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{{Diabetic ketoacidosis}}
{{Diabetic ketoacidosis}}
{{CMG}}
{{CMG}}; {{AE}} {{HK}}
 
==Overview==
Diabetic ketoacidosis (DKA) is a medical emergency. The mainstay of therapy for DKA is medical therapy including [[intravenous]] [[insulin]], [[fluids]], [[potassium]] replacement and [[bicarbonate]] therapy in case of severe [[acidosis]] ([[pH]] <6.9). The basic principles guiding therapy include rapid restoration of adequate [[circulation]] and [[perfusion]], [[insulin]] to reverse [[ketosis]] and lower [[glucose]] levels, and close monitoring to prevent and treat complications if they develop. There are minor differences in the management of DKA in U.S.A. and U.K. which are opinion based and depend on the healthcare setting.


==Medical Therapy==
==Medical Therapy==
Treatment consists of hydration to lower the [[osmolality]] of the blood, replacement of lost electrolytes, insulin to force glucose and [[potassium]] into the cells, and eventually glucose simultaneously with insulin in order to correct other [[metabolic]] abnormalities, such as lowered blood potassium ([[hypokalemia]]) and elevated ketone levels.  Many patients require admission to a step-down unit or an [[intensive care unit]] (ICU) so that [[vital signs]], urine output, and blood tests can be monitored frequently. Brain [[edema]] is not rare, and so this may suggest intensive monitoring as well. In patients with severe alteration of mental status, [[intubation]] and [[mechanical ventilation]] may be required. Survival is dependent on how badly-deranged the metabolism is at presentation to a [[hospital]], but the process is only occasionally fatal.
The United States (US) and United Kingdom (UK) follow slightly different guidelines for the management of diabetic ketoacidosis (DKA) but the basic principles are same.
DKA occurs more commonly in type 1 diabetes because insulin deficiency is most severe, though it can occur in type 2 diabetes. In about a quarter of young people who develop type 1 diabetes, insulin deficiency and hyperglycemia lead to ketoacidosis before the disease is recognized and treated. This can occur at the onset of type 2 diabetes as well, especially in young people. In a person known to have diabetes and being adequately treated, DKA usually results from omission of [[insulin]], mismanagement of acute [[gastroenteritis]], the flu, or the development of a serious new health problem (e.g., [[bacterial infection]], [[myocardial infarction]]).
 
=== <u>Basic principles</u> ===
The basic principles of diabetic ketoacidosis treatment (DKA) are:
* Rapid restoration of adequate [[circulation]] and [[perfusion]] with [[intravenous fluids]].
* Gradual [[rehydration]] and restoration of depleted [[Electrolyte|electrolytes]] (especially [[sodium]] and [[potassium]]), even if [[serum]] levels appear adequate.  
* [[Insulin]] to reverse [[ketosis]] and lower [[glucose]] levels.  
* Careful monitoring to detect and treat complications.
 
=== <u>ADA guidelines</u> ===
The American Diabetes Association (ADA) recommends the following therapy for diabetic ketoacidosis (DKA):<ref name="pmid2699725">{{cite journal |vauthors=Radhakrishna Pillai M, Balaram P, Bindu S, Hareendran NK, Padmanabhan TK, Nair MK |title=Interleukin 2 production in lymphocyte cultures: a rapid test for cancer-associated immunodeficiency in malignant cervical neoplasia |journal=Cancer Lett. |volume=47 |issue=3 |pages=205–10 |year=1989 |pmid=2699725 |doi= |url=}}</ref><ref name="urlDiabetes Care">{{cite web |url=http://care.diabetesjournals.org/content/32/7/1335?ijkey=34356f79daf21d51f95018c32e74e6df627e513c&keytype2=tf_ipsecsha |title=Diabetes Care |format= |work= |accessdate=}}</ref><ref name="pmid21978840">{{cite journal |vauthors=Nyenwe EA, Kitabchi AE |title=Evidence-based management of hyperglycemic emergencies in diabetes mellitus |journal=Diabetes Res. Clin. Pract. |volume=94 |issue=3 |pages=340–51 |year=2011 |pmid=21978840 |doi=10.1016/j.diabres.2011.09.012 |url=}}</ref>


