Hyperosmolar hyperglycemic state medical therapy: Difference between revisions
Jump to navigation
Jump to search
Line 38: | Line 38: | ||
** '''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 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 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. | |||
==References== | ==References== |
Revision as of 14:33, 25 September 2017
Hyperosmolar hyperglycemic state Microchapters |
Differentiating Hyperosmolar hyperglycemic state from other Diseases |
---|
Diagnosis |
Treatment |
Case Studies |
Hyperosmolar hyperglycemic state medical therapy On the Web |
American Roentgen Ray Society Images of Hyperosmolar hyperglycemic state medical therapy |
Hyperosmolar hyperglycemic state medical therapy in the news |
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:
Overview
Medical Therapy
Basic principles
The basic principles of hyperosmolar hyperglycemic state treatment are:
- Rapid restoration of adequate circulation and perfusion with intravenous fluids.
- Correction of plasma osmolality and plasma glucose toward normal.
- Gradual rehydration and restoration of depleted electrolytes (especially sodium and potassium), even if serum levels appear adequate.
- Insulin to lower glucose levels.
- Identifying and treating precipitating events.
- Careful monitoring to detect and treat complications.
The American Diabetes Association (ADA) recommends the following therapy for hyperosmolar hyperglycemic state:[1][2][3][4]
Fluid therapy
- Initial fluid therapy is aimed towards expansion of the intravascular, interstitial, and intracellular volume, all of which are reduced in hyperglycemic crises.
- Fluid restoration also leads to increased renal perfusion and improves renal function.
- The following options may be used for fluid restoration:
- Isotonic saline (0.9% 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 infused at a rate of 250-500 ml/h if serum sodium is low.
- Subsequent choice for fluid replacement depends on hemodynamics, the volume status of the body (signs and symptoms of dehydration), serum electrolyte levels, and urinary output.[5]
- Half normal saline (0.45% NaCl ) infused at 250–500 ml/h is beneficial if the corrected serum sodium is normal or increased.[5][6]
- Successful progress with fluid replacement is judged by, blood pressure monitoring, measurement of fluid input/output, laboratory values, and clinical examination.
- 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 ∼ 300 mg/dl, 5% dextrose should be added to replacement fluids to allow continued insulin administration.
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.
- Insulin therapy helps control hyperglycemia and hyperkalemia in hyperosmolar hyperglycemic state.[7]
- Rate of administration: An initial intravenous dose of regular insulin (0.1 units/kg) followed by infusion of 0.1 units/kg/h insulin.[2]
- 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.[2]
- 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 IV fluids to keep the glucose between 250 - 300 mg/dl until hyperosmolality has resolved or the patient is conscious and alert.[8][4]
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.
References
- ↑ 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.
- ↑ 2.0 2.1 2.2 "Diabetes Care".
- ↑ 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.
- ↑ 4.0 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.
- ↑ 5.0 5.1 "Diabetic Ketoacidosis: Evaluation and Treatment - American Family Physician".
- ↑ 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.
- ↑ "Management of Diabetic Ketoacidosis - American Family Physician".
- ↑ 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.
- ↑ Beigelman PM (1973). "Potassium in severe diabetic ketoacidosis". Am. J. Med. 54 (4): 419–20. PMID 4633105.