eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic
Hyperosmolar Hyperglycemic State: Treatment & Medication
Updated: Oct 28, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Prehospital Care
Standard care for dehydration and altered mental status is appropriate, including airway management, intravenous access, crystalloid, and any medications routinely given to coma patients.
- Airway management is the top priority. In comatose patients in whom airway protection is of concern, endotracheal intubation may be indicated. Cervical spine immobilization is necessary if head or neck injury is a possibility.
- Intravenous access, large bore if possible, is useful, provided that attempts to obtain it do not significantly delay transfer to the nearest ED.
- Bolus of 500 mL isotonic saline is appropriate for nearly all adults who are clinically dehydrated.
- Basic medications given to coma patients in the field may include dextrose (50 mL of D50). This is of benefit to many comatose patients with few adverse effects.
- When possible, fingerstick glucose measurement is obtained prior to dextrose administration. In any case in which fingerstick glucose measurement is unavailable or likely to be delayed, empiric D50 must be administered to comatose patients without delay. Undiagnosed and untreated hypoglycemia, which may present with signs and symptoms very similar to those of HHS, is readily reversible but can be rapidly lethal if not treated promptly.
- Whenever possible, contact the receiving facility while en route to ensure preparation for a comatose, dehydrated, and/or hyperglycemic patient.
- Notify the facility of possible cerebrovascular accident when appropriate.
Emergency Department Care
- Manage the airway as needed, establish intravenous access, initiate vigorous fluid resuscitation, and obtain appropriate laboratory and radiographic studies.
- Fluid deficits in hyperosmolar hyperglycemic state (HHS) are large; the fluid deficit of an adult may be 10 L or more.
- Administer 1-2 L of isotonic saline in the first 2 hours. A higher initial volume may be necessary in patients with severe volume depletion. Slower initial rates may be appropriate in patients with significant cardiac or renal disease. Caution should be taken to not correct hypernatremia too quickly, as this could lead to cerebral edema.
- After the initial bolus, some clinicians recommend changing to half-normal saline, while others continue with isotonic saline. Either fluid likely will replenish intravascular volume and correct hyperosmolarity; a good standard is to switch to half-normal saline once blood pressure and urine output are adequate.
- Once serum glucose drops to 250 mg/dL, the patient must receive dextrose in the intravenous fluid. This may decrease the risk of developing cerebral edema.1
- In pediatric patients with suspected HHS, correcting fluid deficits over a longer time period (48 h) may be appropriate to reduce the risk of developing cerebral edema.4
- Initiate insulin therapy in the ED.
- Although many patients with HHS respond to fluids alone, intravenous insulin in dosages similar to those used in DKA can facilitate correction of hyperglycemia.
- Insulin used without concomitant vigorous fluid replacement increases risk of shock.
- Replete potassium and magnesium as needed. Use of insulin may exacerbate hypokalemia.
- Detection and treatment of an underlying illness is critical. Antibiotics need to be administered early.
- Frequent reevaluation of the patient's clinical and laboratory parameters is necessary. Recheck glucose concentrations every hour. Electrolytes and VBGs should be monitored every 2-4 hours or as clinically indicated.
- All patients diagnosed with HHS require hospitalization, usually to an intensive care unit for close monitoring.
Diagnosis and management guidelines for hyperglycemic crises are available from the American Diabetes Association.7
Consultations
- Generally, no consultation is required to manage HHS in the ED. Virtually all patients need admission to a monitored unit managed by medicine, pediatrics, or the ICU.
- In occasional cases, endocrinology, neurology, or infectious disease consultation may be useful.
- Psychiatry consultation may be useful during the hospitalization.
Medication
Fluids, insulin, and repletion of electrolytes (especially potassium) are the cornerstones of management. Antipyretics, antiemetics, and antibiotics are added, when appropriate, to control fever and vomiting, and treat an underlying infection if suspected.
Insulin
Although many patients with HHS respond to fluids alone, IV insulin in dosages similar to those used in DKA can facilitate correction of hyperglycemia. Insulin used without concomitant vigorous fluid replacement increases risk of shock.
