eMedicine Specialties > Endocrinology > Diabetes Mellitus

Hyperosmolar Coma: Treatment & Medication

Author: J Michael Gonzalez-Campoy, MD, PhD, FACE, Medical Director and CEO, MN Center for Obesity, Metabolism, and Endocrinology
Contributor Information and Disclosures

Updated: Jun 1, 2009

Treatment

Medical Care

All patients with HNS require hospitalization, and most should be admitted directly to the intensive care unit (ICU). When available, an endocrinologist should direct the care of these patients. The main goals of treatment are to (1) vigorously rehydrate the patient while maintaining electrolyte homeostasis; (2) correct hyperglycemia; (3) treat underlying diseases; and (4) monitor and assist cardiovascular, pulmonary, renal, and CNS function.

  • Intravenous fluid hydration and electrolyte homeostasis
    • If a recent record of the patient's weight is available for comparison, the difference between the admission weight and the preadmission weight may provide a rough estimate of the degree of dehydration.
    • Rapid and aggressive intravascular volume replacement is always indicated as the first line of therapy for patients with HNS.
      • Isotonic sodium chloride solution is the fluid of choice to begin treatment, because sodium and water must be replaced in these severely dehydrated patients.
      • Infuse enough volume to allow for the perfusion of vital organs and the kidneys. Usually, 2 liters of 0.9% isotonic sodium chloride solution may be infused safely over the first hour of treatment. Once renal perfusion is accomplished, as evidenced by adequate urinary output, 0.45% saline may be used for continued hydration.
      • A reasonable goal of treatment is to replace half of the estimated volume deficit in the first 12 hours of therapy. The remainder of the volume deficit may then be replaced over the second 12-hour period.
      • Intravenous fluid treatment allows for renal excretion of sugar and dilutes the extracellular fluid volume, causing a dramatic drop in the plasma glucose concentration.
      • At a serum osmolality of less than 320 mOsm/kg, the intravenous fluids may again be switched to 0.9% isotonic sodium chloride solution. When the blood glucose concentration, checked hourly initially, reaches 300 mg/dL, change the infusion to 5% dextrose in 0.9% isotonic sodium chloride solution again. This helps prevent a precipitous fall of glucose, which may be associated with cerebral edema.
    • In most patients, adequately monitoring volume status entails the use of a urinary catheter. In patients with preexisting or acute cardiac disease or with diseases in which third spacing is a problem, use findings from pulmonary capillary wedge pressure monitoring to guide rehydration therapy. Patients with hypotension may require pressor support in the ICU while rehydration is accomplished.
    • Profound potassium depletion requires careful replacement. With rehydration, the potassium concentration is diluted. With the institution of insulin therapy, potassium is driven into cells. A precipitous drop in the potassium concentration may lead to cardiac arrhythmia. Potassium may be added to the infusion fluid and should be started at a potassium level of 5 mEq/L or less. Hypokalemia at the onset of rehydration requires up to 60 mEq/L to correct the serum potassium concentration. Check the potassium level at least every 4 hours until the blood glucose concentration is stabilized.
    • Phosphate, magnesium, and calcium are not replaced routinely, but a patient symptomatic with tetany requires replacement therapy.
  • Correction of hyperglycemia
    • All patients with HNS require treatment with intravenous insulin; however, immediate treatment with insulin is contraindicated in the initial management of patients with HNS. The osmotic pressure that glucose exerts within the vascular space contributes to the maintenance of circulating volume in these severely dehydrated patients. Institution of insulin therapy drives glucose, potassium, and water into cells. This results in circulatory collapse if fluid has not been replaced first.
    • After the kidneys show evidence of being perfused, initiating insulin therapy is safe. This is accomplished most effectively in the ICU, where cardiovascular and respiratory support is available if needed. Infuse insulin separately from other fluids, and do not interrupt or suspend the infusion of insulin once therapy is started. The following guideline for insulin infusion may be used.
      • Begin a continuous insulin infusion of 0.1 U/kg/h.
      • Monitor blood glucose by bedside testing every hour. If stable for 3 hours, then decrease the frequency of testing to every 2 hours.
      • Set the target blood glucose level at 250-300 mg/dL. This may be adjusted downwards after the patient is stabilized.
      • For blood glucose concentrations of less than 250 mg/dL, decrease the insulin infusion rate by 0.5 U/h.
      • For a blood glucose concentration of 250-300 mg/dL, do not change the insulin infusion rate.
      • For a blood glucose concentration of 301-350 mg/dL, increase the insulin infusion rate by 0.5 U/h.
      • For a blood glucose concentration of 351 mg/dL or greater, increase the insulin infusion rate by 1 U/h.
      • Do not discontinue the insulin drip.
      • If a decrease of more than 100 mg/dL occurs between consecutive readings, wait to increase the insulin infusion rate.
    • When the glucose level has been 200-300 mg/dL for at least 1 day and the patient's level of consciousness has improved, glycemic control may be tightened. The recommended level of glycemia for most patients with type 2 DM is 80-120 mg/dL. This correlates to the recommended hemoglobin A1c value of 7% recommended by the American Diabetes Association. All patients who have experienced HNS will probably require intensive management of their diabetes initially, and this includes insulin. The severe hyperglycemia with which these patients present implies profound beta cell dysfunction. In most instances, sufficient recovery of endogenous insulin production is a reasonable expectation, with safe dismissal of the patient from the hospital on oral therapy. After maintaining adequate glycemic control with insulin for several weeks following HNS, consider switching patients to a regimen with an oral agent.
  • Treatment of underlying diseases
    • When an underlying disease is responsible for HNS, identify and treat it. The resolution of HNS often lags pending resolution of the underlying process.
    • Some authors advocate prophylactic heparin treatment and broad-spectrum antibiotic coverage, but prophylactic heparin treatment and broad-spectrum antibiotic coverage have not been studied adequately to recommend their use.
  • Cardiopulmonary monitoring
    • The mortality rate associated with HNS remains high.
    • The profound electrolyte and metabolic abnormalities present during treatment warrant careful cardiorespiratory monitoring.
    • When patients have compromised gas exchange, endotracheal intubation and mechanical ventilation are indicated.
  • Neurological monitoring
    • This is indicated in all patients with HNS who present with altered MS. Hyperosmolarity may trigger many neurological syndromes.
    • If a patient has seizures, phenytoin is not the agent of choice because it inhibits endogenous insulin secretion and because, in general, it is ineffective in persons with HNS.

