eMedicine Specialties > Endocrinology > Diabetes Mellitus

Hypoglycemia

Vasudevan A Raghavan, MBBS, MD, MRCP, Assistant Professor, Department of Internal Medicine, Divisions of Endocrinology, Diabetes and Metabolism and Cardiovascular Sciences, Ohio State University; Co-director of The Ross Heart Hospital Comprehensive Lipid Management Clinic, Ohio State University Medical Center
Vellore A R Srinivasan, MSc, PhD, Associate Professor, Department of Biochemistry, Sri Balaji Vidyapeeth University, Mahatma Gandhi Medical College and Research Institute campus, Puducherry, India; Kenneth J Snow, MD, Associate Chief, Adult Diabetes, Joslin Clinic

Updated: Aug 18, 2009

Introduction

Background

Hypoglycemia is a syndrome characterized by a reduction in plasma glucose concentration to a level that may induce symptoms of low blood sugar. Hypoglycemia typically arises from abnormalities in the mechanisms involved in glucose homeostasis. To diagnose hypoglycemia, the Whipple triad characteristically is present. This triad includes the documentation of low blood sugar, presence of symptoms, and reversal of these symptoms when the blood sugar level is restored to normal. (See image below and Image 1.)

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

Pathophysiology

Hypoglycemic symptoms are related to the brain and the sympathetic nervous system. Decreased levels of glucose lead to deficient cerebral glucose availability (ie, neuroglycopenia) that can manifest as confusion, difficulty with concentration, irritability, hallucinations, focal impairments (eg, hemiplegia), and eventually, coma and death. Stimulation of the sympatho-adrenal nervous system leads to sweating, palpitations, tremulousness, anxiety, and hunger.

The adrenergic symptoms often precede the neuroglycopenic symptoms and, thus, provide an early warning system for the patient. Studies have shown that the primary stimulus for the release of catecholamines is the absolute level of plasma glucose. The rate of decrease of glucose is less important. Previous blood sugar levels can influence an individual's response to a particular level of blood sugar. However, one must appreciate that a patient with chronic hypoglycemia can have almost no symptoms.

Frequency

United States

• The incidence of hypoglycemia in a population is difficult to ascertain. Patients and physicians frequently attribute symptoms (eg, anxiety, irritability, hunger) to hypoglycemia without documenting the presence of low blood sugar. The true prevalence of hypoglycemia, with blood sugar levels below 50 mg/dL, generally occurs in 5-10% of people presenting with symptoms suggestive of hypoglycemia.
  
  
  • Hypoglycemia is a known complication of several medications, and the incidence is difficult to determine with any certainty.
  • Hypoglycemia is a known complication of many therapies for diabetes; therefore, the incidence of hypoglycemia in a population of people with diabetes is very different from that in a population of people without diabetes.^1,2
  • Insulin-producing tumors are a rare but important treatable cause of hypoglycemia, with an annual incidence of 1-2 cases per million persons per year.

Mortality/Morbidity

Reactive hypoglycemia often is treated successfully with dietary changes and is associated with minimal morbidity. Mortality is not observed. Hypoglycemia occurring as a complication of therapy for diabetes is common. Mild hypoglycemia occurs in more than half of all patients with diabetes who are in therapy.

Race

No known racial predilection exists.

Sex

Reactive hypoglycemia is reported most frequently by women. Other causes of hypoglycemia are not associated with a sex predilection.

Age

Reactive hypoglycemia typically is observed in women aged 25-35 years. The average age of a patient diagnosed with an insulinoma is the early 40s, but cases have been reported in patients ranging from birth to age 80 years.³