Insulin deficiency switches many aspects of metabolic balance in a catabolic direction. The liver becomes a net producer of glucose by way of [[gluconeogenesis]] (from protein) and [[glycogenolysis]] (from glycogen, though this source is usually exhausted within hours). Fat in [[adipose tissue]] is reduced to [[triglycerides]] and fatty acids by [[lipolysis]]. Muscle is degraded to release amino acids for gluconeogenesis. The rise of fatty acid levels is accompanied by increasing levels of ketone bodies ([[acetone]], [[acetoacetate]] and beta-hydroxybutyrate; only one, acetone, is chemically a ketone -- the name is an historical accident). As ketosis worsens, it produces a [[metabolic acidosis]], with [[anorexia]], abdominal distress, and eventually vomiting. The rising level of glucose increases the volume of urine produced by the kidneys (an osmolar [[diuresis]]). The high volume of urination ([[polyuria]]) also produces increased losses of electrolytes, especially [[sodium]], [[potassium]], [[chloride]], [[phosphate]], and [[magnesium]]. Reduced fluid intake from [[vomiting]] combined with amplified urination produce dehydration. As the [[metabolic acidosis]] worsens, it induces obvious [[hyperventilation]] (termed [[Kussmaul breathing|Kussmaul respiration]]). [[Kussmaul breathing | Kussmaul's respirations]] are the body's attempt to remove carbon dioxide from the blood that would otherwise form [[carbonic acid]] and further worsen the ketoacidosis.  See also [[arterial blood gas]].
==== Fluid therapy ====
* Initial [[Intravenous fluids|fluid therapy]] is aimed towards expansion of the [[intravascular]], [[interstitial]], and [[intracellular]] volume, all of which are reduced in [[Hyperglycemic crises resident survival guide|hyperglycemic crises]].  
* [[Fluid]] restoration also leads to increased [[renal]] [[perfusion]] and improves [[renal]] function.
* The following options may be used for [[fluid]] restoration:
** [[Saline solution|Isotonic saline]] (0.9% [[Sodium chloride|NaCl]]) is infused at a rate of 15–20 ml/kg/h or 1–1.5 L during the first hour. It may also be [[Infusion|infused]] at a rate of 250-500 ml/h if [[serum]] [[sodium]] is low.
** Subsequent choice for [[Intravenous fluids|fluid]] replacement depends on [[hemodynamics]], the volume status of the body ([[Signs and Symptoms|signs and symptoms]] of [[dehydration]]), [[serum electrolyte]] levels, and [[urinary]] output.<ref name="urlDiabetic Ketoacidosis: Evaluation and Treatment - American Family Physician">{{cite web |url=http://www.aafp.org/afp/2013/0301/p337.html |title=Diabetic Ketoacidosis: Evaluation and Treatment - American Family Physician |format= |work= |accessdate=}}</ref>
** Half [[normal saline]] (0.45% [[Sodium chloride|NaCl]] ) [[Infusion|infused]] at 250–500 ml/h is beneficial if the corrected [[serum]] [[sodium]] is normal or increased.<ref name="urlDiabetic Ketoacidosis: Evaluation and Treatment - American Family Physician" /><ref name="pmid3138479">{{cite journal |vauthors=Kageyama Y, Kawamura J, Ajisawa A, Yamada T, Iikuni K |title=A case of pseudohypoparathyroidism type 1 associated with gonadotropin resistance and hypercalcitoninaemia |journal=Jpn. J. Med. |volume=27 |issue=2 |pages=207–10 |year=1988 |pmid=3138479 |doi= |url=}}</ref>
* Successful progress with fluid replacement is judged by, [[blood pressure]] monitoring, measurement of [[fluid]] input/output, laboratory values, and clinical examination.  
* [[Intravenous fluids|Fluid]] replacement usually leads to successful treatment of volume deficit within the first 24 hours.
* In patients with [[renal]] or [[cardiac]] compromise, monitoring of [[serum]] [[osmolality]] and frequent assessment of [[cardiac]], [[renal]], and [[mental status]] must be performed during [[fluid resuscitation]] to avoid [[iatrogenic]] [[fluid overload]].  
* Aggressive [[rehydration]] with subsequent resolution of the [[hyperosmolar]] state has been shown to be linked to a better response to low dose [[insulin]]. 
* Once the [[plasma]] [[glucose]] is ∼ 200 mg/dl, 5% [[dextrose]] should be added to replacement [[Intravenous fluids|fluids]] to allow continued [[insulin]] administration. 


