. Med. |volume=53 |issue=10 |pages=1071–3 |year=2014 |pmid=24827487 |doi= |url=}}</ref><ref name="pmid20610941">{{cite journal |vauthors=Osuchowski MF, Craciun FL, Schuller E, Sima C, Gyurko R, Remick DG |title=Untreated type 1 diabetes increases sepsis-induced mortality without inducing a prelethal cytokine response |journal=Shock |volume=34 |issue=4 |pages=369–76 |year=2010 |pmid=20610941 |pmc=2941557 |doi=10.1097/SHK.0b013e3181dc40a8 |url=}}</ref><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> | |||
** [[Urinary tract infections|Genitourinary tract infections]]<ref name="pmid19152925">{{cite journal |vauthors=Czaja CA, Rutledge BN, Cleary PA, Chan K, Stapleton AE, Stamm WE |title=Urinary tract infections in women with type 1 diabetes mellitus: survey of female participants in the epidemiology of diabetes interventions and complications study cohort |journal=J. Urol. |volume=181 |issue=3 |pages=1129–34; discussion 1134–5 |year=2009 |pmid=19152925 |pmc=2699609 |doi=10.1016/j.juro.2008.11.021 |url=}}</ref> | |||
* Drugs:<ref name="pmid17604410">{{cite journal |vauthors=Ramaswamy K, Kozma CM, Nasrallah H |title=Risk of diabetic ketoacidosis after exposure to risperidone or olanzapine |journal=Drug Saf |volume=30 |issue=7 |pages=589–99 |year=2007 |pmid=17604410 |doi= |url=}}</ref><ref name="pmid23344556">{{cite journal |vauthors=Guenette MD, Hahn M, Cohn TA, Teo C, Remington GJ |title=Atypical antipsychotics and diabetic ketoacidosis: a review |journal=Psychopharmacology (Berl.) |volume=226 |issue=1 |pages=1–12 |year=2013 |pmid=23344556 |doi=10.1007/s00213-013-2982-3 |url=}}</ref> | |||
** [[Antipsychotic drugs|Antipsychotic agents]] ([[clozapine]], [[olanzapine]], [[risperidone]]) | |||
** Illicit drugs ([[cocaine]] and [[alcohol]]) | |||
** [[Corticosteroids]]<ref name="pmid4327634">{{cite journal |vauthors=Alavi IA, Sharma BK, Pillay VK |title=Steroid-induced diabetic ketoacidosis |journal=Am. J. Med. Sci. |volume=262 |issue=1 |pages=15–23 |year=1971 |pmid=4327634 |doi= |url=}}</ref> | |||
** [[Glucagon]]<ref name="pmid49515">{{cite journal |vauthors=Alberti KG |title=Role of glucagon and other hormones in development of diabetic ketoacidosis |journal=Lancet |volume=1 |issue=7920 |pages=1307–11 |year=1975 |pmid=49515 |doi= |url=}}</ref> | |||
** [[Interferon]]<ref name="pmid21775762">{{cite journal |vauthors=Nakamura K, Kawasaki E, Imagawa A, Awata T, Ikegami H, Uchigata Y, Kobayashi T, Shimada A, Nakanishi K, Makino H, Maruyama T, Hanafusa T |title=Type 1 diabetes and interferon therapy: a nationwide survey in Japan |journal=Diabetes Care |volume=34 |issue=9 |pages=2084–9 |year=2011 |pmid=21775762 |pmc=3161293 |doi=10.2337/dc10-2274 |url=}}</ref> | |||
** [[Pentamidine]]<ref name="pmid8577688">{{cite journal |vauthors=Lu CP, Wu HP, Chuang LM, Lin BJ, Chuang CY, Tai TY |title=Pentamidine-induced hyperglycemia and ketosis in acquired immunodeficiency syndrome |journal=Pancreas |volume=11 |issue=3 |pages=315–6 |year=1995 |pmid=8577688 |doi= |url=}}</ref><ref name="pmid3150636">{{cite journal |vauthors=Lambertus MW, Murthy AR, Nagami P, Goetz MB |title=Diabetic ketoacidosis following pentamidine therapy in a patient with the acquired immunodeficiency syndrome |journal=West. J. Med. |volume=149 |issue=5 |pages=602–4 |year=1988 |pmid=3150636 |pmc=1026553 |doi= |url=}}</ref> | |||
** [[Sympathomimetic agents]] ([[albuterol]], [[dopamine]], [[dobutamine]], [[terbutaline]], [[ritodrine]], [[thiazide diuretics]])<ref name="pmid24459">{{cite journal |vauthors=Borberg C, Gillmer MD, Beard RW, Oakley NW |title=Metabolic effects of beta-sympathomimetic drugs and dexamethasone in normal and diabetic pregnancy |journal=Br J Obstet Gynaecol |volume=85 |issue=3 |pages=184–9 |year=1978 |pmid=24459 |doi= |url=}}</ref><ref name="pmid1684993">{{cite journal |vauthors=Rodgers BD, Rodgers DE |title=Clinical variables associated with diabetic ketoacidosis during pregnancy |journal=J Reprod Med |volume=36 |issue=11 |pages=797–800 |year=1991 |pmid=1684993 |doi= |url=}}</ref> | |||
* [[Myocardial infarction]]<ref name="pmid15887449">{{cite journal |vauthors=Trachtenbarg DE |title=Diabetic ketoacidosis |journal=Am Fam Physician |volume=71 |issue=9 |pages=1705–14 |year=2005 |pmid=15887449 |doi= |url=}}</ref> | |||
* [[Pancreatitis]]<ref name="pmid11051350">{{cite journal |vauthors=Nair S, Yadav D, Pitchumoni CS |title=Association of diabetic ketoacidosis and acute pancreatitis: observations in 100 consecutive episodes of DKA |journal=Am. J. Gastroenterol. |volume=95 |issue=10 |pages=2795–800 |year=2000 |pmid=11051350 |doi=10.1111/j.1572-0241.2000.03188.x |url=}}</ref> | |||
