Hyperosmolar hyperglycemic state medical therapy: Difference between revisions

Jump to navigation Jump to search
No edit summary
 
(15 intermediate revisions by 3 users not shown)
Line 1: Line 1:
__NOTOC__
__NOTOC__
{{Hyperosmolar hyperglycemic state}}
{{Hyperosmolar hyperglycemic state}}
{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} {{HS}}


==Overview==
==Overview==
Hyperosmolar hyperglycemic state (HHS) is a [[medical emergency]] and acute complication of [[diabetes mellitus]]. The basic principles guiding therapy include rapid restoration of adequate [[circulation]] and [[perfusion]], correction of [[hyperosmolality]], [[electrolytes]] balance, [[hyperglycemia]], identifying and treating the underlying precipitating cause and close monitoring to prevent and treat complications if they develop. The mainstay of therapy for HHS is [[medical therapy]] including intravenous [[insulin]], [[fluids|fluids,]] and [[potassium]] replacement therapy.
Hyperosmolar hyperglycemic state (HHS) is a [[medical emergency]] and acute complication of [[diabetes mellitus]]. The basic principles guiding therapy include rapid restoration of adequate [[circulation]] and [[perfusion]], correction of [[hyperosmolality]], [[electrolytes]] balance, [[hyperglycemia]], identifying and treating the underlying precipitating cause and close monitoring to prevent and treat complications if they develop. The mainstay of therapy for HHS is medical therapy including intravenous [[insulin]], [[fluids|fluids,]] and [[potassium]] replacement therapy.


==Medical Therapy==
==Medical Therapy==
Line 31: Line 31:
* Once the [[plasma]] [[glucose]] is ∼ 300 mg/dl, 5% [[dextrose]] should be added to replacement [[Intravenous fluids|fluids]] to allow continued [[insulin]] administration. 
* Once the [[plasma]] [[glucose]] is ∼ 300 mg/dl, 5% [[dextrose]] should be added to replacement [[Intravenous fluids|fluids]] to allow continued [[insulin]] administration. 
==== '''Insulin therapy''' ====
==== '''Insulin therapy''' ====
* Adequate fluids must be given before administring [[insulin]]. If [[insulin]] is given before [[fluids]], it will cause water to move [[intracellulary]] causing worsening of [[hypotension]] and death.
* Adequate fluids must be given before administering [[insulin]]. If [[insulin]] is given before [[fluids]], it will cause water to move intracellularly causing worsening of [[hypotension]] and death.
* [[Insulin]] therapy helps control [[hyperglycemia]] and [[hyperkalemia]] in hyperosmolar hyperglycemic state.<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>
* [[Insulin]] therapy helps control [[hyperglycemia]] and [[hyperkalemia]] in hyperosmolar hyperglycemic state.<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>


Line 37: Line 37:
** The initial [[bolus]] of [[insulin]] may be skipped, if patients receive an hourly [[insulin]] [[infusion]] of 0.14 units/kg body weight.
** 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>  
** 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]] can be doubled until a steady [[glucose]] decline is achieved.
** '''Titration''': If [[plasma]] [[glucose]] does not decrease by 50–75 mg from the initial value in the first hour, the [[insulin]] [[infusion]] can be doubled until a steady [[glucose]] decline is achieved.
** When the [[blood]] [[glucose]] level reaches 300 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]] to keep the [[glucose]] between 250 - 300 mg/dl until hyperosmolality has resolved or the patient is conscious and alert.<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><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=2699725 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19564476  }} </ref>
** When the [[blood]] [[glucose]] level reaches 300 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]] to keep the [[glucose]] between 250 - 300 mg/dl until hyperosmolality has resolved or the patient is conscious and alert.<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><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=2699725 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19564476  }} </ref>
'''Potassium replacement'''
'''Potassium replacement'''
Line 55: Line 55:
'''Identify and treat the precipitating cause'''
'''Identify and treat the precipitating cause'''
* Appropriate investigations can be ordered to find out and treat the precipitating cause.
* Appropriate investigations can be ordered to find out and treat the precipitating cause.
* Empiric antibiotics can be administered, if there is suspicion of sepsis only after taking the blood cultures.
* Empiric [[Antibiotic|antibiotics]] can be administered, if there is suspicion of [[sepsis]] only after taking the [[Blood culture|blood cultures]].
=== <u>Criteria for resolution</u> ===
=== <u>Criteria for resolution</u> ===
* The following criteria must be met for labeling resolution of hyperosmolar hyperglycemic state:
* The following criteria must be met for labeling resolution of hyperosmolar hyperglycemic state:
Line 63: Line 63:
** Regain of normal hemodynamic status
** Regain of normal hemodynamic status


 
===Step-wise management of hyperosmolar hyperglycemic state===
 
 
 
{{familytree/start}}
{{familytree/start}}
{{familytree | | | | | | | | | B01 | | | | | |B01=HHS}}
{{familytree | | | | | | | | | | | | | | | | | B01 | | | | | | | | | | |B01=HHS treatment protocol according to ADA guidelines}}
{{familytree | | |,|-|-|-|-|-|-|+|-|-|-|-|-|-|.| }}
{{familytree | | | | | | |,|-|-|-|-|-|-|-|-|-|-|-|+|-|-|-|-|-|-|-|-|-|-|.| }}
{{familytree | | C01 | | | | | C02 | | | | | C03 |C01=Fluids|C02=Insulin|C03=Potassium}}
{{familytree | | | | | | C01 | | | | | | | | | |C02| | | | | | | | |C03|C01=Fluids|C02=Insulin|C03=Potassium}}
{{familytree | | |!| | | | | | | | | | |!| }}
{{familytree | | | | | | |!| | | | | | | | |,|-|-|^|-|-|.| | | |,|-|-|-|+|-|-|-|-|.| }}
 