Clinical

History

• Symptoms of hypoglycemia may be categorized as neurogenic (adrenergic) or neuroglycopenic.
  • Symptoms due to sympatho-adrenal activation include sweating, shakiness, tachycardia, anxiety, and a sensation of hunger.
  • Neuroglycopenic symptoms include weakness, tiredness, or dizziness; inappropriate behavior (sometimes mistaken for inebriation), difficulty with concentration; confusion; blurred vision; and, in extreme cases, coma and death.
  • The timing of onset of these symptoms relative to the time of meal ingestion is crucial in the evaluation of a patient with hypoglycemia. Fasting hypoglycemia typically occurs in the morning before eating or during the day, particularly in the afternoon if meals are missed or delayed. Postprandial hyperglycemia typically occurs 2-4 hours after eating food, especially when meals contain high levels of simple carbohydrates. Postprandial symptoms are typically due to reactive causes, but some patients with insulinoma also may present with postprandial symptoms. About 4-6 hours after food ingestion, plasma glucose concentrations are 80-90 mg/dL, and rates of glucose utilization and production are approximately 2 mg/kg/min. Glucose production is primarily (70-80%) from hepatic glycogenolysis, with a lesser contribution (20-25%) from hepatic gluconeogenesis.
• Reactive hypoglycemia seldom causes glucose levels to drop low enough to induce severe neuroglycopenic symptoms; therefore, a history of true loss of consciousness is highly suggestive of an etiology other than reactive hypoglycemia.
• Reactive hypoglycemia has been suggested to be more common in people who are insulin-resistant, and it may be a frequent precursor to type-2 diabetes. Therefore, patients who have a family history of type-2 diabetes or insulin-resistance syndrome (ie, hypertension, hyperlipidemia, obesity) may be at higher risk for developing hypoglycemia.
• In a study of maternal hypoglycemia, Pugh et al investigated risk factors for and results of hypoglycemia in pregnancy.⁴ Reporting on 870 obstetric patients, 436 of whom were identified as having hypoglycemia following a glucose challenge test (GCT) and the rest of whom were not hypoglycemic following a GCT, the authors found that hypoglycemia occurred more frequently in women below age 25 years and in women who had a preexisting medical condition. Hypoglycemia was less frequent in women whose prepregnancy body mass index was ³ 30. The investigators also found that patients with hypoglycemia were at greater risk of preeclampsia/eclampsia.

Physical

Physical examination usually does not yield specific findings.

Causes

• Fasting hypoglycemia
  • Nesidioblastosis is characterized by a diffuse budding of insulin-secreting cells from pancreatic duct epithelium and pancreatic microadenomas of such cells; it is a rare cause of fasting hypoglycemia in infants and an extremely rare cause in adults.
  • Causes of fasting hypoglycemia usually diagnosed in infancy or childhood include inherited liver enzyme deficiencies that restrict hepatic glucose release (deficiencies of glucose-6-phosphatase, fructose-1,6-diphosphatase, phosphorylase, pyruvate carboxylase, phosphoenolpyruvate carboxykinase, or glycogen synthetase). Inherited defects in fatty acid oxidation, including that resulting from systemic carnitine deficiency and inherited defects in ketogenesis (3-hydroxy-3-methylglutaryl-CoA lyase deficiency) cause fasting hypoglycemia by restricting the extent to which nonneural tissues can derive their energy from plasma FFA and ketones during fasting or exercise. This results in an abnormally high rate of glucose uptake by nonneural tissues under these conditions.
  • Drugs - Ethanol, haloperidol, pentamidine, quinine, salicylates, and sulfonamides
• Exogenous insulin
  • Insulin-producing tumors of pancreas: Islet cell adenoma or carcinoma (insulinoma) is an uncommon and usually curable cause of fasting hypoglycemia and is most often diagnosed in adults. It may occur as an isolated abnormality or as a component of the type I multiple endocrine neoplasia (MEN) syndrome. Carcinomas account for only 10% of insulin-secreting islet cell tumors. Hypoglycemia in patients with islet cell adenomas results from uncontrolled insulin secretion, which may be clinically determined during fasting and exercise. Approximately 60% of patients with insulinoma are female. Insulinomas are uncommon in persons younger than 20 years and are rare in those younger than 5 years. The median age at diagnosis is about 50 years, except in patients with MEN syndrome, in which it is in the mid 20s. Ten percent of patients with insulinoma are older than 70 years.
  • Non–beta-cell tumors: Hypoglycemia may also be caused by large non–insulin-secreting tumors, most commonly retroperitoneal or mediastinal malignant mesenchymal tumors. The tumor secretes abnormal insulinlike growth factor (large IGF-II), which does not bind to its plasma binding proteins. This increase in free IGF-II exerts hypoglycemia through the IGF-I or the insulin receptors. The hypoglycemia is corrected when the tumor is completely or partially removed and usually recurs when the tumor regrows.
• Autoimmune hypoglycemia - Insulin antibodies and insulin receptor antibodies
• Surreptitious sulfonylurea use/abuse
• Hormonal deficiencies - Hypoadrenalism (Cortisol), hypopituitarism (growth hormone) (in children), glucagons deficiency (rare), and epinephrine (very rare)
• Critical illnesses - Cardiac, hepatic, and renal diseases; sepsis with multiorgan failure
• Combination of one or more of the above, for example, chronic renal failure and sulphonylurea ingestion
• Reactive hypoglycemia
  • Idiopathic
  • Alimentary hypoglycemia is another form of reactive hypoglycemia that occurs in patients who have had prior upper GI surgical procedures (gastrectomy, gastrojejunostomy, vagotomy, pyloroplasty) and allows rapid glucose entry and absorption in the intestine, provoking excessive insulin response to a meal. This may occur within 1-3 hours after a meal. Very rare cases of idiopathic alimentary hypoglycemia occur in patients who have not had GI operations.
  • Congenital enzyme deficiencies - Hereditary fructose intolerance, galactosemia, and leucine sensitivity of childhood: In hereditary fructose intolerance and galactosemia, an inherited deficiency of a hepatic enzyme causes acute inhibition of hepatic glucose output when fructose or galactose is ingested. Leucine provokes an exaggerated insulin secretory response to a meal and reactive hypoglycemia in patients with leucine sensitivity of childhood.