* [[Shock (medical)|Shock]]/[[hypovolemia]]<ref name="pmid15871546">{{cite journal |vauthors=Umpierrez GE, Kitabchi AE |title=Diabetic ketoacidosis: risk factors and management strategies |journal=Treat Endocrinol |volume=2 |issue=2 |pages=95–108 |year=2003 |pmid=15871546 |doi= |url=}}</ref> | |||
* [[Trauma]]<ref name="pmid17585123">{{cite journal |vauthors=Dhatariya KK |title=Diabetic ketoacidosis |journal=BMJ |volume=334 |issue=7607 |pages=1284–5 |year=2007 |pmid=17585123 |pmc=1895683 |doi=10.1136/bmj.39237.661111.80 |url=}}</ref> | |||
* Undiagnosed [[diabetes mellitus]]<ref name="pmid22125712">{{cite journal |vauthors=Razavi Z |title=Frequency of ketoacidosis in newly diagnosed type 1 diabetic children |journal=Oman Med J |volume=25 |issue=2 |pages=114–7 |year=2010 |pmid=22125712 |pmc=3215499 |doi=10.5001/omj.2010.31 |url=}}</ref> | |||
* Noncompliance to [[insulin]] treatment:<ref name="pmid20489639">{{cite journal |vauthors=Borus JS, Laffel L |title=Adherence challenges in the management of type 1 diabetes in adolescents: prevention and intervention |journal=Curr. Opin. Pediatr. |volume=22 |issue=4 |pages=405–11 |year=2010 |pmid=20489639 |pmc=3159529 |doi=10.1097/MOP.0b013e32833a46a7 |url=}}</ref><ref name="pmid25061324">{{cite journal |vauthors=Gosmanov AR, Gosmanova EO, Dillard-Cannon E |title=Management of adult diabetic ketoacidosis |journal=Diabetes Metab Syndr Obes |volume=7 |issue= |pages=255–64 |year=2014 |pmid=25061324 |pmc=4085289 |doi=10.2147/DMSO.S50516 |url=}}</ref> | |||
** Body image issues | |||
** Financial problems | |||
**Lack of [[insulin]]<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> | |||
** [[Psychological]] factors | |||
**Self-neglect | |||
**Accidental | |||
**Neglect by caregivers | |||
== | ==Management== | ||
The diagnostic approach and management management of [[HHS]] and [[DKA]] are based on the ADA guidelines published in 2009.<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 | doi=10.2337/dc09-9032 | pmc=PMC2699725 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19564476 }} </ref> | |||
===General Approach=== | |||
{{Family tree/start}} | |||
{{Family tree |border=2|boxstyle=background: WhiteSmoke;|A1|A1=<div style="float: left; text-align: left; height: 38em; width: 45em; padding:1em;"> '''Characterize the symptoms:''' | |||
---- | |||
❑ [[Polyuria]]<br> | |||
❑ [[Polydipsia]]<br> | |||
❑ [[Weight loss]]<br> | |||
❑ [[Vomiting]]<br> | |||
❑ [[Dehydration]]<br> | |||
❑ Weakness<br> | |||
❑ Mental status change<br> | |||
❑ [[Abdominal pain]] <br> | |||
❑ Vomiting | |||
<br> | |||
---- | |||
'''Examine the patient:''' | |||
---- | |||
❑ Poor skin turgor <br> | |||
❑ [[Kussmaul breathing]]<br> | |||
❑ [[Tachycardia]]<br> | |||
❑ [[Hypotension]]<br> | |||
❑ [[Hypothermia]] or [[hyperthermia]] | |||
<br> | |||
---- | |||
'''Identify precipitating factors:''' | |||
---- | |||
❑ [[Infection]]s <br> ❑ [[Insulin]] deficiency <br> ❑ [[Myocardial infarction]] <br> ❑ New onset [[DM]] type 1 <br> ❑ Pregnancy <br> ❑ Stress </div>}} | |||
{{Family tree |!| }} | |||
{{Family tree |border=2|boxstyle=background: WhiteSmoke;|B1|B1=<div style="float: left; text-align: left; height: 21em; width: 45em; padding:1em;">'''Order tests:'''<br> | |||
❑ Serum glucose <br> ❑ [[ABG]] <br> ❑ [[CBC]] <br> ❑ [[Electrolytes]] <br> ❑ Serum & urinary [[ketone]]s <br> ❑ [[Urinalysis]] <br> ❑ [[BUN]] <br> ❑ [[Creatinine]] <br> ❑ [[Osmolality|Plasma osmolality]] | |||
<br> | |||
---- | |||
❑ [[EKG]] <br> ❑ [[CXR]] <br> ❑ Urine, sputum, blood cultures (not routine)</div>}} | |||
{{Family tree |border=2|boxstyle=background: WhiteSmoke;|D1|D1=<div style="float: left; text-align: left; height: 8em; width: 45em; padding:1em;">'''Start the management of the following SIMULTANEOUSLY: (Urgent)'''<br>'''(Check the algorithms below for more details)'''<br> | |||
❑ [[Hyperglycemic crises resident survival guide#Management: IV Fluids|IV fluids]] <br> | |||
❑ [[Hyperglycemic crises resident survival guide#Management: Insulin|Insulin]] <br> | |||
❑ [[Hyperglycemic crises resident survival guide#Management: Potassium|Potassium]] <br> | |||
❑ [[Hyperglycemic crises resident survival guide#Management: Bicarbonate|Bicarbonate]] | |||
<br> | |||
</div>}} | |||
{{Family tree |!| }} | |||