On presentation to hospital, patients in DKA are typically suffering dehydration and breathing both fast and deeply. [[Abdominal pain]] is common and may be severe. Consciousness level is typically normal until late in the process, when [[obtundation]] (dulled or reduced level of alertness or consciousness) may progress to [[coma]]. Dehydration can become severe enough to cause shock. Laboratory tests typically show [[hyperglycemia]], [[metabolic acidosis]], normal or elevated potassium, and severe [[ketosis]]. Many other tests can be affected.
==== '''Insulin therapy''' ====
* [[Insulin]] therapy helps control [[hyperglycemia]], [[hyperkalemia]] and [[ketosis]].<ref name="urlManagement of Diabetic Ketoacidosis - American Family Physician">{{cite web |url=http://www.aafp.org/afp/1999/0801/p455.html |title=Management of Diabetic Ketoacidosis - American Family Physician |format= |work= |accessdate=}}</ref>
* The following routes and rates of [[insulin]] administration may be used:
** '''Route''': [[Intravenous|Intravenous route]] is preferred because of rapid onset of action, although [[subcutaneous]] route can also be used.
** '''Rate of administration''': An initial [[intravenous]] dose of [[regular insulin]] (0.1 units/kg) followed by [[infusion]] of 0.1 units/kg/h [[insulin]].<ref name="urlDiabetes Care">{{cite web |url=http://care.diabetesjournals.org/content/32/7/1335?ijkey=34356f79daf21d51f95018c32e74e6df627e513c&keytype2=tf_ipsecsha |title=Diabetes Care |format= |work= |accessdate=}}</ref>
** The initial [[bolus]] of [[insulin]] may be skipped, if patients receive an hourly [[insulin]] [[infusion]] of 0.14 units/kg body weight.
** Low-dose [[insulin]] [[infusion]] protocols decrease [[plasma]] [[glucose]] concentration at a rate of 50–75 mg/dl/h.<ref name="urlDiabetes Care">{{cite web |url=http://care.diabetesjournals.org/content/32/7/1335?ijkey=34356f79daf21d51f95018c32e74e6df627e513c&keytype2=tf_ipsecsha |title=Diabetes Care |format= |work= |accessdate=}}</ref>
** '''Titration''':If [[plasma]] [[glucose]] does not decrease by 50–75 mg from the initial value in the first hour, the [[insulin]] [[infusion]] should be increased every hour until a steady [[glucose]] decline is achieved.
** When the [[blood]] [[glucose]] level reaches 200 mg/dl, the rate of [[insulin]] [[infusion]] should be changed to 0.02 units/kg/h - 0.05 units/kg/h and [[dextrose]] may be added to the [[Intravenous|IV]] [[fluids]].<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>
'''Potassium replacement'''
* [[Potassium]] replacement is started when the levels fall below the upper limit of normal (5.0-5.2 mEq/L).<ref name="pmid4633105">{{cite journal |vauthors=Beigelman PM |title=Potassium in severe diabetic ketoacidosis |journal=Am. J. Med. |volume=54 |issue=4 |pages=419–20 |year=1973 |pmid=4633105 |doi= |url=}}</ref>
* Goal is to maintain [[serum]] [[potassium]] levels within the normal range of 4–5 mEq/L.
'''Bicarbonate'''
* The use of [[bicarbonate]] in DKA is controversial. It lacks [[Evidence-based medicine|evidence-based]] [[Prospective cohort study|prospective clinical trials]] (especially in patients with pH <6.85 and [[pediatric]] population), and there has been no proven clinical efficacy of [[bicarbonate]] use.<ref name="pmid219063672">{{cite journal |vauthors=Chua HR, Schneider A, Bellomo R |title=Bicarbonate in diabetic ketoacidosis - a systematic review |journal=Ann Intensive Care |volume=1 |issue=1 |pages=23 |year=2011 |pmid=21906367 |pmc=3224469 |doi=10.1186/2110-5820-1-23 |url=}}</ref><ref name="pmid6091840">{{cite journal |vauthors=Hale PJ, Crase J, Nattrass M |title=Metabolic effects of bicarbonate in the treatment of diabetic ketoacidosis |journal=Br Med J (Clin Res Ed) |volume=289 |issue=6451 |pages=1035–8 |year=1984 |pmid=6091840 |pmc=1443021 |doi= |url=}}</ref><ref name="pmid3096181">{{cite journal |vauthors=Morris LR, Murphy MB, Kitabchi AE |title=Bicarbonate therapy in severe diabetic ketoacidosis |journal=Ann. Intern. Med. |volume=105 |issue=6 |pages=836–40 |year=1986 |pmid=3096181 |doi= |url=}}</ref><ref name="pmid4209917">{{cite journal |vauthors=Munk P, Freedman MH, Levison H, Ehrlich RM |title=Effect of bicarbonate on oxygen transport in juvenile diabetic ketoacidosis |journal=J. Pediatr. |volume=84 |issue=4 |pages=510–4 |year=1974 |pmid=4209917 |doi= |url=}}</ref><ref name="pmid12401775">{{cite journal |vauthors=Latif KA, Freire AX, Kitabchi AE, Umpierrez GE, Qureshi N |title=The use of alkali therapy in severe diabetic ketoacidosis |journal=Diabetes Care |volume=25 |issue=11 |pages=2113–4 |year=2002 |pmid=12401775 |doi= |url=}}</ref><ref name="urlDiabetes Care">{{cite web |url=http://care.diabetesjournals.org/content/25/11/2113 |title=Diabetes Care |format= |work= |accessdate=}}</ref>
* The use of [[bicarbonate]] in emergent settings depends on the clinical judgment, opinion, and expertise. The perceived benefit in acute reversal of severe [[acidemia]] is only based on animal and experimental studies.
* According to ADA guidelines, [[bicarbonate]] is administered if arterial pH is < 6.9 to prevent [[acidotic]] complications.
* 100 mmol [[sodium bicarbonate]] (two ampules) in 400 ml sterile water (an [[isotonic]] solution) with 20 mEq [[Potassium chloride|KCI]] administered at a rate of 200 ml/h for 2 h until the [[venous]] [[pH]] is >7.0.
* [[Bicarbonate]] use may be associated with a higher risk of developing [[cerebral edema]] in patients with high [[blood urea nitrogen]] levels.<ref name="pmid11172153">{{cite journal |vauthors=Glaser N, Barnett P, McCaslin I, Nelson D, Trainor J, Louie J, Kaufman F, Quayle K, Roback M, Malley R, Kuppermann N |title=Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics |journal=N. Engl. J. Med. |volume=344 |issue=4 |pages=264–9 |year=2001 |pmid=11172153 |doi=10.1056/NEJM200101253440404 |url=}}</ref>
'''Phosphate'''
* [[Phosphate]] therapy may be given to avoid potential [[cardiac]] and [[skeletal muscle]] weakness and [[respiratory depression]] due to [[hypophosphatemia]].<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>
* [[Phosphate]] replacement may sometimes be indicated in patients with [[cardiac dysfunction]], [[anemia]], or [[respiratory depression]] and when [[serum]] [[phosphate]] concentration is <1.0 mg/dl.
* Aggressive [[phosphate]] replacement may lead to [[hypocalcemia]].


