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__NOTOC__
__NOTOC__
{{CMG}}; {{AE}}; {{VB}}


==Definition==
'''For more information about DKA, click [[DKA|here]].'''


Diabetic ketoacidosis is a life threatening complication of untreated or inadequately treated Diabetes Mellitus, usually Type 1 but sometimes also seen in Type 2. It is a metabolic abnormality with hypoglycemia, metabolic acidosis and ketonuria/ketonemia. It is seen when there is lack of insulin in body, so that instead of sugars, fats are burned as fuel.
{{CMG}}; {{AE}} {{HK}}, {{HS}}
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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]]
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! 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==
It sometimes occurs as an initial presentation in undiagnosed cases of type 1 DM, however it can also occur in people with type 2 DM. In both the types it may be precipitated by one or more of the following causes. It is a life-threatening condition in itself.


==Life Threatening Causes==
===Life Threatening Causes===
Diabetic ketoacidosis is a life-threatening condition and must be treated as such irrespective of the causes.  Life-threatening conditions may result in death or permanent disability within 24 hours if left untreated.
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>
 


==Most Common Causes==
* 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>


* '''Intercurrent illnesses''' - such as infections, is the most common risk factor precipitating DKA. Urinary tract infection's and Pneumonia being the 2 most common.<ref name="Umpierrez-2003">{{Cite journal  | last1 = Umpierrez | first1 = GE. | last2 = Kitabchi | first2 = AE. | title = Diabetic ketoacidosis: risk factors and management strategies. | journal = Treat Endocrinol | volume = 2 | issue = 2 | pages = 95-108 | month = | year = 2003 | doi = | PMID = 15871546 }}</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


* '''Pregnancy'''.<ref name="Parker-2007">{{Cite journal  | last1 = Parker | first1 = JA. | last2 = Conway | first2 = DL. | title = Diabetic ketoacidosis in pregnancy. | journal = Obstet Gynecol Clin North Am | volume = 34 | issue = 3 | pages = 533-43, xii | month = Sep | year = 2007 | doi = 10.1016/j.ogc.2007.08.001 | PMID = 17921013 }}</ref>
|}


* '''Stress''' such as that caused from surgery, infections etc which leads to a release of stress hormones , which are counter-regulatory to insulin.<ref name="MacGillivray-1981">{{Cite journal  | last1 = MacGillivray | first1 = MH. | last2 = Bruck | first2 = E. | last3 = Voorhess | first3 = ML. | title = Acute diabetic ketoacidosis in children: role of the stress hormones. | journal = Pediatr Res | volume = 15 | issue = 2 | pages = 99-106 | month = Feb | year = 1981 | doi = 10.1203/00006450-198102000-00002 | PMID = 6789292 }}</ref>
===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}}


* '''Dehydration'''.
<br>
<br>


* '''Medications''' such as corticosteroid, pentamidine,<ref name="Lambertus-1988">{{Cite journal  | last1 = Lambertus | first1 = MW. | last2 = Murthy | first2 = AR. | last3 = Nagami | first3 = P. | last4 = Goetz | first4 = 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 | month = Nov | year = 1988 | doi =  | PMID = 3150636 }}</ref> clozapine. <ref name="Ai-1998">{{Cite journal  | last1 = Ai | first1 = D. | last2 = Roper | first2 = TA. | last3 = Riley | first3 = JA. | title = Diabetic ketoacidosis and clozapine. | journal = Postgrad Med J | volume = 74 | issue = 874 | pages = 493-4 | month = Aug | year = 1998 | doi | PMID = 9926128 }}</ref>
===Management: Insulin===
{{familytree/start}}
{{familytree | | | A01 | | | A01= '''Check K<sup>+</sup> before administering insulin'''}}
{{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 | |`| 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 | | | C01 | | | C01= ❑ '''Check if serum glucose falls by 10% in the first hour'''}}
{{familytree | |,|-|^|-|.| | }}
{{familytree | D01 | | D02 | D01= Yes| D02= No}}
{{familytree | |!| | | |!| | }}
{{familytree | |!| | | E01 | E01= ❑ Administer IV bolus of 0.14 U/Kg,<br> then continue previous treatment}}
{{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 
----
❑ '''Keep serum glucose between 150-200 mg/dL until'''<br> '''resolution (200-300 mg/dL for HHS) '''}}
{{familytree | | | |!| | | | }}
{{familytree | | | G01 | | | G01= ❑ Check glucose, BUN, electrolytes, creatinine, venous pH every 3-4 hours until stable}}
{{familytree | | | |!| | | | }}
{{familytree | | | G02 | | | G02= ❑ '''Confirm resolution and'''<br> '''assess ability to eat'''}}
{{familytree | |,|-|^|-|.| | }}
{{familytree | H01 | | H02 | H01= Inability to eat| H02= Able to eat}}
{{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}}