Differential Diagnoses

Other Problems to Be Considered

Hepatic failure
Simulating hypoglycemia
Transient ischemic attacks
Cardiac dysrhythmia
Pheochromocytoma
Substance abuse, eg, cocaine

Workup

Laboratory Studies

• During hypoglycemic episodes, patients should test their glucose at home to document hypoglycemia that is occurring with the episodes. Take into consideration that meter readings may not be accurate enough to establish the diagnosis.
• Test glucose and insulin levels simultaneously to document low glucose levels occurring in conjunction with inappropriate insulin levels.
• Administer an oral glucose tolerance test if reactive hypoglycemia is suspected. An oral glucose tolerance test provides little benefit for the evaluation of fasting hypoglycemia. Perform the test for 5 hours while simultaneously testing glucose and insulin levels. To be meaningful, low blood sugar during the test should be accompanied by typical symptoms. Response to a mixed meal may be more representative.
• A supervised fast is the most reliable diagnostic test for the evaluation of fasting hypoglycemia. Continue the fast for as long as 72 hours or until symptoms develop in the presence of hypoglycemia (blood sugar <45 mg/dL for women, <55 mg/dL for men). Obtain simultaneous insulin levels every 6 hours, when glucose is low and when symptoms develop. Glucose and/or glucagon must be administered after blood sample withdrawal to abort hypoglycemic symptoms.
• Obtain C-peptide levels any time an elevated insulin level is obtained. Endogenous hyperinsulinemia from insulinoma is associated with elevated C-peptide concentrations with concurrent hypoglycemia. Exogenous hyperinsulinemia from injected insulin results in low concentrations of C-peptide, both because of the effect of the associated hypoglycemia and because of the direct suppressive effect of insulin on the pancreatic beta cell.
• Other causes of hypoglycemia should be properly investigated. For example, a morning cortisol level determination and/or adrenocorticotropic hormone (ACTH) stimulation testing should be performed if adrenal insufficiency is suspected. 
• Remember that whole blood glucose values may be spuriously low in polycythemia rubra vera because of the unequal distribution of glucose between erythrocytes and plasma, excessive glycolysis by erythrocytes, or both. Low blood glucose values in leukemia are due to excessive glycolysis by leukocytes and in hemolytic crisis from excessive glycolysis by nucleated erythrocytes. In the polycythemic patient or in serum of the leukemic or hemolytic patient, prompt measurement of glucose in plasma to which an antiglycolytic agent has been added should provide accurate results.

