Hypoglycemia Medication

  • Author: Osama Hamdy, MD, PhD, FACE; Chief Editor: George T Griffing, MD   more...
 
Updated: Feb 3, 2012
 

Medication Summary

The mainstay of therapy for hypoglycemia is glucose. Other medications may be administered based on the underlying cause or the accompanying symptoms; however, these medications are not addressed in this article.

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Glucose Supplement

Class Summary

Glucose supplements are used to raise the patient's serum glucose.

Dextrose (Glucose-D)

 

Dextrose is a monosaccharide absorbed from intestine and distributed, stored, and used by tissues. Parenterally injected, dextrose is used in patients unable to obtain adequate oral (PO) intake. Direct oral absorption results in rapid increase of blood glucose concentrations.

Dextrose is effective in small doses, and there is no evidence that it may cause toxicity. Concentrated dextrose infusions provide higher amounts of glucose and increased caloric intake with minimum fluid volume. The long-term management of hypoglycemia is dictated by its cause (eg, insulinoma).

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Glucose-Elevating Agents

Class Summary

Glucose-elevating agents can act in the pancreas or the peripheral tissues to increase blood glucose levels.

Glucagon

 

Pancreatic alpha cells of islets of Langerhans produce glucagon, a polypeptide hormone. This agent exerts effects opposite of insulin on blood glucose and elevates blood glucose levels by inhibiting glycogen synthesis and enhancing formation of glucose from noncarbohydrate sources, such as proteins and fats (gluconeogenesis).

Glucagon also increases hydrolysis of glycogen to glucose (glycogenolysis) in the liver. This agent accelerates hepatic glycogenolysis and lipolysis in adipose tissue by stimulating cyclic AMP (cAMP) synthesis via adenylyl cyclase and enhancing phosphorylase kinase activity.

Glucagon may be useful when intravenous (IV) access is problematic. This agent may be administered as part of emergency medical services (EMS) protocol in patients with altered mental status and no IV access.

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Inhibitors of insulin secretion

Class Summary

Agents that inhibit insulin secretion increase glucose levels by reducing peripheral glucose metabolism.

Diazoxide (Proglycem)

 

Diazoxide is a direct inhibitor of insulin secretion. This agent increases hepatic glucose output by inhibiting pancreatic insulin release and, possibly, through an extrapancreatic effect, as well as decreases cellular glucose uptake. Although, diazoxide has a very limited role in treating hypoglycemia, it can help improve symptoms of hypoglycemia caused by increased insulin secretion in patients awaiting surgery or those with nonresectable disease and may be indicated in some cases of insulinoma or overdosage with oral (PO) hypoglycemic agents.

Hyperglycemic effect starts within 1 hour, lasting a maximum of 8 hours if the patient's renal function normal. Patients with refractory hypoglycemia may require high dosages.

Octreotide (Sandostatin)

 

This agent Inhibits insulin secretion. Octreotide acts primarily on somatostatin receptor subtypes II and V. It also inhibits growth hormone secretion and has a multitude of other endocrine and nonendocrine effects, including inhibition of glucagon, vasoactive intestinal peptides (VIP), and gastrointestinal peptides.

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Antineoplastic agents

Class Summary

Antineoplastic agents inhibit cell growth and proliferation.

Streptozocin (Zanosar)

 

Streptozocin has a high affinity for neuroendocrine cells, inhibits cell proliferation, and is cytolytic. This agent interferes with normal DNA function by alkylation and protein modification.

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Contributor Information and Disclosures
Author

Osama Hamdy, MD, PhD, FACE  Medical Director, Obesity Clinical Program, Director of Inpatient Diabetes Management, Joslin Diabetes Center; Assistant Professor of Medicine, Harvard Medical School

Osama Hamdy, MD, PhD, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists and American Diabetes Association

Disclosure: Merck Inc Honoraria Speaking and teaching

Coauthor(s)

Vellore A R Srinivasan, MSc, PhD  Professor, Department of Biochemistry, Mahatma Gandhi Memorial Medical College and Research Institute, Sri Balaji Vidyapeeth University, India

Disclosure: Sri Balaji Vidyapeeth University, Mahatma Gandhi Medical College and Research Institute campus , Pondicherry ( Puducherry ) , India . P.C. 607 402 Salary Employment

Kenneth J Snow, MD  Associate Chief, Adult Diabetes, Joslin Clinic

Kenneth J Snow, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American Diabetes Association, and Endocrine Society

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.

Additional Contributors

Vasudevan A Raghavan, MBBS, MD, MRCP(UK) Director, Cardiometabolic and Lipid (CAMEL) Clinic Services, Division of Endocrinology, Scott and White Hospital, Texas A&M Health Science Center College of Medicine

Vasudevan A Raghavan, MBBS, MD, MRCP(UK) is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Heart Association, Endocrine Society, National Lipid Association, and Royal College of Physicians

Disclosure: Nothing to disclose.

David S Schade, MD Chief, Division of Endocrinology and Metabolism, Professor, Department of Internal Medicine, 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.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
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  11. Lin YY, Hsu CW, Sheu WH, Chu SJ, Wu CP, Tsai SH. Use of therapeutic responses to glucose replacement to predict glucose patterns in diabetic patients presenting with severe hypoglycaemia. Int J Clin Pract. Aug 2009;63(8):1161-6. [Medline].

  12. Egi M, Bellomo R, Stachowski E, et al. Hypoglycemia and outcome in critically ill patients. Mayo Clin Proc. Mar 2010;85(3):217-24. [Medline].

  13. Goh HK, Chew DE, Miranda IG, Tan L, Lim GH. 24-Hour observational ward management of diabetic patients presenting with hypoglycaemia: a prospective observational study. Emerg Med J. Oct 2009;26(10):719-23. [Medline].

  14. Sinert R, Su M, Secko M, Zehtabchi S. The utility of routine laboratory testing in hypoglycaemic emergency department patients. Emerg Med J. Jan 2009;26(1):28-31. [Medline].

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Diagnostic algorithm. A systematic approach is often required to establish the true cause of hypoglycemia, using an algorithmic approach.
 
 
 
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