* '''Failure of pump therapy''' - This has been recognized as a potential adverse effect of pump use and hence incidence has reduced. <ref name="Rosenbloom-2010">{{Cite journal  | last1 = Rosenbloom | first1 = AL. | title = The management of diabetic ketoacidosis in children. | journal = Diabetes Ther | volume = 1 | issue = 2 | pages = 103-20 | month = Dec | year = 2010 | doi = 10.1007/s13300-010-0008-2 | PMID = 22127748 }}</ref><ref name="Baird-2009">{{Cite journal  | last1 = Baird | first1 = JS. | title = Relapse of diabetic ketoacidosis secondary to insulin pump malfunction diagnosed by capillary blood 3-hydroxybutyrate: a case report. | journal = Cases J | volume = 2 | issue =  | pages = 8012 | month =  | year = 2009 | doi = 10.4076/1757-1626-2-8012 | PMID = 19918445 }}</ref>
<br>
<br>


==Management==
===Management: Potassium===
{{familytree/start |summary=Diabetic ketoacidosis}}
{{familytree/start}}
{{familytree | | | | | | | | | | | | | | | | | | | | | | | | A01 | | | |A01=Diabetic ketoacidosis}}
{{familytree | | | | | A01 | | | A01= ❑ Assess K<sup>+</sup> level <br> ❑ Establish adequate renal function<br> (urine output 50 ml/hour)}}
{{familytree | | | | | | | | | | | | | | | | | | | | | | | | |!| | | | |}}
{{familytree | |,|-|-|-|+|-|-|-|.| | }}
{{familytree | | | | | | | | | | | | | | | | | | | | | | | | B01 | | | |B01='''H/o''' - vomiting, abdominal pain, drowsiness, altered mentation, fever, & malaise.'''Precipitating factors''' - Insulin deficiency, Intercurrent illness, stress, MI, Pregnancy, new onset DM type 1.}}
{{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 | |!| | | |!| | | | | | }}
{{familytree | | | | | | | | | | | | | | | | | | | | | | | | C01 | | | |C01='''Check labs''' - CBC, Chem 7, ABG, EKG, CXR, urine dipstick & routine }}
{{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 | |!| | | |!| | | |!| | }}
{{familytree | | | | | | | | | | | | | | | | | | | | | | | | D01 | | | |D01='''Diagnostic criteria'''Blood glucose > 250 mg/dL pH < 7.3 Serum bicarbonate < 18 mEq/L<br>Serum ketones (+)<br>Anion gap > 10 }}
{{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 | | | | | | | | | |,|-|-|-|-|-|-|-|-|-|v|-|-|-|-|^|-|-|-|-|v|-|-|-|-|-|-|-|-|-|.| | }}
{{familytree | | | | | | | | | E01 | | | | | | | | E02 | | | | | | | | E03 | | | | | | | | E04 | | | |E01='''i.v fluid therapy''' |E02='''Insulin''' |E03='''Need for K<sup>+</sup> replacement?''' |E04='''Need for bicarbonate replacement?'''}}
{{familytree | | | | | | | | | |!| | | | | | | |,|-|^|-|.| | | |,|-|-|-|+|-|-|-|.| | | |,|-|^|-|.| | |}}
{{familytree | | | | | | | | | F01 | | | | | | F02 | | F03 | | F04 | | F05 | | F06 | | F07 | | F08 | |F01=Check hydration status |F02=i.v. |F03=s.c. for uncomplicated DKA |F04= '''<3.3 mEq/dL''' |F05= 3.3-5.3 mEq/dL |F06= >5.3 mEq/dL |F07='''pH < 6.9''' |F08=pH > 7.0 }}
{{familytree | | | | | |,|-|-|-|+|-|-|-|.| | | |!| | | |!| | | |!| | | |!| | | |!| | | |!| | | |!| |}}