Imaging Studies

• For the evaluation of insulinomas, CT scan and ultrasound often are not helpful because most of these tumors are small. MRI may be better.
• Selective arteriography often is helpful.
• Selective percutaneous transhepatic venous sampling often is helpful for localizing an insulinoma to the head, body, or tail of the pancreas.
• Octreotide scanning localizes insulinomas in approximately half the cases.
• Intraoperative ultrasound can be used as a diagnostic aid.
• Retroperitoneal tumors that are producing insulin-like growth factor (IGF) usually are imaged easily using a CT scan.

Other Tests

• Proinsulin normally represents less than 20% of total immunoreactive insulin. In patients with islet-cell tumors, proinsulin may contribute as much as 70% of insulin immunoreactivity.
• Provocative tests involving the administration of arginine, leucine, calcium, glucagon, or tolbutamide generally are of limited value because their sensitivity or specificity is inadequate.⁵
• Diagnostic algorithm: A systematic approach is often required to establish the true cause of hypoglycemia, using an algorithmic approach. One such algorithm is given below (see image below and Image 1).

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

Treatment

Medical Care

If dietary therapy is inadequate, medical care for patients with fasting hypoglycemia may include intravenous (IV) glucose infusion. However, IV octreotide is effective for suppressing endogenous insulin secretion. Reactive hypoglycemia does not require medical care.

Surgical Care

Definitive treatment for fasting hypoglycemia caused by a tumor is surgical resection. The success rate is good for benign islet-cell adenomas, and the success rate for malignant islet-cell tumors can be as high as 50%.

Diet

• Dietary therapy may be effective for improving symptoms in patients with fasting hypoglycemia. Frequent meals/snacks are preferred, especially at night, with complex carbohydrates.
• For patients with reactive hypoglycemia, initiate a carbohydrate restriction. Patients should avoid simple sugars, increase the frequency of their meals, and reduce the size of their meals. Patients may require 6 small meals and 2-3 snacks per day.

Activity

Because exercise burns carbohydrates and increases sensitivity to insulin, patients with fasting hypoglycemia should avoid significant activity. On the other hand, patients with reactive hypoglycemia often find that their symptoms improve after embarking on a routine exercise program.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Inhibitors of insulin secretion

These drugs increase glucose levels by reducing peripheral glucose metabolism.

Diazoxide (Hyperstat)

Can help improve symptoms of hypoglycemia caused by increased insulin secretion in patients awaiting surgery or those with nonresectable disease. Increases blood glucose by inhibiting pancreatic insulin release and, possibly, through an extrapancreatic effect. With normal renal function, hyperglycemic effects start within 1 h and usually last a maximum of 8 h.

Dosing

Adult

IV: 100-200 mg bid/tid; refractory hypoglycemia may require higher dosages
PO: Usually 300-400 mg/d; may be as high as 800 mg

Pediatric

Infants and newborns: 8-15 mg/kg/d IV q8-12h
Children: Administer as in adults

Interactions

Highly bound to serum proteins and displaces other substances that also are highly bound (eg, Coumadin), resulting in higher levels; may decrease serum hydantoins, possibly resulting in decreased anticonvulsant effects; thiazide diuretics may potentiate hyperuricemic and antihypertensive effects

Contraindications

Documented hypersensitivity; aortic coarctation, aortic aneurysm, arteriovenous shunts, pheochromocytoma

Precautions

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

Causes salt and water retention; caution in congestive heart failure or decreased cardiac output; causes relaxation of smooth muscle in peripheral arterioles, leading to hypotension; do not administer within 6 h of administering beta-blockers, hydralazine, methyldopa, minoxidil, nitrites, prazosin, reserpine, and papaverinelike compounds; patients with diabetes mellitus may require treatment for hyperglycemia; when given prior to delivery, may produce fetal or neonatal hyperbilirubinemia, thrombocytopenia, altered carbohydrate metabolism, and other adverse reactions

Octreotide (Sandostatin)

Acts primarily on somatostatin receptor subtypes II and V. Inhibits GH secretion and has a multitude of other endocrine and nonendocrine effects, including inhibition of glucagon, VIP peptides, and GI peptides.

