Hypoglycemia

Hypoglycemia is a clinical syndrome characterized by episodes of low blood glucose (sugar). These episodes can be accompanied by marked autonomic manifestations. There are no specific symptoms of hypoglycemia, but they may include hunger, feelings of anxiety, sweating, nausea, trembling, dizziness, visual disturbances, drowsiness, difficulty speaking, fatigue, palpitations, confusion, and headache. Serum glucose is measured and classified as being low, normal, or elevated. Currently, 70 to 100 mg/dL is considered to be normal. Symptoms of hypoglycemia usually occur when blood glucose levels are less than 50 to 60 mg/dL. Hypoglycemia is a syndrome with diverse etiologies; therefore, treatment should be aimed toward the specific etiology.

Glucose is a form of sugar that the body uses as fuel. Carbohydrates are the main dietary sources of glucose. After a meal, glucose is absorbed into the bloodstream and distributed to the body's cells where it is used for energy. Blood glucose homeostasis involves complex interactions between the central nervous system and the endocrine system. The primary glucoregulatory organs are the liver, pancreas, adrenal glands, and pituitary gland. These organs regulate glucose through the release of hormones including insulin, glucagon, epinephrine, norepinephrine, glucocorticoids, and growth hormone.

Insulin is the primary regulator of glucose metabolism; it acts predominantly on the liver, skeletal muscle, and adipose (fat) tissue. Insulin is produced by the pancreas and acts to suppress endogenous glucose production, stimulates glucose use, and promotes conversion to glycogen for storage. Ultimately, it acts to lower the blood glucose levels. When hypoglycemia occurs, the body acts in defense by decreasing insulin secretion. Glucagon [Page 875]and epinephrine also protect the body from acute hypoglycemia by stimulating the release of glucose from the liver. They do this through two processes: glycogenolysis and gluconeogenesis. The former process is the breakdown of glycogen into glucose for immediate use. The latter is generation of new glucose. Other hormones such as growth hormone and cortisol protect from hypoglycemia over prolonged periods of time.

Evaluating a patient with hypoglycemia can be quite complex. Koch's postulates of hypoglycemia underlines the steps to evaluating patients with hypoglycemia. First, recognize the patient's symptoms could be caused by hypoglycemia. Second, document that the patient's serum glucose concentrations are low while the patient is symptomatic. Third, show that the symptoms can be relieved by the administration of glucose. The goal is to diagnose hypoglycemia and any other clinically relevant associated diseases.

A patient with serum glucose less than 60 should be evaluated for a hypoglycemic disorder. A patient with low blood glucose in the absence of symptoms does not need further evaluation. However, repeated episodes of hypoglycemia necessitate evaluation. In healthy persons, isolated episodes of hypoglycemia may result from accidental or intentional drug ingestion such as alcohol, salicylates, sulfa medications, haloperidol, pentamidine, and quinine. It may also be factitious, caused by accidental or intentional ingestion of hypoglycemic agents such as insulin, or a side effect of certain medications. Insulinomas are rare tumors that produce excessive amounts of the hormone insulin, which leads to hypoglycemia.

Hypoglycemic disorders can be categorized as fasting or postprandial/reactive, or insulin mediated or noninsulin mediated. However, it is more useful to classify the patient according to symptoms and differentiate the sick from not sick. The patient may have hypoglycemia alone or it may be part of a disorder. A detailed evaluation is key with a thorough review of the patient's past medical history and medication history. The differential diagnosis is different for different age groups.

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