{{Family tree |border=2|boxstyle=background: WhiteSmoke;|E1|E1=<div style="float: left; text-align: left; height: 9em; width: 45em; padding:1em;">'''Check the following every two hours until the patient is stable:'''<br> ❑ Glucose <br>❑ [[Electrolytes]] <br> ❑ [[BUN]] <br> ❑ Venous pH <br> ❑ [[Creatinine]] </div>}} | |||
{{Family tree |!| }} | |||
{{Family tree |border=2|boxstyle=background: WhiteSmoke;|F1|F1=<div style="float: left; text-align: left; height: 15em; width: 45em; padding:1em;">'''Determine the resolution of HHS:'''<br> | |||
❑ Blood glucose <200 mg/dl, '''AND'''<br> | |||
❑ Two of the following criteria:<br> | |||
- Serum bicarbonate level >15 mEq/l<br>- Venous pH >7.3<br>- Calculated anion gap12 mEq/l | |||
---- | |||
'''Determine the resolution of HHS:'''<br> | |||
❑ Normal osmolality<br> | |||
❑ Regain of normal mental status<br></div>}} | |||
{{Family tree/end}} | |||
<br> | |||
* | * The diagnosis of [[diabetic ketoacidosis]] is made in the presence of: | ||
**[[Hyperglycemia]]- [[Plasma glucose]] > 250 mg/dL | |||
**[[Metabolic acidosis|Anion gap metabolic acidosis]]- pH < 7.3; [[Serum bicarbonate]] < 15 mEq/L | |||
**[[Ketonemia]]/ [[Ketonuria]] | |||
* Shown below is a table summarizing the diagnosis of [[Diabetic ketoacidosis]] according the the American Diabetes Association (ADA) guidelines. <ref name="pmiddoi.org/10.2337/dc09-9032">{{cite journal| author=Schmoldt A, Benthe HF, Haberland G| title=Digitoxin metabolism by rat liver microsomes. | journal=Biochem Pharmacol | year= 1975 | volume= 24 | issue= 17 | pages= 1639-41 | pmid=doi.org/10.2337/dc09-9032 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10 }} </ref> <ref name="pmid11194218">{{cite journal| author=Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI | display-authors=etal| title=Management of hyperglycemic crises in patients with diabetes. | journal=Diabetes Care | year= 2001 | volume= 24 | issue= 1 | pages= 131-53 | pmid=11194218 | doi=10.2337/diacare.24.1.131 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11194218 }} </ref> | |||
{| class="wikitable" | |||
! colspan="1" rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |VARIABLE | |||
! colspan="3" rowspan="1" align="center" style="background:#4479BA; color: #FFFFFF;" + |DIABETIC KETOACIDOSIS | |||
|- | |||
! colspan="1" rowspan="1" align="center" style="background:#4479BA; color: #FFFFFF;" + |MILD (Plasma Glucose > 250mg/dL or 13.88 mmol/L) | |||
! colspan="1" rowspan="1" align="center" style="background:#4479BA; color: #FFFFFF;" + |MODERATE (Plasma Glucose > 250mg/dL or 13.88 mmol/L) | |||
! colspan="1" rowspan="1" align="center" style="background:#4479BA; color: #FFFFFF;" + |SEVERE (Plasma Glucose > 250mg/dL or 13.88 mmol/L) | |||
|- | |||
| colspan="1" rowspan="1" |'''[[Arterial]] [[pH]]''' | |||
| colspan="1" rowspan="1" |7.25 to 7.30 | |||
| colspan="1" rowspan="1" |7.00 to < 7.24 | |||
| colspan="1" rowspan="1" |< 7.00 | |||
|- | |||
| colspan="1" rowspan="1" |'''[[Serum]] [[bicarbonate]]''' | |||
| colspan="1" rowspan="1" |15 to 18 mEq/L | |||
| colspan="1" rowspan="1" |10 to < 15 mEq/L | |||
| colspan="1" rowspan="1" |< 10 mEq/L | |||
|- | |||
| colspan="1" rowspan="1" |'''[[Urine]] [[ketone]] (Nitroprusside reaction method)''' | |||
| colspan="1" rowspan="1" |Positive | |||
| colspan="1" rowspan="1" |Positive | |||
| colspan="1" rowspan="1" |Positive | |||
|- | |||
| colspan="1" rowspan="1" |'''[[Serum]] [[ketone]] (Nitroprusside reaction method)''' | |||
| colspan="1" rowspan="1" |Positive | |||
| colspan="1" rowspan="1" |Positive | |||
| colspan="1" rowspan="1" |Positive | |||
|- | |||
| colspan="1" rowspan="1" |'''[[Osmolarity|Effective serum osmolality]]''' | |||
| colspan="1" rowspan="1" |Variable | |||
| colspan="1" rowspan="1" |Variable | |||
| colspan="1" rowspan="1" |Variable | |||
|- | |||
| colspan="1" rowspan="1" |'''[[Anion gap]]''' | |||
| colspan="1" rowspan="1" |> 10 mEq/L (10 mmol/L) | |||
| colspan="1" rowspan="1" |> 12 mEq/L (12 mmol/L) | |||
| colspan="1" rowspan="1" |> 12 mEq/L (12 mmol/L) | |||
|- | |||
| colspan="1" rowspan="1" |'''[[Mental status]]''' | |||
| colspan="1" rowspan="1" |Alert | |||
| colspan="1" rowspan="1" |Alert/drowsy | |||
| colspan="1" rowspan="1" |Stupor/coma | |||
|} | |||
===Management: IV Fluids=== | |||
{{familytree/start}} | |||
{{familytree | | | | | | | B01 | | | | | | B01= '''Initial IV fluid''' <br> ❑ 0.9% NaCl (15-20ml/kg/hour), OR <br> ❑ 1-1.5L during the first hour}} | |||
{{familytree | | | | | | | |!| | | | | | | }} | |||
{{familytree | | | | | | | C01 | | | | | | C01= ❑ '''Evaluate the hydration status'''}} | |||