Dosing

Adult

Initial: 50 mcg SC tid; may increase dose to 500 mcg SC tid; doses of 300-600 mcg/d or higher seldom result in additional biochemical benefit

Pediatric

1-10 mcg/kg SC tid

Interactions

May reduce effects of cyclosporine; patients on insulin, oral hypoglycemics, beta-blockers, and calcium channel blockers may need dosage adjustments

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Biliary tract abnormalities (eg, stones, sludge, biliary duct dilatation) can occur; adverse effects primarily related to altered GI motility include nausea, abdominal pain, diarrhea, increased incidence of gallstones, and biliary sludge; because of alterations in counter-regulatory hormones (eg, insulin, glucagon, GH), hypoglycemia or hyperglycemia may occur; bradycardia, cardiac conduction abnormalities, and arrhythmias have been reported; because of inhibition of TSH secretion, hypothyroidism may occur; caution in renal impairment; cholelithiasis may occur

Antineoplastic agents

These agents inhibit cell growth and proliferation.

Streptozocin (Zanosar)

Has a high affinity for neuroendocrine cells, inhibits cell proliferation, and is cytolytic. Interferes with normal function of DNA by alkylation and protein modification.

Dosing

Adult

500 mg/m² IV for 5 d q6wk

Pediatric

Administer as in adults

Interactions

Aminoglycosides, loop diuretics, and doxorubicin may increase nephrotoxicity; phenytoin may decrease effects

Contraindications

Documented hypersensitivity

Precautions

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

Severe nausea and vomiting are common; liver dysfunction can occur; renal toxicity is dose-related and cumulative; closely monitor renal, hepatic, and hematologic function

Follow-up

Further Outpatient Care

• If the patient has fasting hypoglycemia and the cause is treatable, long-term follow-up usually is not needed. If the cause cannot be treated definitively (eg, inoperable pancreatic insulinoma), diazoxide can be used to elevate blood glucose levels and chemotherapy that specifically targets the beta cell (ie, using cytotoxic agents such as streptozotocin) should be considered.
• If the patient has reactive hypoglycemia, periodic outpatient monitoring is warranted to assess the continued presence of symptoms.

Complications

• Untreated fasting hypoglycemia can lead to severe neuroglycopenia and, possibly, death.
• Untreated reactive hypoglycemia may cause significant discomfort to the patient, but long-term sequelae are not likely.

Prognosis

• Prognosis depends on the cause of the hypoglycemia. If the cause of fasting hypoglycemia is identified and curable, prognosis is excellent. If the problem is not curable, such as an inoperable malignant tumor, long-term prognosis is poor. However, note that these tumors may progress rather slowly.
• If the patient has reactive hypoglycemia, symptoms often spontaneously improve over time, and long-term prognosis is very good.

Patient Education

For excellent patient education resources, visit eMedicine's Diabetes Center. Also, see eMedicine's patient education article, Hypoglycemia (Low Blood Sugar).

Miscellaneous

Medicolegal Pitfalls

• Failure to identify the presence of fasting hypoglycemia rather than postprandial hypoglycemia
• Failure to evaluate fasting hypoglycemia with a prolonged fast (ie, as long as 72 h)
• Failure to document true hypoglycemia as a cause of symptoms

Multimedia

Media file 1: Diagnostic algorithm. A systematic approach is often required to establish the true cause of hypoglycemia, using an algorithmic approach.

References

1. Hill NR, Thompson B, Bruce J, et al. Glycaemic risk assessment in children and young people with Type 1 diabetes mellitus. Diabet Med. Jul 2009;26(7):740-3. [Medline].

2. Turnbull FM, Abraira C, Anderson RJ, et al. Intensive glucose control and macrovascular outcomes in type 2 diabetes. Diabetologia. Aug 5 2009;[Medline].

3. Garza H. Minimizing the risk of hypoglycemia in older adults: a focus on long-term care. Consult Pharm. Jun 2009;24 Suppl B:18-24. [Medline].

4. Pugh SK, Doherty DA, Magann EF, et al. Does hypoglycemia following a glucose challenge test identify a high risk pregnancy?. Reprod Health. Jul 14 2009;6:10. [Medline].

5. 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].

