Hyperosmolar hyperglycemic state medical therapy: Difference between revisions
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* 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 antibiotics can be administered, if there is suspicion of sepsis only after taking the blood cultures. | ||
=== <u>Criteria for resolution</u> === | |||
* The following criteria must be met for labeling resolution of hyperosmolar hyperglycemic state: | |||
** [[Plasma glucose]] < 300 mg/dl | |||
** [[Plasma osmolality]] < 320 mOsm/kg | |||
** Regain of normal mental status | |||
** Regain of normal hemodynamic status | |||
==References== | ==References== |
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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.
Other electrolytes
- There is insufficient evidence that treatment with phosphate, calcium, and magnesium alters the outcome in the hyperosmolar hyperglycemic state.[10]
- Phosphate therapy may be given to avoid potential cardiac and skeletal muscle weakness and respiratory depression due to hypophosphatemia.[8]
- 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.
- Magnesium should be checked as it is important in preventing renal wasting of potassium.
Vitamins
- Patients with hyperosmolar hyperglycemic state and diabetes are vulnerable to develop refeeding syndrome.[11]
- The administration of thiamine can prevent refeeding syndrome.
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:
- Plasma glucose < 300 mg/dl
- Plasma osmolality < 320 mOsm/kg
- Regain of normal mental status
- Regain of normal hemodynamic status
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".
- ↑ 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.
- ↑ Beigelman PM (1973). "Potassium in severe diabetic ketoacidosis". Am. J. Med. 54 (4): 419–20. PMID 4633105.
- ↑ 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.
- ↑ 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.