{{familytree | |,|-|-|-|-|-|^|-|-|-|.| |}} | |||
{{familytree | D01 | | | | D02 | | D03 | D01= '''Severe hypovolemia'''|D02= '''Mild hypovolemia'''| | D03= '''[[Cardiogenic shock resident survival guide|Cardiogenic shock]]'''<br> ❑ Hemodynamic monitoring/pressors}} | |||
{{familytree | |!| | | | | |!| | | }} | |||
{{familytree | |!| | | | | E01 | | E01= ❑ '''Assess the corrected [Na<sup>+</sup>]'''}} | |||
{{familytree | |!| | | | |,|^|.| | }} | |||
{{familytree | F01 | | F02 | | F03 | | F01= ❑ Administer 0.9% NaCl (1.0L/hour)|F02= '''High or normal [Na<sup>+</sup>]'''<br> ❑ Administer 0.45% NaCl (250-500 ml/hour)<br> depending on the hydration status|F03= '''Low [Na<sup>+</sup>]'''<br> ❑ Administer 0.9% NaCl (250-500 ml/hour)<br> depending on the hydration status }} | |||
{{familytree | |!| | | |!| | | |!| | | }} | |||
{{familytree | |`|-|-|-|^| G01 |'| | | | | G01= '''Hemodynamic monitoring:'''<br><div style="float: left; text-align: left; line-height: 150% ">❑ [[Blood pressure]] <br> ❑ Laboratory results<br> ❑ Input/output of fluids <br> ❑ Clinical status </div>}} | |||
{{familytree | | | | | | | |!| | | | | | | }} | |||
{{familytree | | | | | | | H01 | | | | | | H01= '''When serum glucose reaches <br> 200mg/dL in DKA and 300mg/dl in HHS'''<br> ❑ Change to 5% dextrose with 0.45% NaCl<br>(150-250 mL/hour) }} | |||
{{familytree/end}} | |||
<br> | |||
<br> | |||
==Management== | ===Management: Insulin=== | ||
{{familytree/start | {{familytree/start}} | ||
{{familytree | {{familytree | | | A01 | | | A01= '''Check K<sup>+</sup> before administering insulin'''}} | ||
{{familytree | | | | | | | | | | | | | | | | {{familytree | |,|-|^|-|.| | }} | ||
{{familytree | | | {{familytree | A02 | | A03 | A02= '''K<sup>+</sup><3.3 mEq/L''' <br> ❑ Hold insulin and give K<sup>+</sup> 20-30 mEq/h <br> until K<sup>+</sup>>3.3 mEq/L | A03= '''K<sup>+</sup>>5.5 mEq/L''' <br>❑ Do not give K <br> ❑ Proceed with insulin}} | ||
{{familytree | {{familytree | |!| | | |!| | }} | ||
{{familytree | {{familytree | |`| B01 |'| | B01= '''Administer initial IV dose of insulin'''<br>❑ Continuous IV infusion of 0.14 U/Kg/h, '''OR''' <br>❑ IV bolus of 0.1 U/Kg, then continuous IV <br>infusion of 0.1 U/Kg/h}} | ||
{{familytree | | | | | | | | | | | | | | | | {{familytree | | | |!| | | | }} | ||
{{familytree | | | | | | | {{familytree | | | C01 | | | C01= ❑ '''Check if serum glucose falls by 10% in the first hour'''}} | ||
{{familytree | | | | | | | {{familytree | |,|-|^|-|.| | }} | ||
{{familytree | | | | | | | {{familytree | D01 | | D02 | D01= Yes| D02= No}} | ||
{{familytree | | | | | | | | | {{familytree | |!| | | |!| | }} | ||
{{familytree | | | | | | | | | {{familytree | |!| | | E01 | E01= ❑ Administer IV bolus of 0.14 U/Kg,<br> then continue previous treatment}} | ||
{{familytree | {{familytree | |!| | | |!| | }} | ||
{{familytree | | | | | | {{familytree | |`| F01 |'| | F01= '''When serum glucose reaches 250mg/dl in DKA and 300mg/dl in HHS:''' <br>❑ Reduce IV regular insulin infusion to 0.02-0.05 U/kg/h, '''OR''' <br>❑ Administer SC rapid acting insulin at 0.1 U/kg every 2 hours | ||
{{familytree | ---- | ||
{{familytree | | | | | | ❑ '''Keep serum glucose between 150-200 mg/dL until'''<br> '''resolution (200-300 mg/dL for HHS) '''}} | ||
{{familytree | |,|-|-|-|+|-|-|-|. | {{familytree | | | |!| | | | }} | ||
{{familytree | | {{familytree | | | G01 | | | G01= ❑ Check glucose, BUN, electrolytes, creatinine, venous pH every 3-4 hours until stable}} | ||
{{familytree | {{familytree | | | |!| | | | }} | ||
{{familytree | | | | {{familytree | | | G02 | | | G02= ❑ '''Confirm resolution and'''<br> '''assess ability to eat'''}} | ||
{{familytree | {{familytree | |,|-|^|-|.| | }} | ||
{{familytree | H01 | | H02 | H01= Inability to eat| H02= Able to eat}} | |||
{{familytree | |!| | | |!| | }} | |||
{{familytree | | | {{familytree | I01 | | I02 | I01= ❑ Continue IV insulin infusion<br> and IV fluid replacement| I02= '''Transfer from IV to SC insulin''' <br>❑ Initiate SC multidose insulin <br> ❑ Continue IV insulin 1-2 hours after<br> SC insulin is initiated}} | ||
{{familytree | | | |,|-|^|-|.|}} | |||
{{familytree | | | J01 | | J02 | J01='''Patient previously on insulin?'''<br> ❑ Recommence the insulin home dose | J02= '''Insulin naive patient?''' <br> ❑ Start at a multidose of 0.5-0.8 U/kg/day}} | |||
{{familytree/end}} | |||
<br> | |||
<br> | |||
===Management: Potassium=== | |||
{{familytree/start}} | |||