At this point the patient is urgently in need of intravenous fluids. The basic principles of DKA treatment are:
=== <u>Criteria for resolution</u> ===
* Rapid restoration of adequate circulation and perfusion with [[isotonic]] intravenous fluids
* According to [[American Diabetes Association]], the following criteria must be met for labeling resolution of DKA:
* Gradual rehydration and restoration of depleted electrolytes (especially sodium and potassium), even if serum levels appear adequate
** [[Blood glucose]] <200mg/dl
* Insulin to reverse ketosis and lower glucose levels
'''PLUS'''
* Careful monitoring to detect and treat complications
* Any two of the following:
** [[Bicarbonate]] greater than equal to 15 mEq/L
** [[Venous]] [[pH]] > 7.3
** [[Anion gap]] less than equal to 12 mEq/L
* [[Bicarbonate]] level should not be relied upon to assess the resolution of DKA. This is because high volumes of [[Normal saline|0.9 % saline]] ([[Sodium chloride|NaCl]]) may lead to [[hyperchloremia]] in patients. The [[hyperchloremic acidosis]] will lower the [[bicarbonate]] and thus lead to difficulty is assessing whether the [[ketosis]] has resolved. The [[hyperchloremic acidosis]] may cause [[renal]] [[vasoconstriction]] and be a cause of [[oliguria]].
* DKA usually resolves in 24 hours with appropriate treatment.


