Vitamin A deficiency
Vitamin A deficiency: Excerpt from Professional Guide to Diseases (Eighth Edition)
A fat-soluble vitamin absorbed in the GI tract, vitamin A maintains epithelial tissue and retinal function. Consequently, deficiency of this vitamin may result in night blindness, decreased color adjustment, keratinization of epithelial tissue, and poor bone growth. Healthy adults have adequate vitamin A reserves to last up to a year; children often don’t.
Causes and incidence
Vitamin A deficiency usually results from inadequate intake of foods high in vitamin A (liver, kidney, butter, milk, cream, cheese, and fortified margarine) or carotene, a precursor of vitamin A found in dark green leafy vegetables and yellow or orange fruits and vegetables. (Six mg of beta-carotene is equal to 1 mg of vitamin A.) The recommended daily allowance for vitamin A is 1 mg for adult males and 0.8 mg for adult females.
Less common causes include:
❑ malabsorption due to celiac disease, sprue, cirrhosis, obstructive jaundice, cystic fibrosis, giardiasis, or habitual use of mineral oil as a laxative
❑ massive urinary excretion caused by cancer, tuberculosis, pneumonia, nephritis, or urinary tract infection
❑ decreased storage and transport of vitamin A due to hepatic disease.
Each year, more than 80,000 people worldwide — mostly children in underdeveloped countries — lose their sight from severe vitamin A deficiency. This condition is rare in the United States, although many disadvantaged children have substandard levels of vitamin A. With therapy, the chance of reversing symptoms of night blindness and milder conjunctival changes is excellent. When corneal damage is pres-ent, emergency treatment is necessary.
Signs and symptoms
Typically, the first symptom of vitamin A deficiency is night blindness (nyctalopia), which usually becomes apparent when the patient enters a dark place or is caught in the glare of oncoming headlights while driving at night. This condition can progress to xerophthalmia, or drying of the conjunctivas, with development of gray plaques (Bitot’s spots); if unchecked, perforation, scarring, and blindness may result. Keratinization of epithelial tissue causes dry, scaly skin; follicular hyperkeratosis; and shrinking and hardening of the mucous membranes, possibly leading to infections of the eyes and the respiratory or genitourinary tract. An infant with severe vitamin A deficiency shows signs of failure to thrive and apathy, along with dry skin and corneal changes, which can lead to ulceration and rapid destruction of the cornea.
Diagnosis
Dietary history and typical ocular lesions suggest vitamin A deficiency. Carotene levels less than 40 mcg/dl also suggest vitamin A deficiency, but they vary with seasonal ingestion of fruits and vegetables.
Confirming diagnosis A serum level of vitamin A that falls below 10 mcg/dl confirms the diagnosis. Levels between 10 and 19 mcg/dl are also considered low but the patient isn’t likely to have developed significant symptoms.
Treatment
Mild conjunctival changes or night blindness requires vitamin A replacement in the form of cod liver oil or halibut liver oil. Acute deficiency requires aqueous vitamin A solution I.M., especially when corneal changes have occurred. Therapy for underlying biliary obstruction consists of administration of bile salts; for pancreatic insufficiency, pancreatin. Dry skin responds well to cream-based or petroleum-based products.
In patients with chronic malabsorption of fat-soluble vitamins, and in those with low dietary intake, prevention of vitamin A deficiency requires aqueous I.V. supplements or an oral water-miscible preparation.
Special considerations
❑ Administer oral vitamin A supplements with or after meals or parenterally, as ordered. Watch for signs of hypercarotenemia (orange coloration of the skin and eyes) and hypervitaminosis A (rash, hair loss, anorexia, transient hydrocephalus, and vomiting in children; bone pain, hepatosplenomegaly, diplopia, and irritability in adults). If these signs occur, discontinue supplements and notify the physician immediately. (Hypercarotenemia is relatively harmless; hypervitaminosis A may be toxic.)
❑ Because vitamin A deficiency usually results from dietary insufficiency, provide nutritional counseling. Tell the patient that vitamin A comes from animal sources, such as eggs, meat, milk, cheese, cream, liver, kidney, and cod and halibut fish oil, but that healthier choices, such as carrots, pumpkins, sweet potatoes, and most dark green, leafy vegetables are good sources of beta-carotene, vitamin A’s precursor form. Instruct the patient that the more intense the color of a fruit or vegetable, the higher its beta-carotene content. Provide referrals to appropriate community agencies if necessary.
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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