{{familytree | | | | | A01 | | | A01= ❑ Assess K<sup>+</sup> level <br> ❑ Establish adequate renal function<br> (urine output 50 ml/hour)}} | |||
{{familytree | |,|-|-|-|+|-|-|-|.| | }} | |||
{{familytree | B01 | | B02 | | B03 |B01= '''K<sup>+</sup><3.3 mEq/L'''| B02= '''K<sup>+</sup>= 3.3-5.2 mEq/L'''| B03= '''K<sup>+</sup>>5.2 mEq/L'''}} | |||
{{familytree | |!| | | |!| | | | | | }} | |||
{{familytree | C01 | | C02 | | C03 | C01= ❑ Hold insulin <br>❑ Administer 20-30 mEq/hour <br>until K<sup>+</sup>>3.3 mEq/L| C02= ❑ Administer 20-30 mEq/hour in each<br> liter of IV fluid to keep serum K<sup>+</sup><br> between 4 and 5 mEq/L | C03= ❑ Do not give K<sup>+</sup>}} | |||
{{familytree | |!| | | |!| | | |!| | }} | |||
{{familytree | |`|-|-| D01 |-|-|'| | D01= '''Keep K<sup>+</sup>= 4-5 mEq/L''' <br> ❑ Check K<sup>+</sup> every 2 hours<br> until resolution of HHS}} | |||
{{familytree/end}} | {{familytree/end}} | ||
==Do's== | ==Do's== | ||
* Check labs initially and every 2-4 hours | * Check labs initially and every 2-4 hours. | ||
* | * Immediately check urine for ketones with dipstick and send urine to the lab for analysis. | ||
* Initiate | * Initiate [[Insulin|IV insulin]] as soon as the patient arrives and satisfies the diagnostic criteria of DKA. | ||
* Assess | * Assess the trigger that precipitated DKA and treat the cause. | ||
* Admit the patient | * In patients with [[potassium]](K) < 3.3 mEq/L, [[Fluid|fluids]] and [[potassium]] replacement must be done '''before''' initiating [[insulin]] therapy, to prevent further [[hypokalemia]]. | ||
* | * Admit the patient to the floor; however, if the pH < 7.0 or the patient is unconscious then admit to ICU. | ||
* Make sure to calculate the corrected sodium level when evaluating the sodium level. Sodium can be falsely low due to the elevated glucose level; in order to correct for this, add 1.6 mmol/L of Na+ for every 100 mg/dL of glucose > 100 mg/dL. | |||
* | * Monitor for complications of DKA itself or of the therapy. | ||
* In case the patient has cardiac or renal compromise, monitor serum [[osmolality]] and frequently assess the cardiac, renal and mental status. | |||
==Don'ts== | ==Don'ts== | ||
* | * Do not stop [[Insulin|IV insulin]] until DKA has resolved. | ||
* Do not stop | * Do not stop [[Insulin|IV insulin]], even if subcutaneous insulin is administered because it needs time to kick in. | ||
* | * Do not give insulin if K+ levels are below 3.3 mEq/l because it may further exacerbate the [[hypokalemia]]. | ||
* Do not use 0.9% NaCl if corrected Na+ levels > 145 mEq/l, use 0.45% instead | * Do not use 0.9% NaCl if corrected Na+ levels > 145 mEq/l, use 0.45% instead. | ||
* Do not supplement phosphate | * Avoid rapid correction of [[plasma osmolality]] and [[Sodium|serum sodium]], to prevent fatal [[cerebral edema]]. | ||
* Maximum reduction in [[plasma osmolality]] should be 3 mOsmol/kg per hour. | |||
* Do not supplement [[phosphate]] excessively, clinical trials have not shown any benefits. Supplement [[phosphate]] only if there is an actual deficit. | |||
* DO not use [[Subcutaneous tissue|subcutaneous]] sliding scale [[insulin]] in management of [[hyperglycemia]] due to [[diabetes type 1]].<ref name="pmid33515493">{{cite journal| author=Pasquel FJ, Lansang MC, Dhatariya K, Umpierrez GE| title=Management of diabetes and hyperglycaemia in the hospital. | journal=Lancet Diabetes Endocrinol | year= 2021 | volume= 9 | issue= 3 | pages= 174-188 | pmid=33515493 | doi=10.1016/S2213-8587(20)30381-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=33515493 }} </ref> | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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Latest revision as of 07:41, 29 April 2021
For more information about DKA, click here.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2], Husnain Shaukat, M.D [3]
Hyperglycemic crises Resident Survival Guide Microchapters |
---|
Overview |
Classification |
Causes |
FIRE |
Diagnosis |
Treatment |
Do's |
Don'ts |
Overview
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are life threatening complications of untreated or inadequately treated diabetes mellitus. HHS is characterized by hyperglycemia, hyperosmolarity and dehydration; whereas DKA is characterized by hyperglycemia, acidosis, and ketosis.[1]
Causes
Life Threatening Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. Hyperosmolar hyperglycemic state is a life-threatening condition and must be treated as such irrespective of the causes.
