Vitamin A Deficiency and Hypervitaminosis

On this page
  1. Direct answer
  2. What you must remember
  3. Worked example: a toddler who cannot see at dusk
  4. Where carotenes and retinol get confused
  5. Frequently asked questions
  6. Related topics

Direct answer

Vitamin A deficiency causes night blindness, then Bitot spots, corneal ulceration and keratomalacia, through impaired rhodopsin regeneration and epithelial change. Excess preformed vitamin A causes raised intracranial pressure, hepatotoxicity and teratogenicity. Dietary carotenoids are not toxic in the same way, which is the examiner's central distinction between the two.

What you must remember

  • First sign: night blindness from impaired rhodopsin regeneration in rod photoreceptors, which precedes conjunctival and corneal change.
  • Bitot spots: foamy, keratinised plaques on the lateral bulbar conjunctiva, a marker of established deficiency most often seen in children.
  • Xerophthalmia spectrum: conjunctival xerosis, Bitot spots, corneal xerosis, corneal ulceration and keratomalacia, the last causing irreversible blindness.
  • Systemic effects: impaired immunity raises the risk of measles, diarrhoea and respiratory infection, and phrynoderma with follicular hyperkeratosis is described.
  • Acute toxicity: headache, vomiting and bulging fontanelle in infants from raised intracranial pressure; chronic toxicity causes dry skin, alopecia, bone pain, hepatosplenomegaly and hyperostosis.
  • Teratogenicity: high-dose preformed vitamin A and isotretinoin cause neural crest and cardiac outflow defects, so pregnancy must be excluded and prevented during treatment.
  • Carotenaemia: yellow skin sparing the sclerae comes from carotenoids, not jaundice, and is harmless.
  • Indian programme: biannual vitamin A prophylaxis for children aged nine months to five years runs through the national programme, and high-dose oral vitamin A treats xerophthalmia.

Worked example: a toddler who cannot see at dusk

A two-year-old with recent measles and diarrhoea is brought because she bumps into furniture in dim light. Examination shows Bitot spots on both lateral conjunctivae and dull, dry corneas, which is xerophthalmia until proven otherwise.

  1. Protect the cornea: The cornea is the urgent concern, since ulceration can progress to keratomalacia within days. Eye protection is given, with urgent referral if the cornea is ulcerated.
  2. Give high-dose vitamin A: The xerophthalmia protocol uses high-dose oral vitamin A on day one, again on day two and again about two weeks later.
  3. Treat the infection: Measles and diarrhoea drain vitamin A stores and worsen the outcome, so both are treated.
  4. Take the diet history: It covers green leafy vegetables, orange fruits, liver and fortified foods.
  5. Cover the household: The household is referred for supplementation under the national programme so that siblings are covered too.

Contrast an adult taking large amounts of retinol capsules for skin problems, who presents with headache, dry skin and bone pain. Here the cause is preformed vitamin A rather than diet, and the workup includes liver function, pregnancy testing and dose reduction.

Where carotenes and retinol get confused

Vitamin A questions turn on a few distinctions.

  • Trap: treating yellow palms as a sign of toxicity. Correct: beta-carotene from vegetables is converted only as needed, so yellow palms are benign, whereas retinol and retinyl esters from animal sources are toxic in excess.
  • Trap: waiting for Bitot spots as the first sign. Correct: night blindness is the earliest symptom, and Bitot spots indicate established deficiency.
  • Trap: swapping teratogenic and non-teratogenic agents. Correct: isotretinoin and acitretin are teratogenic and require pregnancy prevention, while carotenoids are not.
  • Trap: attributing a bulging infant fontanelle to hydrocephalus. Correct: acute hypervitaminosis A is a differential for raised intracranial pressure in an infant, a useful stem clue when a large vitamin A dose is mentioned.

Frequently asked questions

What is the earliest clinical sign of vitamin A deficiency?

Night blindness is the earliest clinical sign of vitamin A deficiency, caused by impaired rhodopsin regeneration in rod photoreceptors. It usually precedes conjunctival changes such as Bitot spots, so it is the symptom to ask about in a child with a poor diet.

What causes Bitot spots in vitamin A deficiency?

Bitot spots are foamy, keratinised plaques on the bulbar conjunctiva, produced by keratinising squamous metaplasia in vitamin A deficiency. They indicate established deficiency and carry a risk of corneal ulceration and keratomalacia if untreated.

Why is vitamin A teratogenic in high doses?

High-dose preformed vitamin A and isotretinoin are teratogenic because retinoic acid regulates neural crest and cardiac outflow development. Exposure in early pregnancy can cause craniofacial, cardiac and central nervous system malformations, so pregnancy must be excluded before treatment.

What are the features of acute vitamin A toxicity in infants?

Acute vitamin A toxicity in infants causes raised intracranial pressure, with headache, vomiting and a bulging anterior fontanelle, after a single very large dose. Chronic toxicity in older patients causes dry skin, alopecia, bone pain and hepatosplenomegaly.

How is carotenaemia distinguished from jaundice?

Carotenaemia causes yellow skin, especially on the palms and soles, while the sclerae are spared, whereas jaundice colours the sclerae. Carotenaemia is harmless and fades when carotene-rich foods are reduced, unlike the hepatic causes of jaundice.

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