Insulin (Humulin, Humalog, Novolin)
Used to reduce blood glucose levels and decrease ketogenesis. Some authors favor lower bolus and infusion dosages, with rationale that fluids are cornerstone of therapy and that disorder is more one of insulin resistance than of insulin deficiency. Furthermore, lowering serum glucose and serum osmolarity overly rapidly can result in complications.
Adult
0.1 U/kg IV once, followed by 0.1 U/kg/h. Alternatively, 0.14 U/kg/h without a bolus dose can be used.
Pediatric
0.1 U/kg IV once (not to exceed 10 U), followed by 0.1 U/kg/h
Some authors recommend omitting loading dose; alternatively, IV doses of regular insulin can be given q1h, especially in patients who are not critically ill
Medications that may decrease hypoglycemic effects of insulin include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine, isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid, estrogens, ethacrynic acid, calcitonin, oral contraceptives, diazoxide, dobutamine, phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin
Medications that may increase hypoglycemic effects of insulin include calcium, ACE inhibitors, alcohol, tetracyclines, beta-blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAOIs, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone
Documented hypersensitivity; hypoglycemia
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Hyperthyroidism may increase renal clearance of insulin, increasing need for insulin, while hypothyroidism may delay insulin turnover, decreasing need for insulin; monitor glucose level carefully; dose adjustments may be necessary in patients with renal or hepatic dysfunction
Electrolytes
These agents are used to replenish electrolytes depleted because of the presence of high blood glucose level.
Potassium chloride (Klor-Con, K-Dur, Micro-K)
Initial serum potassium in even reference range suggests intracellular potassium depletion. In virtually all cases of HHS, supplemental potassium is necessary, as serum level drops secondary to insulin therapy and correction of metabolic acidosis.
Do not start until initial serum level is ascertained. Administer IV potassium cautiously, with attention to proper dosing and concentration. If patient can tolerate oral medications or has gastric tube in place, KCl can be repleted orally up to 60 mEq per dose, with dosing based upon frequently obtained lab values.
Adult
10-20 mEq IV over 1 h and prn based on frequently obtained lab values; adjust dosage to obtain serum levels of 4.5 mEq/L
In severe hypokalemia, consider infusions of up to 40 mEq over 1 h
Pediatric
0.5-0.75 mEq/kg slow IV infusion over 1-2 h initial dose; not to exceed 3 mEq/kg/d; adjust dosage to reach final serum levels of 4.5 mEq/dL
ACE inhibitors may result in elevated serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; digoxin in patients with hypokalemia may result in digoxin toxicity (caution if discontinuing potassium administration in patients maintained on digoxin)
Hyperkalemia; renal failure; conditions in which potassium is retained; oliguria or azotemia; crush syndrome; severe hemolytic reactions; anuria; adrenocortical insufficiency
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Do not infuse rapidly; high plasma concentrations may cause death due to cardiac depression, arrhythmias, or arrest; plasma levels do not necessarily reflect tissue levels
Always administer IV potassium therapy with an infusion pump system designed to administer precise quantities per minute
Dosages and dilutions must be double checked to ensure they are correct; institute nursing protocols at each institution to ensure no dosing errors occur
Monitor potassium replacement therapy whenever possible by continuous or serial ECG; when concentration >40 mEq/L is infused, local pain and phlebitis may follow; vein sclerosis may occur in peripheral IV sites
Alkalinizing agent
No evidence is found that sodium bicarbonate provides any benefit to patients with HHS. It may be considered if a patient has significant acidosis (pH <7.0), particularly if inotropic agents are required to maintain blood pressure.
Sodium bicarbonate (NaHCO3)
Bicarbonate ion produced on dissociation neutralizes hydrogen ions and raises urinary and blood pH.