Common Causes
Common causes of hyperosmolar hyperglycemic state (HHS) include:
- Infections:
- Drugs:[7][8]
- Myocardial infarction[16]
- Pancreatitis[17]
- Shock/hypovolemia[18]
- Trauma[19]
- Undiagnosed diabetes mellitus[20]
- Noncompliance to insulin treatment:[21][22]
- Body image issues
- Financial problems
- Lack of insulin[5]
- Psychological factors
- Self-neglect
- Accidental
- Neglect by caregivers
Management
The diagnostic approach and management management of HHS and DKA are based on the ADA guidelines published in 2009.[1]
General Approach
Characterize the symptoms:
❑ Polyuria Examine the patient: ❑ Poor skin turgor Identify precipitating factors: ❑ Infections ❑ Insulin deficiency ❑ Myocardial infarction ❑ New onset DM type 1 ❑ Pregnancy ❑ Stress | |||||
Order tests: ❑ Serum glucose ❑ EKG ❑ CXR ❑ Urine, sputum, blood cultures (not routine) | |||||
Start the management of the following SIMULTANEOUSLY: (Urgent) (Check the algorithms below for more details) ❑ IV fluids | |||||
Check the following every two hours until the patient is stable: ❑ Glucose ❑ Electrolytes ❑ BUN ❑ Venous pH ❑ Creatinine | |||||
Determine the resolution of HHS: ❑ Blood glucose <200 mg/dl, AND Determine the resolution of HHS: | |||||
- The diagnosis of diabetic ketoacidosis is made in the presence of:
- Hyperglycemia- Plasma glucose > 250 mg/dL
- Anion gap metabolic acidosis- pH < 7.3; Serum bicarbonate < 15 mEq/L
- Ketonemia/ Ketonuria
- Shown below is a table summarizing the diagnosis of Diabetic ketoacidosis according the the American Diabetes Association (ADA) guidelines. [23] [24]
VARIABLE | DIABETIC KETOACIDOSIS | ||
---|---|---|---|
MILD (Plasma Glucose > 250mg/dL or 13.88 mmol/L) | MODERATE (Plasma Glucose > 250mg/dL or 13.88 mmol/L) | SEVERE (Plasma Glucose > 250mg/dL or 13.88 mmol/L) | |
Arterial pH | 7.25 to 7.30 | 7.00 to < 7.24 | < 7.00 |
Serum bicarbonate | 15 to 18 mEq/L | 10 to < 15 mEq/L | < 10 mEq/L |
Urine ketone (Nitroprusside reaction method) | Positive | Positive | Positive |
Serum ketone (Nitroprusside reaction method) | Positive | Positive | Positive |
Effective serum osmolality | Variable | Variable | Variable |
Anion gap | > 10 mEq/L (10 mmol/L) | > 12 mEq/L (12 mmol/L) | > 12 mEq/L (12 mmol/L) |
Mental status | Alert | Alert/drowsy | Stupor/coma |
Management: IV Fluids
Initial IV fluid ❑ 0.9% NaCl (15-20ml/kg/hour), OR ❑ 1-1.5L during the first hour | |||||||||||||||||||||||||||||
❑ Evaluate the hydration status | |||||||||||||||||||||||||||||
Severe hypovolemia | Mild hypovolemia | Cardiogenic shock ❑ Hemodynamic monitoring/pressors | |||||||||||||||||||||||||||
❑ Assess the corrected [Na+] | |||||||||||||||||||||||||||||
❑ Administer 0.9% NaCl (1.0L/hour) | High or normal [Na+] ❑ Administer 0.45% NaCl (250-500 ml/hour) depending on the hydration status | Low [Na+] ❑ Administer 0.9% NaCl (250-500 ml/hour) depending on the hydration status | |||||||||||||||||||||||||||
Hemodynamic monitoring: | |||||||||||||||||||||||||||||
When serum glucose reaches 200mg/dL in DKA and 300mg/dl in HHS ❑ Change to 5% dextrose with 0.45% NaCl (150-250 mL/hour) | |||||||||||||||||||||||||||||
Management: Insulin
Check K+ before administering insulin | |||||||||||||||||
K+<3.3 mEq/L ❑ Hold insulin and give K+ 20-30 mEq/h until K+>3.3 mEq/L | K+>5.5 mEq/L ❑ Do not give K ❑ Proceed with insulin | ||||||||||||||||
Administer initial IV dose of insulin ❑ Continuous IV infusion of 0.14 U/Kg/h, OR ❑ IV bolus of 0.1 U/Kg, then continuous IV infusion of 0.1 U/Kg/h | |||||||||||||||||
❑ Check if serum glucose falls by 10% in the first hour | |||||||||||||||||
Yes | No | ||||||||||||||||
❑ Administer IV bolus of 0.14 U/Kg, then continue previous treatment | |||||||||||||||||