Treatment usually results in full recovery, though death can result from inadequate treatment or a variety of complications, such as cerebral edema (occurs mainly in children).
=== <u>Differences in management between US and UK</u> ===
* [[American Diabetes Association]] guidelines recommend treating DKA based on the severity.
* Joint British Diabetes Societies in the UK recommend treating DKA based on rate of fall of [[glucose]] and [[serum]] [[ketones]], with a corresponding rise in [[bicarbonate]].
The following are differences in management of DKA between the US and UK:<ref name="pmid2699725">{{cite journal |vauthors=Radhakrishna Pillai M, Balaram P, Bindu S, Hareendran NK, Padmanabhan TK, Nair MK |title=Interleukin 2 production in lymphocyte cultures: a rapid test for cancer-associated immunodeficiency in malignant cervical neoplasia |journal=Cancer Lett. |volume=47 |issue=3 |pages=205–10 |year=1989 |pmid=2699725 |doi= |url=}}</ref><ref name="pmid3096181">{{cite journal |vauthors=Morris LR, Murphy MB, Kitabchi AE |title=Bicarbonate therapy in severe diabetic ketoacidosis |journal=Ann. Intern. Med. |volume=105 |issue=6 |pages=836–40 |year=1986 |pmid=3096181 |doi= |url=}}</ref><ref name="pmid1443021">{{cite journal |vauthors=Fleming TN, Runge PE, Charles ST |title=Diode laser photocoagulation for prethreshold, posterior retinopathy of prematurity |journal=Am. J. Ophthalmol. |volume=114 |issue=5 |pages=589–92 |year=1992 |pmid=1443021 |doi= |url=}}</ref><ref name="pmid21906367">{{cite journal |vauthors=Chua HR, Schneider A, Bellomo R |title=Bicarbonate in diabetic ketoacidosis - a systematic review |journal=Ann Intensive Care |volume=1 |issue=1 |pages=23 |year=2011 |pmid=21906367 |pmc=3224469 |doi=10.1186/2110-5820-1-23 |url=}}</ref><ref name="pmid28364357">{{cite journal |vauthors=Dhatariya KK, Vellanki P |title=Treatment of Diabetic Ketoacidosis (DKA)/Hyperglycemic Hyperosmolar State (HHS): Novel Advances in the Management of Hyperglycemic Crises (UK Versus USA) |journal=Curr. Diab. Rep. |volume=17 |issue=5 |pages=33 |year=2017 |pmid=28364357 |pmc=5375966 |doi=10.1007/s11892-017-0857-4 |url=}}</ref>
{| class="wikitable"
! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" + |Region
! colspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" + |Treatment
|-
|'''Insulin'''
|'''Intravenous fluids'''
|'''Bicarbonate'''
|-
|United states
|
* Use [[regular insulin]]
* Use a [[bolus]] (priming dose) of 10 U after [[Intravenous fluids|fluid therapy]] and then continue at a rate of 0.1U/kg/h
|
* [[Normal saline]] ([[Normal saline|0.9 %]]) at a rate of 15-20 ml/kg/h (1-1.5 L)
* Switch to 5 % [[dextrose]] with half [[normal saline]] (0.45 %) when serum glucose reaches 150-200mg/dl
|
* Use [[bicarbonate]] if pH < 6.9
|-
|United Kingdom
|
* Mainly use [[regular insulin]] but also advocate the use of long acting basal [[insulin]] to prevent rebound [[hyperglycemia]]
* Do not advocate the use of [[bolus]] (priming dose)
|
* [[Normal saline]] (0.9 %) at a rate of 1 L in each of first 2 hours
|
* Do not advocate use of [[bicarbonate]]
|}