{{familytree | | | | | |D01| | | | | | | |D02| | |D03| |D04| |D05| | |D06| |D01=Hydration status|D02=0.1 u/kg/B.WT. as IV bolus|D03=0.14 u/kg/B.WT/hr as continous IV infusion|D04=K < 3.3 mEq/L|D05=K = 3.3 - 5.2 mEq/L |D06=K > 5.2 mEq/L}}
{{familytree | | | | | | |   | | | | | | | |!| | | E01 | | | | | | | | E02 | | E03 | | | E04 |E01=K < 3.2|E02=K =3.2 - 5.2|E03=k> 5.2|E04=E04}}
{{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 300 mg/dl, reduce regular insulin to 0.02-0.05 U/Kg/hour, maintain serum glucose between 200 mg/dl to 300 mg/dl until patient is alert}}
{{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 300 mg/dl, switch to 5% dextrose with 0.45% NaCl at 150-250 ml/hour }}
{{familytree/end}}
{{familytree/end}}
{{Summary= HHS protocol according to American diabetes association}}


==References==
==References==
Line 84: Line 88:
{{WH}}
{{WH}}
{{WS}}
{{WS}}
[[Category:Medicine]]
[[Category:Endocrinology]]
[[Category:Up-To-Date]]
[[Category:Emergency medicine]]

Latest revision as of 19:35, 23 October 2017

Hyperosmolar hyperglycemic state Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Hyperosmolar hyperglycemic state from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic study of choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Hyperosmolar hyperglycemic state medical therapy On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Hyperosmolar hyperglycemic state medical therapy

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Hyperosmolar hyperglycemic state medical therapy

CDC on Hyperosmolar hyperglycemic state medical therapy

Hyperosmolar hyperglycemic state medical therapy in the news

Blogs on Hyperosmolar hyperglycemic state medical therapy

Directions to Hospitals Treating Psoriasis

Risk calculators and risk factors for Hyperosmolar hyperglycemic state medical therapy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Husnain Shaukat, M.D [2]

Overview

Hyperosmolar hyperglycemic state (HHS) is a medical emergency and acute complication of diabetes mellitus. The basic principles guiding therapy include rapid restoration of adequate circulation and perfusion, correction of hyperosmolality, electrolytes balance, hyperglycemia, identifying and treating the underlying precipitating cause and close monitoring to prevent and treat complications if they develop. The mainstay of therapy for HHS is medical therapy including intravenous insulin, fluids, and potassium replacement therapy.

Medical Therapy

Basic principles

The basic principles of hyperosmolar hyperglycemic state treatment are:

The American Diabetes Association (ADA) recommends the following therapy for hyperosmolar hyperglycemic state:[1][2][3][4]

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).[9]
  • Goal is to maintain serum potassium levels within the normal range of 3.3–5.2 mEq/L.
  • If serum potassium levels are < 3.3 mEq/L; hold the insulin and add 20 - 30 mEq/ hr of potassium to each litre infusion fluids.
  • If serum potassium levels are > 5.2 mEq/L; do not add potassium but check for serum potassium every 2 hours.

Other electrolytes

Vitamins

Identify and treat the precipitating cause

  • Appropriate investigations can be ordered to find out and treat the precipitating cause.
  • Empiric antibiotics can be administered, if there is suspicion of sepsis only after taking the blood cultures.

Criteria for resolution

  • The following criteria must be met for labeling resolution of hyperosmolar hyperglycemic state:

Step-wise management of hyperosmolar hyperglycemic state

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
HHS treatment protocol according to ADA guidelines
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Fluids
 
 
 
 
 
 
 
 
 
Insulin
 
 
 
 
 
 
 
 
Potassium
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Hydration status
 
 
 
 
 
 
 
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 300 mg/dl, reduce regular insulin to 0.02-0.05 U/Kg/hour, maintain serum glucose between 200 mg/dl to 300 mg/dl until patient is alert
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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 300 mg/dl, switch to 5% dextrose with 0.45% NaCl at 150-250 ml/hour
 
 
 
 
 
 
 
 
 

References

  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 "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 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.
  5. 5.0 5.1 "Diabetic Ketoacidosis: Evaluation and Treatment - American Family Physician".
  6. 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.
  7. "Management of Diabetic Ketoacidosis - American Family Physician".
  8. 8.0 8.1 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.
  9. Beigelman PM (1973). "Potassium in severe diabetic ketoacidosis". Am. J. Med. 54 (4): 419–20. PMID 4633105.
  10. Winter RJ, Harris CJ, Phillips LS, Green OC (1979). "Diabetic ketoacidosis. Induction of hypocalcemia and hypomagnesemia by phosphate therapy". Am. J. Med. 67 (5): 897–900. PMID 116547.
  11. Solomon SM, Kirby DF (1990). "The refeeding syndrome: a review". JPEN J Parenter Enteral Nutr. 14 (1): 90–7. doi:10.1177/014860719001400190. PMID 2109122.

Template:WH Template:WS