When serum glucose reaches 250mg/dl in DKA and 300mg/dl in HHS: ❑ Reduce IV regular insulin infusion to 0.02-0.05 U/kg/h, OR ❑ Administer SC rapid acting insulin at 0.1 U/kg every 2 hours ❑ Keep serum glucose between 150-200 mg/dL until resolution (200-300 mg/dL for HHS) | |||||||||||||||||
❑ Check glucose, BUN, electrolytes, creatinine, venous pH every 3-4 hours until stable | |||||||||||||||||
❑ Confirm resolution and assess ability to eat | |||||||||||||||||
Inability to eat | Able to eat | ||||||||||||||||
❑ Continue IV insulin infusion and IV fluid replacement | Transfer from IV to SC insulin ❑ Initiate SC multidose insulin ❑ Continue IV insulin 1-2 hours after SC insulin is initiated | ||||||||||||||||
Patient previously on insulin? ❑ Recommence the insulin home dose | Insulin naive patient? ❑ Start at a multidose of 0.5-0.8 U/kg/day | ||||||||||||||||
Management: Potassium
❑ Assess K+ level ❑ Establish adequate renal function (urine output 50 ml/hour) | |||||||||||||||||||||||
K+<3.3 mEq/L | K+= 3.3-5.2 mEq/L | K+>5.2 mEq/L | |||||||||||||||||||||
❑ Hold insulin ❑ Administer 20-30 mEq/hour until K+>3.3 mEq/L | ❑ Administer 20-30 mEq/hour in each liter of IV fluid to keep serum K+ between 4 and 5 mEq/L | ❑ Do not give K+ | |||||||||||||||||||||
Keep K+= 4-5 mEq/L ❑ Check K+ every 2 hours until resolution of HHS | |||||||||||||||||||||||
Do's
- Check labs initially and every 2-4 hours.
- Immediately check urine for ketones with dipstick and send urine to the lab for analysis.
- Initiate IV insulin as soon as the patient arrives and satisfies the diagnostic criteria of DKA.
- Assess the trigger that precipitated DKA and treat the cause.
- In patients with potassium(K) < 3.3 mEq/L, fluids and potassium replacement must be done before initiating insulin therapy, to prevent further hypokalemia.
- Admit the patient to the floor; however, if the pH < 7.0 or the patient is unconscious then admit to ICU.
- Make sure to calculate the corrected sodium level when evaluating the sodium level. Sodium can be falsely low due to the elevated glucose level; in order to correct for this, add 1.6 mmol/L of Na+ for every 100 mg/dL of glucose > 100 mg/dL.
- Monitor for complications of DKA itself or of the therapy.
- In case the patient has cardiac or renal compromise, monitor serum osmolality and frequently assess the cardiac, renal and mental status.
Don'ts
- Do not stop IV insulin until DKA has resolved.
- Do not stop IV insulin, even if subcutaneous insulin is administered because it needs time to kick in.
- Do not give insulin if K+ levels are below 3.3 mEq/l because it may further exacerbate the hypokalemia.
- Do not use 0.9% NaCl if corrected Na+ levels > 145 mEq/l, use 0.45% instead.
- Avoid rapid correction of plasma osmolality and serum sodium, to prevent fatal cerebral edema.
- Maximum reduction in plasma osmolality should be 3 mOsmol/kg per hour.
- Do not supplement phosphate excessively, clinical trials have not shown any benefits. Supplement phosphate only if there is an actual deficit.
- DO not use subcutaneous sliding scale insulin in management of hyperglycemia due to diabetes type 1.[25]
References
- ↑ 1.0 1.1 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. PMC 2699725. PMID 19564476.
- ↑ Bouter KP, Diepersloot RJ, van Romunde LK, Uitslager R, Masurel N, Hoekstra JB, Erkelens DW (1991). "Effect of epidemic influenza on ketoacidosis, pneumonia and death in diabetes mellitus: a hospital register survey of 1976-1979 in The Netherlands". Diabetes Res. Clin. Pract. 12 (1): 61–8. PMID 1906798.
- ↑ Nakamura K, Inokuchi R, Doi K, Fukuda T, Tokunaga K, Nakajima S, Noiri E, Yahagi N (2014). "Septic ketoacidosis". Intern. Med. 53 (10): 1071–3. PMID 24827487.
- ↑ Osuchowski MF, Craciun FL, Schuller E, Sima C, Gyurko R, Remick DG (2010). "Untreated type 1 diabetes increases sepsis-induced mortality without inducing a prelethal cytokine response". Shock. 34 (4): 369–76. doi:10.1097/SHK.0b013e3181dc40a8. PMC 2941557. PMID 20610941.
