Patients with xerophthalmia generally present with irritation associated with a sensation of a foreign body in their eyes as well as some mild pain. The symptoms are exacerbated in dry environments, in the presence of air conditioning and during exposure to a computer monitor. They also frequently worsen at the end of the day. Xerophthalmia associated with meibomian gland dysfunction, however, is usually worse when the patient wakes up and is distinguished by eyelids that are red and sticky.

Other associated symptoms include fatigue, avoidance of light and itching sensations. Patients also experience a reduction of tears during emotional moments or when peeling onions. Some patients, however, may complain from excessive tearing. This is caused by an increasingly sensitized reflex to corneal dryness and may be particularly prominent in windy conditions.

On physical examination, the eyes are commonly normal or slightly erythematous. Conjunctivitis or ulcers in the cornea may be evident if the condition is especially severe. Physicians should additionally look for evidence implicating direct causes such as any signs for Parkinson's, joint or skin involvement and local disease of the eyes.

Important signs that are especially worrisome and may need urgent referral are photophobia, excessive erythema involving only one eye, an acute onset, pain in the eyes that is either moderate or severe, double vision (diplopia) and any nonspecific systemic signs (for example, fever or weight loss).

Xerophthalmia is definitively diagnosed with special tests after referral to an ophthalmologist. They include symptoms questionnaires that help in assessing the severity of the condition, Schirmer's test, the slit-lamp exam, tear break-up time and corneal damage assessment performed with stains such as fluorescein, lissamine green or rose Bengal. Furthermore, laboratory blood tests can also help elucidate potential underlying causes (for example, thyroid or immunological diseases).

The tear break-up time is performed with a slit lamp in addition to a cobalt blue filter. Initially, fluorescein is injected into the lower fornix and the patient is asked to blink. The tear break-up time corresponds to the period separating the last blink from the appearance of a corneal black spot. Eye dryness is suggested by a tear break-up time less than 10 second.

Treatment is targeted at symptomatic relief, prevention of corneal damage and resolution of underlying causes.
Mild disease is treated by a reduction of exacerbating factors such as smoking (first or second-hand). Patients are additionally advised to decrease their exposure to television and computer monitors as they are associated with reduced blinking. Contact lenses are best avoided but, in cases where it may be necessary to wear them, gas-permeable or silicone-hydrogen are recommended. The cornerstone of treatment remains tear substitutes in the form of ointments, drops or gels.

Patients who do not respond to the above regimen or who suffer from moderate to severe disease should increase their intake of omega-3 fatty acids through supplements or by increasing their intake of oily fish [9]. Anti-inflammatory drugs may also be helpful and evidence suggests that they work better than tear substitutes. These include topical steroids, pilocarpine, tetracyclines and topical cyclosporine A. Topical steroids are not preferred because of their side effects profile and azithromycin or clarithromycin can be used instead of tetracyclines in cases of intolerance.

Other potential treatment modalities include ocular inserts, punctal plugs and secretagogues. Ocular inserts work by slowly releasing lubricant material after they are inserted in the conjunctival sac but they may also lead to discomfort. Secretagogues like pilocarpine work by increasing tear production but are limited by their side effects. Punctal plugs are placed over lacrimal ducts to decrease the drainage of tears. Evidence suggests that they lead to a relief of associated symptoms but they should be placed only after inflammation is controlled [10].

Artificial tears may be substituted by autologous serum tears. The latter are characterized by an absence of any artificial preservatives and are rich in nutritive and anti-inflammatory agents. Nonetheless, their efficacy has not yet been proven.
Surgery is the treatment of last resort. It is employed for punctal closure or on the conjunctiva. The latter involves grafts or transplants, salivary gland autotransplantation or a transplantation of the amniotic membrane.

The course of the xerophthalmia is not well studied, but it is thought to be relatively long. Prognosis is variable, depending on the underlying cause. In rare instances, severe complications such as corneal ulceration and visual loss may occur.

The causes underlying dryness of the eyes are various but they can be generally categorized into four divisions. They are either due to a poor production of tears, an excessive amount of tear loss, problems with eye lids or with blinking and disruptions in the composition of tears. Eye dryness is intimately linked with inflammation. It can cause inflammation and also result from the process. Redness is not necessarily concomitantly present with inflammation. The administration of artificial tears that contain benzalkonium chloride can also exacerbate the condition.

Xerophthalmia can be caused by a range of common factors that are not necessarily linked with a disease process. They include drug side effects, allergies, decreased air humidity due to air conditioning, strong winds or heating, increased exposure to computer screens or microscopes resulting in lower rates of blinking and wider lid apertures and finally blepharitis with a resulting decreased amount of tear production.

Furthermore, systemic disease can also underlie the condition, in particular diabetes, rosacea, diseases of the thyroid gland, Parkinson's disease and administration of antihistamines and antidepressants [2].

