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Introduction

Spontaneous hypoglycemia in adults is of two principal types: fasting and postprandial. Symptoms begin at plasma glucose levels in the range of 60 mg/dL and impairment of brain function at approximately 50 mg/dL. Fasting hypoglycemia is often subacute or chronic and usually presents with neuroglycopenia as its principal manifestation; postprandial hypoglycemia is relatively acute and is often heralded by symptoms of neurogenic autonomic discharge (sweating, palpitations, anxiety, tremulousness).

Differential Diagnosis

Fasting hypoglycemia may occur in certain endocrine disorders, such as hypopituitarism, Addison's disease, or myxedema; in disorders related to liver malfunction, such as acute alcoholism or liver failure; and in instances of renal failure, particularly in patients requiring dialysis.

Clinical Findings

These conditions are usually obvious, with hypoglycemia being only a secondary feature. When fasting hypoglycemia is a primary manifestation developing in adults without apparent endocrine disorders or inborn metabolic diseases from childhood, the principal diagnostic possibilities include (1) hyperinsulinism, due to either pancreatic B cell tumors or islet hyperplasia or surreptitious administration of insulin (or sulfonylureas), and (2) hypoglycemia due to non-insulin-producing extrapancreatic tumors.

Postprandial (reactive) hypoglycemia may be classified as early (within 2-3 hours after a meal) or late (3-5 hours after eating). Early, or alimentary, hypoglycemia occurs when there is a rapid discharge of ingested carbohydrate into the small bowel followed by rapid glucose absorption and hyperinsulinism. It may be seen after gastrointestinal surgery and is particularly associated with the dumping syndrome after gastrectomy. In some cases, it is functional and may represent overactivity of the parasympathetic nervous system mediated via the vagus nerve. Rarely, it results from defective counterregulatory responses such as deficiencies of growth hormone, glucagon, cortisol, or autonomic responses.

Alcohol-related hypoglycemia is due to hepatic glycogen depletion combined with alcohol-mediated inhibition of gluconeogenesis. It is most common in malnourished alcohol abusers but can occur in anyone who is unable to ingest food after an acute alcoholic episode followed by gastritis and vomiting.