{{familytree | | | | | G01 | | G02 | | G03 | | G04 | | G05 | | G06 | | G07 | | G08 | | G09 | | G10 | |G01=Mild dehydration |G02=Severe dehydration |G03=Cardiogenic shock |G04=Regular insulin @ 0.1 U/kg bolus. |G05=Rapid action insulin 0.3 U/kg then 0.2 U/kg after 1 Hr. |G06=Hold insulin, supplement K<sup>+</sup> @ 20-30 mEq/Hr till K<sup>+</sup> > 3.3 mEq/L |G07=Administer 20-30 mEq K<sup>+</sup> per L of fluid. |G08=Don't supplement, check 2 hourly. |G09=Dilute NaHCo<sub>3</sub> (100 mmol) in 400 ml H<sup>2</sup>O with 20 mEq KCl infused over 2 Hrs |G10=No bicarbonate needed. }}
{{familytree | | | | | |!| | | |!| | | |!| | | |!| | | |!| | | | | | | | | | | | | | | |!| | | | | | }}
{{familytree | | | | | H01 | | H02 | | H03 | | H04 | | H05 | | | | | | | | | | | | | | H06 | | | | | |H01=Evaluate for corrected Na<sup>+</sup> levels |H02=Start 0.9% NaCl @ 1L/Hr initially.|H03=Pressors/ Monitor hemodynamics. |H04=Continous infusion @ 0.1 U/kg/Hr |H05=s.c. insulin 0.2 U/kg every 2 Hrs.  |H06= Recheck }}
{{familytree | |,|-|-|-|+|-|-|-|.| | | | | | | |`|-|v|-|'| | | | | | | | | | | | | | | | | | | }}
{{familytree | I01 | | I02 | | I03 | | | | | | | | I04 | | | | | | | | |I01=High Na<sup>+</sup> levels |I02=Normal Na<sup>+</sup> levels |I03=Low Na<sup>+</sup> levels |I04=Double insulin infusion if blood sugar doesnt fall by 50-70 mg/dL in first Hr. }}
{{familytree | |`|-|v|-|'| | | |!| | | | | | | | | |!| | | | | | | | | |}}
{{familytree | | | J01 | | | | J02 | | | | | | | | J03 | | | | | | | | | |J01=Switch to 0.45% NaCl (250-500mL/Hr) |J02=Continue to 0.9% NaCl (250-500mL/Hr) |J03=At serum glucose = 200 mg/dL reduce i.v. insulin to 0.02-0.05 U/kg/Hr or s.c. insulin @ 0.1 U/kg every 2 hrs. Target blood sugar - 150-200 mg/dL till DKA resolves.}}
{{familytree | | | |`|-|-|v|-|-|'| | | | | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | | K01 | | | | | | | | | | | |!| | | | | | | | | | |K01=Check blood glucose levels }}
{{familytree | | | | | | |!| | | | | | | | | | | | |!| | | | | | | | | |}}
{{familytree | | | | | | L01 |-|-|-|-|-|-|-|-|-|-| L02 | | | | | L03 | | |L01='''At serum glucose levels ~ 200 mg/dL''' switch to 5% dextrose with 0.45% NaCl @ 150-250 ml/Hr|L02=Check labs every 2-4 hrs, once pt. tolerates oral feeds transition to s.c. insulin @ 0.8 U/kg/day. Stop i.v. insulin gradually. |L03=Look out for following complications.<br>Hypogylcemia<br>Hypokalemia<br>Cerebral edema<br>Respiratory distress<br>Sepsis<br>Acute gastric dilation
}}
{{familytree | | | | | | | | | | | | | | | | | | | | | | | | | | | | | |}}
{{familytree/end}}
{{familytree/end}}
The managment protocol is based on the recommendations given by American Diabetes Association (ASA) and other sources.<ref name="Nyenwe-2011">{{Cite journal  | last1 = Nyenwe | first1 = EA. | last2 = Kitabchi | first2 = AE. | title = Evidence-based management of hyperglycemic emergencies in diabetes mellitus. | journal = Diabetes Res Clin Pract | volume = 94 | issue = 3 | pages = 340-51 | month = Dec | year = 2011 | doi = 10.1016/j.diabres.2011.09.012 | PMID = 21978840 }}</ref>