====Contraindicated medications====
===Step-wise approach to management of diabetic ketoacidosis===
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{{familytree | | | | | | |,|-|-|-|-|-|-|-|-|-|-|v|-|-|-|-|-|-|-|-|+|-|-|-|-|-|-|-|-|-|-|.| }}
{{familytree | | | | | | C01 | | | | | | | | |C02| | | | | | |C03| | | | | | | | |C04|C01=Fluids|C02=Bicarbonate|C03=Insulin|C04=Potassium}}
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{{familytree | | |,|-|-|-|+|-|-|-|.| | | | | | | | | | | | | |!| | | | |!| | | |!| | | |!| | | | |!| | | | }}
{{familytree | | E01 | |E02| |E03| | | | | | | | | | | |E04| | | |!| | |E05| |E06| | |E07| |E01=Severe hypovolemia|E02= Mild dehydration|E03= Cardiogenic shock|E04=0.1 u/kg/B.WT. as IV continous infusion|E05= Hold insulin and give 20-30mEq/L of potassium until K+ > 3.3mEq/L|E06= Give 20-30mEq/L in each liter of IV fluids to maintain serum K 4-5mEq/L|E07= Do not give potassium but check serum potassium every 2 hours}}
{{familytree | | |!| | | |!| | |!| | | | | | | | | | | | | | |!| | | | |!| | | | | | | | | | | }}
{{familytree | |F01 | |F02| |F03| | | | | | | | | | | | |!| | | | |!| | | | | | | | | | |F01= 0.9% Nacl (1L/hr) as IV infusion|F02= Check corrected serum sodium|F03=Hemodynamic monitoring and add pressors accordingly}}
{{familytree | | | | | | | |!| | | | | | | | | | | | | | | | |`|L01|-|'|L01=If serum glucose does not fall by 10 % within one hour of therapy then give 0.14 U/Kg as IV bolus and continue previous regimen}}
{{familytree | | | |,|-|-|-|+|-|-|-|.| | | | | | | | | | | | | | |!| | }}
{{familytree | | |G01| |G02| |G03| | | | | | | | | | | | |G04| G01= High serum Na (>145 mEq/L)|G02=Normal serum Na (135-145 mEq/L)|G03= Low serum Na (< 135 mEq/L)|G04= When serum glucose drops to 200 mg/dl, reduce regular insulin to 0.02-0.05 U/Kg/hour, or give rapid-acting insulin at 0.1 U/kg SC every 2 hours, maintain serum glucose between 150 mg/dl to,200 mg/dl until resolution}}
{{familytree | | | |!| | | |!| | | |!| | }}
{{familytree | | | |`|H01|'| | |H02| |H01=0.45% NaCl (250-500 ml per hour depending on hydration status|H02=0.9% NaCl (200-500 ml per hour) depending on hydration status }}
{{familytree | | | | | |!| | | | | |!| | | }}
{{familytree | | | | | |`|-|I01|-|'| | |I01=When serum glucose decreases to 200 mg/dl, switch to 5% dextrose with 0.45% NaCl at 150-250 ml/hour }}
{{familytree/end}}
 