- ↑ 5.0 5.1 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.
- ↑ Czaja CA, Rutledge BN, Cleary PA, Chan K, Stapleton AE, Stamm WE (2009). "Urinary tract infections in women with type 1 diabetes mellitus: survey of female participants in the epidemiology of diabetes interventions and complications study cohort". J. Urol. 181 (3): 1129–34, discussion 1134–5. doi:10.1016/j.juro.2008.11.021. PMC 2699609. PMID 19152925.
- ↑ Ramaswamy K, Kozma CM, Nasrallah H (2007). "Risk of diabetic ketoacidosis after exposure to risperidone or olanzapine". Drug Saf. 30 (7): 589–99. PMID 17604410.
- ↑ Guenette MD, Hahn M, Cohn TA, Teo C, Remington GJ (2013). "Atypical antipsychotics and diabetic ketoacidosis: a review". Psychopharmacology (Berl.). 226 (1): 1–12. doi:10.1007/s00213-013-2982-3. PMID 23344556.
- ↑ Alavi IA, Sharma BK, Pillay VK (1971). "Steroid-induced diabetic ketoacidosis". Am. J. Med. Sci. 262 (1): 15–23. PMID 4327634.
- ↑ Alberti KG (1975). "Role of glucagon and other hormones in development of diabetic ketoacidosis". Lancet. 1 (7920): 1307–11. PMID 49515.
- ↑ Nakamura K, Kawasaki E, Imagawa A, Awata T, Ikegami H, Uchigata Y, Kobayashi T, Shimada A, Nakanishi K, Makino H, Maruyama T, Hanafusa T (2011). "Type 1 diabetes and interferon therapy: a nationwide survey in Japan". Diabetes Care. 34 (9): 2084–9. doi:10.2337/dc10-2274. PMC 3161293. PMID 21775762.
- ↑ Lu CP, Wu HP, Chuang LM, Lin BJ, Chuang CY, Tai TY (1995). "Pentamidine-induced hyperglycemia and ketosis in acquired immunodeficiency syndrome". Pancreas. 11 (3): 315–6. PMID 8577688.
- ↑ Lambertus MW, Murthy AR, Nagami P, Goetz MB (1988). "Diabetic ketoacidosis following pentamidine therapy in a patient with the acquired immunodeficiency syndrome". West. J. Med. 149 (5): 602–4. PMC 1026553. PMID 3150636.
- ↑ Borberg C, Gillmer MD, Beard RW, Oakley NW (1978). "Metabolic effects of beta-sympathomimetic drugs and dexamethasone in normal and diabetic pregnancy". Br J Obstet Gynaecol. 85 (3): 184–9. PMID 24459.
- ↑ Rodgers BD, Rodgers DE (1991). "Clinical variables associated with diabetic ketoacidosis during pregnancy". J Reprod Med. 36 (11): 797–800. PMID 1684993.
- ↑ Trachtenbarg DE (2005). "Diabetic ketoacidosis". Am Fam Physician. 71 (9): 1705–14. PMID 15887449.
- ↑ Nair S, Yadav D, Pitchumoni CS (2000). "Association of diabetic ketoacidosis and acute pancreatitis: observations in 100 consecutive episodes of DKA". Am. J. Gastroenterol. 95 (10): 2795–800. doi:10.1111/j.1572-0241.2000.03188.x. PMID 11051350.
- ↑ Umpierrez GE, Kitabchi AE (2003). "Diabetic ketoacidosis: risk factors and management strategies". Treat Endocrinol. 2 (2): 95–108. PMID 15871546.
- ↑ Dhatariya KK (2007). "Diabetic ketoacidosis". BMJ. 334 (7607): 1284–5. doi:10.1136/bmj.39237.661111.80. PMC 1895683. PMID 17585123.
- ↑ Razavi Z (2010). "Frequency of ketoacidosis in newly diagnosed type 1 diabetic children". Oman Med J. 25 (2): 114–7. doi:10.5001/omj.2010.31. PMC 3215499. PMID 22125712.
- ↑ Borus JS, Laffel L (2010). "Adherence challenges in the management of type 1 diabetes in adolescents: prevention and intervention". Curr. Opin. Pediatr. 22 (4): 405–11. doi:10.1097/MOP.0b013e32833a46a7. PMC 3159529. PMID 20489639.
- ↑ Gosmanov AR, Gosmanova EO, Dillard-Cannon E (2014). "Management of adult diabetic ketoacidosis". Diabetes Metab Syndr Obes. 7: 255–64. doi:10.2147/DMSO.S50516. PMC 4085289. PMID 25061324.
- ↑ Schmoldt A, Benthe HF, Haberland G (1975). "Digitoxin metabolism by rat liver microsomes". Biochem Pharmacol. 24 (17): 1639–41. PMID doi.org/10.2337/dc09-9032 Check
|pmid=
value (help). - ↑ Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI; et al. (2001). "Management of hyperglycemic crises in patients with diabetes". Diabetes Care. 24 (1): 131–53. doi:10.2337/diacare.24.1.131. PMID 11194218.
- ↑ Pasquel FJ, Lansang MC, Dhatariya K, Umpierrez GE (2021). "Management of diabetes and hyperglycaemia in the hospital". Lancet Diabetes Endocrinol. 9 (3): 174–188. doi:10.1016/S2213-8587(20)30381-8. PMID 33515493 Check
|pmid=
value (help).