==Do's==
==Do's==


* Check labs initially and every 2-4 hours.  
* Check labs initially and every 2-4 hours.
* Check urine for ketones immediately with dipstick and send urine to lab for analysis.
* Immediately check urine for ketones with dipstick and send urine to the lab for analysis.
* Initiate i.v. insulin as soon as the patient arrives and satisfies criteria for DKA.  
* Initiate [[Insulin|IV insulin]] as soon as the patient arrives and satisfies the diagnostic criteria of DKA.
* Assess to understand what precipitated DKA and treat the cause.  
* Assess the trigger that precipitated DKA and treat the cause.
* Admit the patient. If pH < 7.0, pt unconscious admit to ICU else may be shifted directly to floor.
* 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]].
* Assess hydration status of the patient, treat aggressively.
* Admit the patient to the floor; however, if the pH < 7.0 or the patient is unconscious then admit to ICU.
* switch to Dextrose with normal saline once blood sugar falls to 200 mg/dL.
* 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.
* Check for complications from the condition itself as well as those developing due to therapy.  
* 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 i.v. insulin until DKA has resolved.
* Do not stop [[Insulin|IV insulin]] until DKA has resolved.
* Do not stop i.v. insulin, as soon as s.c. insulin is administered, as it needs time to kick in.  
* 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 3.5 mEq/l, may further cause hypokalemia.
* 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.
 
* Avoid rapid correction of [[plasma osmolality]] and [[Sodium|serum sodium]], to prevent fatal [[cerebral edema]].
* Do not supplement phosphate overzealously, clinical trials have not shown any benefits. Give only if there is am actual deficiency.   
* 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:

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
Polydipsia
Weight loss
Vomiting
Dehydration
❑ Weakness
❑ Mental status change
Abdominal pain
❑ Vomiting


Examine the patient:


❑ Poor skin turgor
Kussmaul breathing
Tachycardia
Hypotension
Hypothermia or hyperthermia


Identify precipitating factors:


Infections
Insulin deficiency
Myocardial infarction
❑ New onset DM type 1
❑ Pregnancy
❑ Stress
 
 
 
Order tests:

❑ Serum glucose
ABG
CBC
Electrolytes
❑ Serum & urinary ketones
Urinalysis
BUN
Creatinine
Plasma osmolality


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
Insulin
Potassium
Bicarbonate

 
 
 
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
❑ Two of the following criteria:
- Serum bicarbonate level >15 mEq/l
- Venous pH >7.3
- Calculated anion gap12 mEq/l


Determine the resolution of HHS:
❑ Normal osmolality

❑ Regain of normal mental status



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:
Blood pressure
❑ Laboratory results
❑ Input/output of fluids
❑ Clinical status
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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

References

  1. 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.
  2. 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.
  3. 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.
  4. 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. 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.
  6. 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.
  7. 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.
  8. 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.
  9. Alavi IA, Sharma BK, Pillay VK (1971). "Steroid-induced diabetic ketoacidosis". Am. J. Med. Sci. 262 (1): 15–23. PMID 4327634.
  10. Alberti KG (1975). "Role of glucagon and other hormones in development of diabetic ketoacidosis". Lancet. 1 (7920): 1307–11. PMID 49515.
  11. 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.
  12. 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.
  13. 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.
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