Consultations

  • An emergent consultation with an endocrinologist is indicated for all patients with HNS.
  • Consider a consultation with a neurologist for most patients with altered MS. A neurologist should monitor the cases of any patients with underlying neurological disease, such as a cerebrovascular accident or a history of seizures.
  • A pulmonologist or critical care specialist should monitor the cases of patients requiring intubation and mechanical ventilation.
  • Obtain consultations with other specialists as appropriate.

Diet

  • Provide adequate nutritional support for all patients. Most patients with HNS are not able to eat for several days, given the comorbidities with which they present.
  • Patients in the ICU who require prolonged mechanical ventilation, patients with impaired airway defenses, and all patients with prolonged MS changes are candidates for enteral or parenteral nutrition. The use of parenteral nutrition often induces insulin resistance and leads to increased insulin requirements.
  • Once HNS is resolved, provide dietary counseling for all patients. A registered dietitian with expertise in counseling patients with diabetes helps accomplish this most effectively.

Medication

Insulin and intravenous fluid management are cornerstones in the management of HNS. Aggressive rehydration with intravenous fluids, including isotonic sodium chloride solution, is indicated in every patient with HNS (see Medical Care). Frequently monitoring electrolyte concentrations is indicated when patients are treated with intravenous fluids. Volume overload is the only other potential problem when treating patients with intravenous fluids; therefore, regular assessment of the hydration state is indicated.

Antihyperglycemic agents

Reduce serum glucose concentration.


Regular insulin (Humulin, Novolin)

Stimulates proper use of glucose by cells and reduces blood sugar levels.

