Hypoglycemia
Hypoglycemia: Excerpt from Professional Guide to Diseases (Eighth Edition)
Hypoglycemia is an abnormally low glucose level in the bloodstream. It occurs when glucose burns up too rapidly, when the glucose release rate falls behind tissue demands, or when excessive insulin enters the bloodstream. Hypoglycemia is classified as reactive or fasting. Reactive hypoglycemia results from the reaction to the disposition of meals or the administration of excessive insulin. Fasting hypoglycemia causes discomfort during long periods of abstinence from food, for example, in the early morning before breakfast. Although hypoglycemia is a specific endocrine imbalance, its symptoms are often vague and depend on how quickly the patient’s glucose levels drop. If not corrected, severe hypoglycemia may result in coma and irreversible brain damage.
Causes and incidence
Reactive hypoglycemia may take several forms. In a diabetic patient, it may result from administration of too much insulin or, less commonly, too much oral antidiabetic medication. In a mildly diabetic patient (or one in the early stages of diabetes mellitus), reactive hypoglycemia may result from delayed and excessive insulin production after carbohydrate ingestion. Similarly, a nondiabetic patient may suffer reactive hypoglycemia from a sharp increase in insulin output after a meal. Sometimes called postprandial hypoglycemia, this type of reactive hypoglycemia usually disappears when the patient eats something sweet. In some patients, reactive hypoglycemia has no known cause (idiopathic reactive) or may result from gastric dumping syndrome and from impaired glucose tolerance.
Fasting hypoglycemia usually results from an excess of insulin or insulin-like substance or from a decrease in counterregulatory hormones. It can be exogenous, resulting from such external factors as alcohol or drug ingestion, or endogenous, resulting from organic problems.
Endogenous hypoglycemia may result from tumors or liver disease. Insulinomas, small islet cell tumors in the pancreas, secrete excessive amounts of insulin, which inhibit hepatic glucose production. They’re generally benign (in 90% of patients). Extrapancreatic tumors, though uncommon, can also cause hypoglycemia by increasing glucose utilization and inhibiting glucose output. Such tumors occur primarily in the mesenchyma, liver, adrenal cortex, GI system, and lymphatic system. They may be benign or malignant. Among nonendocrine causes of fasting hypoglycemia are severe liver diseases, including hepatitis, cancer, cirrhosis, and liver congestion associated with heart failure. All of these conditions reduce the uptake and release of glycogen from the liver. Some endocrine causes include adrenocortical insufficiency, which contributes to hypoglycemia by reducing the production of cortisol and cortisone needed for gluconeogenesis; and pituitary insufficiency, which reduces corticotropin and growth hormone levels.
Hypoglycemia is at least as common in neonates and children as it is in adults and affects 1 out of 1,000 people. Usually, infants develop hypoglycemia because of an increased number of cells per unit of body weight and because of increased demands on stored liver glycogen to support respirations, thermoregulation, and muscular activity. In full-term neonates, hypoglycemia may occur 24 to 72 hours after birth and is usually transient. In neonates who are premature or small for gestational age, onset of hypoglycemia is much more rapid (it can occur as soon as 6 hours after birth) because of their small, immature livers, which produce much less glycogen. Maternal disorders that can produce hypoglycemia in neonates within 24 hours after birth include diabetes mellitus, toxemia, erythroblastosis, and glycogen storage disease.
Signs and symptoms
Signs and symptoms of reactive hypoglycemia include fatigue, malaise, nervousness, irritability, trembling, tension, headache, hunger, cold sweats, and rapid heart rate. These same clinical effects usually characterize fasting hypoglycemia. In addition, fasting hypoglycemia may also cause central nervous system (CNS) disturbances; for example, blurry or double vision, confusion, motor weakness, hemiplegia, seizures, or coma.
In infants and children, signs and symptoms of hypoglycemia are vague. A neonate’s refusal to feed may be the primary clue to underlying hypoglycemia. Associated CNS effects include tremors, twitching, weak or high-pitched cry, sweating, limpness, seizures, and coma.
Diagnosis
A blood glucose monitor or glucose reagent strips provide quick screening methods for determining the blood glucose level. A reading less than 45 mg/dl indicates the need for a venous blood sample.
Confirming diagnosis Laboratory testing confirms the diagnosis by showing decreased blood glucose levels. The following values indicate hypoglycemia:
❑ Full-term infants:
– less than 30 mg/dl before feeding
– less than 40 mg/dl after feeding
❑ Preterm infants:
– less than 20 mg/dl before feeding
– less than 30 mg/dl after feeding
❑ Children and adults:
– less than 40 mg/dl before meal
– less than 50 mg/dl after meal.
In addition, a 5-hour glucose tolerance test may be administered to provoke reactive hypoglycemia. Following a 12-hour fast, laboratory testing to detect plasma insulin and plasma glucose levels may identify fasting hypoglycemia. (See Diagnosing hypoglycemia.)
Treatment
Effective treatment of reactive hypoglycemia requires dietary modification to help delay glucose absorption and gastric emptying. Usually this includes small, frequent meals; ingestion of complex carbohydrates, fiber, and fat; and avoidance of simple sugars, alcohol, and fruit drinks. The patient may also receive anticholinergic drugs to slow gastric emptying and intestinal motility and to inhibit vagal stimulation of insulin release.
For fasting hypoglycemia, surgery and drug therapy are usually required. In patients with insulinoma, tumor removal is the treatment of choice. Drug therapy may include nondiuretic thiazides such as diazoxide to inhibit insulin secretion; streptozocin; and hormones, such as glucocorticoids and long-acting glycogen.
Therapy for neonates who have hypoglycemia or who are at risk of developing it includes preventive measures. A hypertonic solution of 10% dextrose, calculated at 5 to 10 ml/kg of body weight administered I.V. over 10 minutes and followed by 4 to 8 mg/kg/minute for maintenance, should correct a severe hypoglycemic state in neonates. To reduce the chance of hypoglycemia in high-risk neonates, they should receive feedings (either breast milk or a solution of 5% to 10% glucose and water) as soon after birth as possible.
Special considerations
❑ Watch for and report signs of hypoglycemia, such as poor feeding, in high-risk neonates.
❑ Monitor infusion of hypertonic glucose in the neonate to avoid hyperglycemia, circulatory overload, and cellular dehydration. Terminate glucose solutions gradually to prevent hypoglycemia caused by hyperinsulinemia.
❑ Explain the purpose and procedure for any diagnostic tests. Collect blood samples at the appropriate times, as ordered.
❑ Monitor the effects of drug therapy and watch for the development of any adverse effects.
❑ Teach the patient or his family which foods to include in his diet (complex carbohydrates, fiber, fat) and which foods to avoid (simple sugars, alcohol). Refer the patient and his family for dietary counseling as appropriate.
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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