Adult
44-88 mEq (1-2 ampules) IV q1-2h prn; if administered for very severe acidosis, almost always administer as IV infusion, not as IV bolus or push IV
Pediatric
1 mEq/kg IV q1-2h prn, as an IV infusion
Urinary alkalinization induced by increased sodium bicarbonate concentrations may cause decreased levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; increases levels of amphetamines, pseudoephedrine, flecainide, anorexiants, mecamylamine, ephedrine, quinidine, and quinine
Alkalosis; hypernatremia; hypocalcemia; severe pulmonary edema
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Sodium bicarbonate should be used to treat only documented metabolic acidosis and hyperkalemia-induced cardiac arrest; can cause alkalosis, decreased plasma potassium, hypocalcemia, and hypernatremia; caution in electrolyte imbalances such as in patients with CHF, cirrhosis, edema, corticosteroid use, or renal failure; avoid extravasation since can cause tissue necrosis
More on Hyperosmolar Hyperglycemic State |
| Overview: Hyperosmolar Hyperglycemic State |
| Differential Diagnoses & Workup: Hyperosmolar Hyperglycemic State |
 Treatment & Medication: Hyperosmolar Hyperglycemic State |
| Follow-up: Hyperosmolar Hyperglycemic State |
| References |
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References
Kitabchi AE, Umpierrez GE, Murphy MB, et al. Management of hyperglycemic crises in patients with diabetes. Diabetes Care. Jan 2001;24(1):131-53. [Medline].
Nugent BW. Hyperosmolar hyperglycemic state. Emerg Med Clin North Am. Aug 2005;23(3):629-48, vii. [Medline].
Trence DL, Hirsch IB. Hyperglycemic crises in diabetes mellitus type 2. Endocrinol Metab Clin North Am. Dec 2001;30(4):817-31. [Medline].
Kershaw MJ, Newton T, Barrett TG, Berry K, Kirk J. Childhood diabetes presenting with hyperosmolar dehydration but without ketoacidosis: a report of three cases. Diabet Med. May 2005;22(5):645-7. [Medline].
Bhowmick SK, Levens KL, Rettig KR. Hyperosmolar hyperglycemic crisis: an acute life-threatening event in children and adolescents with type 2 diabetes mellitus. Endocr Pract. Jan-Feb 2005;11(1):23-9. [Medline].
Middleton P, Kelly AM, Brown J, Robertson M. Agreement between arterial and central venous values for pH, bicarbonate, base excess, and lactate. Emerg Med J. Aug 2006;23(8):622-4. [Medline].
[Guideline] Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI, et al. Hyperglycemic crises in diabetes. Diabetes Care. Jan 2004;27 Suppl 1:S94-102. [Medline]. [Full Text].
Keenan CR, Murin S, White RH. High risk for venous thromboembolism in diabetics with hyperosmolar state: comparison with other acute medical illnesses. J Thromb Haemost. Jun 2007;5(6):1185-90. [Medline].
Rosa EC, Lopes AC, Liberatori Filho AW, et al. Rhabdomyolysis due to hyperosmolarity leading to acute renal failure. Ren Fail. Mar 1997;19(2):295-301. [Medline].
Kitabchi AE, Murphy MB, Spencer J, Matteri R, Karas J. Is a priming dose of insulin necessary in a low-dose insulin protocol for the treatment of diabetic ketoacidosis?. Diabetes Care. Nov 2008;31(11):2081-5. [Medline].
Kitabchi AE, Nyenwe EA. Hyperglycemic crises in diabetes mellitus: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Endocrinol Metab Clin North Am. Dec 2006;35(4):725-51, viii. [Medline].
Kitabchi AE, Umpierrez GE, Murphy MB, Kreisberg RA. Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association. Diabetes Care. Dec 2006;29(12):2739-48. [Medline].
MacIsaac RJ, Lee LY, McNeil KJ, et al. Influence of age on the presentation and outcome of acidotic and hyperosmolar diabetic emergencies. Intern Med J. Aug 2002;32(8):379-85. [Medline].
Singhi SC. Hyperglycemic hyperosmolar state and type 2 diabetes mellitus: yet another danger of childhood obesity. Pediatr Crit Care Med. Jan 2005;6(1):86-7. [Medline].
Further Reading
Keywords
hyperglycemic hyperosmolar nonketotic coma, hyperosmolar hyperglycemic state, hyperglycemic, diabetic coma, hyperosmolar coma, diabetic nonketotic coma, hyperosmolar nonketotic state, diabetic hyperosmolarity, diabetes, hyperglycemia, diabetic ketoacidosis, DKA, adult-onset diabetes
