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Xerophthalmia: Wikis


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Classification and external resources
ICD-10 E50.6-E50.7
ICD-9 264.6-264.7
DiseasesDB 34035
MeSH D014985

Xerophthalmia (Greek for dry eyes) is a medical condition in which the eye fails to produce tears. It may be caused by a deficiency in vitamin A and is sometimes used to describe that lack, although there may be other causes.

Xerophthalmia caused by a severe vitamin A deficiency is described by pathologic dryness of the conjunctiva and cornea. The conjunctiva becomes dry, thick and wrinkled. If untreated, it can lead to corneal ulceration and ultimately in blindness as a result of corneal damage.

Xerophthalmia is a term that usually implies a destructive dryness of the conjunctival epithelium due to dietary vitamin A deficiency — a rare condition in developed countries, but still causing much damage in developing countries. Other forms of dry eye are associated with aging, poor lid closure, scarring from previous injury, or autoimmune diseases such as rheumatoid arthritis, and these can all cause chronic conjunctivitis. Radioiodine therapy can also induce xerophthalmia, often transiently, although in some patients late onset or persistent xerophthalmia has been observed [1].

The damage to the cornea in vitamin A associated xerophthalmia is quite different from damage to the retina at the back of the globe, a type of damage which can also be due to lack of vitamin A, but which is caused by lack of other forms of vitamin A which work in the visual system. Xerophthalmia from hypovitaminosis A is specifically due to lack of the hormone-like vitamin A metabolite retinoic acid, since (along with certain growth-stunting effects) the condition can be reversed in vitamin A deficient rats by retinoic acid supplementation (however the retinal damage continues). Since retinoic acid cannot be reduced to retinal or retinol, these effects on the cornea must be specific to retinoic acid. This is in keeping with retinoic acid's known requirement for good health in epithelial cells, such as those in the cornea.


Epidemiology and mechanical etiology

Xerophthalmia usually affects children under nine years old and "accounts for 20,000-100,000 new cases of childhood blindness each year in the developing countries." The disease is largely found in developing countries like many of those in Africa and Southern Asia. The condition is not congenital and develops over the course of a few months as the lacrimal glands fail to produce tears. Other conditions involved in the progression already stated include the appearance of Bitot's spots, which are clumps of keratin debris that build up inside the conjuctiva and night blindess, which precedes corneal ulceration and total blindness. Other causes of cyanosis include the following:

  • Methemoglobin
    • Normal hemoglobin unbound to oxygen is called reduced hemoglobin and is symbolized HbFe+2. Methemoglobin (metHb), the oxidized form of hemoglobin, is HbFe+3. Normally, as much as 2% of hemoglobin is in the form of metHb. Because metHb is unable to bind with oxygen, arterial oxygen saturation is reduced by the same amount that metHb is increased.
    • MetHb imparts an intense bluish tinge to the skin; therefore, the cyanosis that comes with methemoglobinemia is not related to reduced hemoglobin but to oxidized hemoglobin.7,8 Methemoglobinemia usually occurs as a drug reaction, especially to nitrite or nitrate-containing compounds (eg, nitroglycerin) and to some topical anesthetics. Dahshan and Donovan report a case of severe methemoglobinemia from topical benzocaine in a toddler.9 Dapsone, a drug used in HIV and non-HIV conditions, can also cause methemoglobinemia.
    • Although excess metHb reduces the measured SaO2, PaO2 is not affected; this is because metHb does not affect transfer of oxygen from the atmosphere to the lungs. A low PaO2 in a patient with excess metHb suggests a concomitant pulmonary problem. MetHb can be measured in a co-oximeter, a companion to the blood gas machine available in most hospital blood gas laboratories. The co-oximeter also measures carboxyhemoglobin, hemoglobin content, and SaO2. Note that standard pulse oximeters, which measure SaO2 using 2 wavelengths of light, do not measure metHb (or carboxyhemoglobin). However, a new generation of pulse oximeters that uses 8 wavelengths of light does have the ability to measure carboxyhemoglobin and metHb (Barker 2006).of light does have the ability to measure COHb and metHb.10
  • Sulfhemoglobin
    • Sulfhemoglobinemia is a rare condition caused by sulfur binding with hemoglobin so that oxygen cannot be bound.
    • Unlike metHb, the iron moiety remains in the reduced state (HbFe+2).
    • Sulfhemoglobin is similar to metHb in causing low SaO2 but not affecting PaO2 and in imparting an intense bluish color to the skin.
  • Peripheral cyanosis
    • Peripheral cyanosis is a dusky or bluish tinge to the fingers and toes and may occur with or without central cyanosis (ie, with or without hypoxemia).
    • When unaccompanied by hypoxemia, as determined by blood gas analysis, peripheral cyanosis is caused by peripheral vasoconstriction.
  • Pseudocyanosis
    • Pseudocyanosis is a bluish tinge to the skin and/or mucous membranes that is not associated with either hypoxemia or peripheral vasoconstriction. Most causes are related to metals (eg, silver nitrate, silver iodide, silver, lead) or drugs (eg, phenothiazines, amiodarone, chloroquine hydrochloride). One report describes blue-gray discoloration in a man who for years ingested colloidal silver for a urinary tract infection11 ; his oxygen levels were normal.
    • One report describes a girl with intensely blue skin from food coloring.12 Consider pseudocyanosis when the patient has no cardiopulmonary symptoms and the skin does not blanch under pressure. To be sure of the diagnosis, obtain a pulse oximetry or arterial blood gas measurement.lBefore the era of rapid blood gas analysis, clinicians often assessed hypoxemia on clinical grounds alone, primarily by looking for cyanosis in the perioral area and fingers.1 Clinical assessment of hypoxemia is now known to be notoriously unreliable for the following reasons:
  • A host of factors, from natural skin pigment to room lighting, can affect detection of cyanosis. As with many other physical examination findings, significant interobserver variation occurs in detecting cyanosis.2 Physicians may diagnose cyanosis as an indicator of hypoxemia when the patient has normal oxygen saturation; alternatively, physicians may miss cyanosis when it should be present (the patient has very low oxygen saturation with normal hemoglobin).3
  • Approximately 5 g/dL of unoxygenated hemoglobin in the capillaries generates the dark blue color appreciated clinically as cyanosis. For this reason, patients who are anemic may be hypoxemic without showing any cyanosis.
  • Ancillary signs and symptoms of hypoxemia (eg, tachycardia, tachypnea, mental status changes) are nonspecific and of no value in reliably detecting hypoxemia. For example, patients may be dyspneic at rest for reasons other than hypoxemia (ie, they have normal PaO2 and SaO2). Conversely, many patients who are chronically hypoxemic (low PaO2 and/or low SaO2) are perfectly lucid and without any obvious physical signs of their low oxygen state (at least while at rest).


Treatment can occur in two ways: treating symptoms and treating the deficiency. Treatment of symptoms usually includes use of artificial tears in the form of eye drops, increasing the humidity of the environment with humidifiers, and wearing wrap around glasses when outdoors. Treatment of the deficiency can be accomplished with a Vitamin A or multivitamin supplement or by eating foods rich in Vitamin A. Treatment with supplements and/or diet can be successful until the disease progresses as far as corneal ulceration, at which point only an extreme surgery can offer a chance of returning sight.

See also


  1. ^ Solans, R; Bosch, JA; Galofre, P; others (2001), "Salivary and lacrimal gland dysfunction (sicca syndrome) after radioiodine therapy.", Journal of Nuclear Medicine 42 (5): 738–43, PMID 11337569 


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