6. Cryer PE, Polonsky KS. Glucose homeostasis and hypoglycemia. In: Wilson JD, Foster DW, Kronenberg HM, Larsen PR, eds. Williams Textbook of Endocrinology. 9^th ed. Philadelphia, Pa: WB Saunders; 1998:939-71.

7. Field JB. Hypoglycemia. Definition, clinical presentations, classification, and laboratory tests. Endocrinol Metab Clin North Am. Mar 1989;18(1):27-43. [Medline].

8. Ibarra JD Jr. Hypoglycemia. Postgrad Med. Feb 1972;51(2):88-93. [Medline].

9. Koch B. Selected topics of hypoglycemia care. Can Fam Physician. Apr 2006;52:466-71. [Medline].

10. Service FJ. Classification of hypoglycemic disorders. Endocrinol Metab Clin North Am. Sep 1999;28(3):501-17, vi. [Medline].

11. Service FJ. Diagnostic approach to adults with hypoglycemic disorders. Endocrinol Metab Clin North Am. Sep 1999;28(3):519-32, vi. [Medline].

12. Service FJ. Hypoglycemia. Endocrinol Metab Clin North Am. Dec 1997;26(4):937-55. [Medline].

13. Service FJ. Hypoglycemic disorders. N Engl J Med. Apr 27 1995;332(17):1144-52. [Medline].

14. Shamoon H. Hypoglycemia. In: Endocrinology and Metabolism. 3^rd ed. New York, NY: McGraw-Hill; 1995:1251-69.

Keywords

hypoglycemia, blood sugar, blood glucose, low blood sugar, high blood sugar, type 2 diabetes, diabetes mellitus, plasma glucose disorder, glucose disorder, low blood sugar, Whipple triad, decreased glucose, insulin-producing tumor, neuroglycopenic symptoms, reactive hypoglycemia, fasting hypoglycemia, hypoglycemic disorder, hypoglycemic

Contributor Information and Disclosures

Author

Vasudevan A Raghavan, MBBS, MD, MRCP, Assistant Professor, Department of Internal Medicine, Divisions of Endocrinology, Diabetes and Metabolism and Cardiovascular Sciences, Ohio State University; Co-director of The Ross Heart Hospital Comprehensive Lipid Management Clinic, Ohio State University Medical Center
Vasudevan A Raghavan, MBBS, MD, MRCP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, Endocrine Society, National Lipid Association, and Royal College of Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Vellore A R Srinivasan, MSc, PhD, Associate Professor, Department of Biochemistry, Sri Balaji Vidyapeeth University, Mahatma Gandhi Medical College and Research Institute campus, Puducherry, 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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Yoram Shenker, MD, Chief of Endocrinology Section, Veterans Affairs Medical Center of Madison; Interim Chief, Associate Professor, Department of Internal Medicine, Section of Endocrinology, Diabetes and Metabolism, University of Wisconsin at Madison
Yoram Shenker, MD is a member of the following medical societies: American Heart Association, 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.

Related eMedicine topics:
Diabetes Mellitus, Type 1 [Endocrinology]
Diabetes Mellitus, Type 1 [Pediatrics: General Medicine]
Diabetes Mellitus, Type 1 - A Review
Diabetes Mellitus, Type 2 [Endocrinology]
Diabetes Mellitus, Type 2 [Pediatrics: General Medicine]
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Disorders of Carbohydrate Metabolism
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Insulinoma
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Clinical guidelines:
Neonatal hypoglycemia: initial and follow up management.
Barbara Bush Children's Hospital at Maine Medical Center - Private Nonprofit Organization.  2004 Apr.  4 pages.  NGC:004293

Guidelines for glucose monitoring and treatment of hypoglycemia in breastfed neonates.
Academy of Breastfeeding Medicine - Professional Association.  1999 (revised 2006).  7 pages.  NGC:005865

Standards of medical care in diabetes. V. Diabetes care.
American Diabetes Association - Professional Association.  1998 (revised 2008 Jan).  8 pages.  NGC:006281

Clinical trials:
Insulin Analogues and Severe Hypoglycaemia

Mechanisms Responsible for Hypoglycemia Associated Autonomic Failure (HAAF)

Sulfonylurea Effects on Glucagon Regulation During Hypoglycemia in Type 1 DM

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