===Contraindicated medications===


{{MedCondContrAbs
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==References==
==References==
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{{Reflist|2}}


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Latest revision as of 19:30, 3 November 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Overview

Diabetic ketoacidosis (DKA) is a medical emergency. The mainstay of therapy for DKA is medical therapy including intravenous insulin, fluids, potassium replacement and bicarbonate therapy in case of severe acidosis (pH <6.9). The basic principles guiding therapy include rapid restoration of adequate circulation and perfusion, insulin to reverse ketosis and lower glucose levels, and close monitoring to prevent and treat complications if they develop. There are minor differences in the management of DKA in U.S.A. and U.K. which are opinion based and depend on the healthcare setting.

Medical Therapy

The United States (US) and United Kingdom (UK) follow slightly different guidelines for the management of diabetic ketoacidosis (DKA) but the basic principles are same.

Basic principles

The basic principles of diabetic ketoacidosis treatment (DKA) are:

ADA guidelines

The American Diabetes Association (ADA) recommends the following therapy for diabetic ketoacidosis (DKA):[1][2][3]

Fluid therapy

Insulin therapy

Potassium replacement

  • Potassium replacement is started when the levels fall below the upper limit of normal (5.0-5.2 mEq/L).[8]
  • Goal is to maintain serum potassium levels within the normal range of 4–5 mEq/L.

Bicarbonate

Phosphate

Criteria for resolution

PLUS

Differences in management between US and UK

The following are differences in management of DKA between the US and UK:[1][11][15][16][17]

Region Treatment
Insulin Intravenous fluids Bicarbonate
United states
United Kingdom

Step-wise approach to management of diabetic ketoacidosis

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
DKA treatment protocol according to ADA guidelines
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Fluids
 
 
 
 
 
 
 
 
Bicarbonate
 
 
 
 
 
 
Insulin
 
 
 
 
 
 
 
 
Potassium
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hydration status
 
 
 
 
 
 
pH greater than equal to 6.9
 
pH less than 6.9
 
 
0.1 u/kg/B.WT. as IV bolus
 
 
0.14 u/kg/B.WT/hr as continous IV infusion
 
K < 3.3 mEq/L
 
K = 3.3 - 5.2 mEq/L
 
 
K > 5.2 mEq/L
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Severe hypovolemia
 
Mild dehydration
 
Cardiogenic shock
 
 
 
 
 
 
 
 
 
 
 
0.1 u/kg/B.WT. as IV continous infusion
 
 
 
 
 
 
 
Hold insulin and give 20-30mEq/L of potassium until K+ > 3.3mEq/L
 
Give 20-30mEq/L in each liter of IV fluids to maintain serum K 4-5mEq/L
 
 
Do not give potassium but check serum potassium every 2 hours
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
0.9% Nacl (1L/hr) as IV infusion
 
Check corrected serum sodium
 
Hemodynamic monitoring and add pressors accordingly
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
If serum glucose does not fall by 10 % within one hour of therapy then give 0.14 U/Kg as IV bolus and continue previous regimen
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
High serum Na (>145 mEq/L)
 
Normal serum Na (135-145 mEq/L)
 
Low serum Na (< 135 mEq/L)
 
 
 
 
 
 
 
 
 
 
 
 
When serum glucose drops to 200 mg/dl, reduce regular insulin to 0.02-0.05 U/Kg/hour, or give rapid-acting insulin at 0.1 U/kg SC every 2 hours, maintain serum glucose between 150 mg/dl to,200 mg/dl until resolution
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
0.45% NaCl (250-500 ml per hour depending on hydration status
 
 
 
 
0.9% NaCl (200-500 ml per hour) depending on hydration status
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
When serum glucose decreases to 200 mg/dl, switch to 5% dextrose with 0.45% NaCl at 150-250 ml/hour
 
 
 
 
 
 
 
 
 

Contraindicated medications

Diabetic ketoacidosis is considered an absolute contraindication to the use of the following medications:

References

  1. ↑ 1.0 1.1 Radhakrishna Pillai M, Balaram P, Bindu S, Hareendran NK, Padmanabhan TK, Nair MK (1989). "Interleukin 2 production in lymphocyte cultures: a rapid test for cancer-associated immunodeficiency in malignant cervical neoplasia". Cancer Lett. 47 (3): 205–10. PMID 2699725.
  2. ↑ 2.0 2.1 2.2 2.3 "Diabetes Care".
  3. ↑ Nyenwe EA, Kitabchi AE (2011). "Evidence-based management of hyperglycemic emergencies in diabetes mellitus". Diabetes Res. Clin. Pract. 94 (3): 340–51. doi:10.1016/j.diabres.2011.09.012. PMID 21978840.
  4. ↑ 4.0 4.1 "Diabetic Ketoacidosis: Evaluation and Treatment - American Family Physician".
  5. ↑ Kageyama Y, Kawamura J, Ajisawa A, Yamada T, Iikuni K (1988). "A case of pseudohypoparathyroidism type 1 associated with gonadotropin resistance and hypercalcitoninaemia". Jpn. J. Med. 27 (2): 207–10. PMID 3138479.
  6. ↑ "Management of Diabetic Ketoacidosis - American Family Physician".
  7. ↑ 7.0 7.1 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.
  8. ↑ Beigelman PM (1973). "Potassium in severe diabetic ketoacidosis". Am. J. Med. 54 (4): 419–20. PMID 4633105.
  9. ↑ Chua HR, Schneider A, Bellomo R (2011). "Bicarbonate in diabetic ketoacidosis - a systematic review". Ann Intensive Care. 1 (1): 23. doi:10.1186/2110-5820-1-23. PMC 3224469. PMID 21906367.
  10. ↑ Hale PJ, Crase J, Nattrass M (1984). "Metabolic effects of bicarbonate in the treatment of diabetic ketoacidosis". Br Med J (Clin Res Ed). 289 (6451): 1035–8. PMC 1443021. PMID 6091840.
  11. ↑ 11.0 11.1 Morris LR, Murphy MB, Kitabchi AE (1986). "Bicarbonate therapy in severe diabetic ketoacidosis". Ann. Intern. Med. 105 (6): 836–40. PMID 3096181.
  12. ↑ Munk P, Freedman MH, Levison H, Ehrlich RM (1974). "Effect of bicarbonate on oxygen transport in juvenile diabetic ketoacidosis". J. Pediatr. 84 (4): 510–4. PMID 4209917.
  13. ↑ Latif KA, Freire AX, Kitabchi AE, Umpierrez GE, Qureshi N (2002). "The use of alkali therapy in severe diabetic ketoacidosis". Diabetes Care. 25 (11): 2113–4. PMID 12401775.
  14. ↑ Glaser N, Barnett P, McCaslin I, Nelson D, Trainor J, Louie J, Kaufman F, Quayle K, Roback M, Malley R, Kuppermann N (2001). "Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics". N. Engl. J. Med. 344 (4): 264–9. doi:10.1056/NEJM200101253440404. PMID 11172153.
  15. ↑ Fleming TN, Runge PE, Charles ST (1992). "Diode laser photocoagulation for prethreshold, posterior retinopathy of prematurity". Am. J. Ophthalmol. 114 (5): 589–92. PMID 1443021.
  16. ↑ Chua HR, Schneider A, Bellomo R (2011). "Bicarbonate in diabetic ketoacidosis - a systematic review". Ann Intensive Care. 1 (1): 23. doi:10.1186/2110-5820-1-23. PMC 3224469. PMID 21906367.
  17. ↑ Dhatariya KK, Vellanki P (2017). "Treatment of Diabetic Ketoacidosis (DKA)/Hyperglycemic Hyperosmolar State (HHS): Novel Advances in the Management of Hyperglycemic Crises (UK Versus USA)". Curr. Diab. Rep. 17 (5): 33. doi:10.1007/s11892-017-0857-4. PMC 5375966. PMID 28364357.

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