Hyperosmolar hyperglycemic state medical therapy
|
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: 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:
- 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
| HHS | |||||||||||||||||||||||||||||||||||||||||||
| Fluids | Insulin | Potassium | |||||||||||||||||||||||||||||||||||||||||
| Hydration status | |||||||||||||||||||||||||||||||||||||||||||
Template:Summary= HHS protocol according to American diabetes association
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.