Adult

Begin 0.1 U/kg/h IV infusion
See Medical Care for management of infusion rate based on treatment goals

Pediatric

Administer as in adults

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 may decrease hypoglycemic effects
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 may increase hypoglycemic effects

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 and may require more insulin to treat hyperkalemia; hypothyroidism may delay turnover, requiring less insulin to treat hyperkalemia; monitor glucose carefully; dose adjustments may be necessary in patients with renal and hepatic dysfunction

More on Hyperosmolar Coma

Overview: Hyperosmolar Coma
Differential Diagnoses & Workup: Hyperosmolar Coma
Treatment & Medication: Hyperosmolar Coma
Follow-up: Hyperosmolar Coma
References
Further Reading

References

  1. Campanella LM, Lartey R, Shih R. Severe hyperglycemic hyperosmolar nonketotic coma in a nondiabetic patient receiving aripiprazole. Ann Emerg Med. Feb 2009;53(2):264-6. [Medline].

  2. Ahuja N, Palanichamy N, Mackin P, et al. Olanzapine-induced hyperglycaemic coma and neuroleptic malignant syndrome: case report and review of literature. J Psychopharmacol. Nov 21 2008;[Medline].

  3. Bartoli E, Sainaghi PP, Bergamasco L, et al. Hyperosmolar coma due to exclusive glucose accumulation: recognition and computations. Nephrology (Carlton). Apr 2009;14(3):338-44. [Medline].

  4. Bartoli E, Bergamasco L, Castello L, et al. Methods for the quantitative assessment of electrolyte disturbances in hyperglycaemia. Nutr Metab Cardiovasc Dis. Jan 2009;19(1):67-74. [Medline].

  5. American Diabetes Association. Hospital admission guidelines for diabetes. Diabetes Care. Jan 2004;27 Suppl 1:S103. [Medline][Full Text].

  6. Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic crises in diabetes. Diabetes Care. Jan 2004;27 Suppl 1:S94-102. [Medline][Full Text].

  7. Fishbein H, Palumbo PJ. Acute Metabolic Complications in Diabetes. In: National Diabetes Data Group. Diabetes in America. 2nd ed. Bethesda, Md: National Institute of Diabetes and Digestive and Kidney Disease; 1995:283-91.

  8. Gonzalez-Campoy JM, Robertson RP. Diabetic ketoacidosis and hyperosmolar nonketotic state: gaining control over extreme hyperglycemic complications. Postgrad Med. Jun 1996;99(6):143-52. [Medline].

  9. Stoner GD. Hyperosmolar hyperglycemic state. Am Fam Physician. May 1 2005;71(9):1723-30. [Medline][Full Text].

Keywords

hyperosmolar coma, diabetic coma, hyperosmolar nonketotic, hyperosmolar nonketotic coma, diabetes, diabetes mellitus, diabetes type 1, diabetes type 2, type 2 diabetes, type 1 diabetes, diabetes 2, diabetes 1, diabeticinsulin, insulin resistance, glucose, blood sugar, hyperglycemia, hyperosmolar nonketotic state

hyperglycemic hyperosmolar nonketotic syndrome, hyperosmolar hyperglycemic syndrome, diabetic hyperosmolar state, hyperosmolar hyperglycemic nonketotic coma, nonketotic hypertonicity, diabetes mellitus type2, diabetes mellitus type 1, type 2 diabetes mellitus, type 1 diabetes mellitus

Contributor Information and Disclosures

Author

J Michael Gonzalez-Campoy, MD, PhD, FACE, Medical Director and CEO, MN Center for Obesity, Metabolism, and Endocrinology
J Michael Gonzalez-Campoy, MD, PhD, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, American Medical Association, and Minnesota Medical Association
Disclosure: Nothing to disclose.

Medical Editor

David S Schade, MD, Chief, Division of Endocrinology and Metabolism, Department of Internal Medicine, Professor, University of New Mexico School of Medicine and Health Sciences Center
David S Schade, MD is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, New Mexico Medical Society, New York Academy of Sciences, and Society for Experimental Biology and Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Don S Schalch, MD, Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics
Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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