Several factors, while not directly causing xerophthalmia, may increase its risk of occurrence. They include estrogen therapy (particularly in the postmenopausal stage), deficiency of vitamin A, malignant neoplasms arising from chemotherapy or radiotherapy, contact lenses, diets deficient in omega-3 or having a low ratio of omega 6 to omega 3, low humidity, prolonged reading time, female sex, old age and smoking [3].

Approximately 15% to 33% of individuals above the age of 65 suffer from dry eyes. The condition increases with age and is considerably more common among women than men.

Nutritional deficiency is a major cause of xerophthalmia and keratomalacia. In fact, blindness due to malnutrition is directly related to those conditions [4].

Vitamin A deficiency is particularly linked to xerophthalmia. Vitamin A associated with protein is first released in the stomach in the form of provitamin A. In the small intestines, retinyl ester is converted to retinol which is much better absorbed. On the other hand, carotenoids pass through in a different process. They are first transformed into retinaldehyde before being reduced to retinol. Retinol is subsequently converted into retinyl ester in an esterification reaction. Following the biochemical reactions in the digestive system, retinyl esters and retinol are transferred to the liver within chylomicrons through the lymphatic system. Up to 80% of vitamin A is stored in the liver. The rest is usually stored in fatty tissues, the pulmonary system and in the kidneys in the form of retinyl palmitate. When vitamin A is required by peripheral tissue, it undergoes esterification in the liver and is moved into the blood where it binds to the RBP protein. The latter requires both zinc and amino acids for its synthesis.

A deficiency in vitamin A can result from various causes. It can be due to decreased intake, abnormalities in vitamin A absorption in the small bower, changes in the normal metabolism in the body and elevated tissue requirements. The adult liver has the ability to store vitamin A for a year whereas vitamin A stores last only for several weeks in children. Vitamin A levels in the body can be accessed from retinol serum values. The latter, however, does not decrease unless vitamin A stores are severely depleted. It may also vary depending on the presence of infection, zinc and iron levels, overall status of nutrition and the synthesis level of RBP proteins in the liver [5].

Other essential elements involved in the pathophysiology of vitamin A deficiency are zinc and iron. Deficiency in zinc leads to abnormalities in the synthesis of RBP in the liver. The mechanisms linking iron and vitamin A deficiencies are poorly understood but it is known that supplementation with vitamin A is not sufficient when there's an accompanying iron deficiency.

Only 40% to 60% of ingested carotene from vegetarian sources is absorbed whereas the body usually takes up to 90% of ingested animal sources of vitamin A in the form retinyl esters. Deficiency in protein and zinc as well as abetalipoproteinemia can further exacerbate carotene absorption. Furthermore, because vitamin A is a fat soluble vitamin, malabsorption diseases can also result in deficiency, in particular pancreatic insufficiency, cholestasis, inflammatory bowel diseases (IBD), sprue, cystic fibrosis and in patients who have undergone bowel bypass surgery. Alcoholic patients are at an increased risk because of the role of alcohol dehydrogenase in catalyzing the transformation of retinol into retinaldehyde.

Supplementation with vitamin A is generally recommended in children aged 6 to 24 months who are hospitalized because of measles [6]. Studies have found a corresponding decrease in mortality especially with doses of 200,000 IU that are given for at least 2 days [7] [8].

Xerophthalmia in children can be prevented with vitamin A supplementation. WHO recommendations depend on the age of the child. Infants who are younger than 6 months are advised to take 50,000 IU in total. Those aged 6 to 12 months or infants with weight below 8 kg require 100,000 IU every 3 to 6 months. Finally, children above 1 year of age but less than 6 year old need 200,000 IU every 6 months.

Xerophthalmia describes eye dryness and can potentially lead to ulcerations of the cornea and blindness if not properly treated. It is most strongly associated with vitamin A deficiency although several systemic diseases or local diseases of the eye can ultimately result in its occurrence [1]. Patients normally present with irritation, a foreign body sensation and very mild pain. The condition is usually exacerbated by dry environments, places with air conditioning or central heating, prolonged exposure to computer monitors and first or second-hand smoking. It is also more prevalent among women and individuals older than 65. Signs that should indicate prompt referral to a specialist include moderate to severe pain, visual loss, an acute onset, diplopia and nonspecific signs such as weight loss or fever. History is generally sufficient for diagnosis although the condition can be diagnosed definitively only with specialized testing such as Schirmer's test or the tear break-up time test. Treatment depends on the severity of the disease. Mild xerophthalmia is generally treated with artificial tears as well as an avoidance of exacerbating conditions. Moderate to severe xerophthalmia may necessitate the use ocular inserts, secretagogues or punctual plugs. In very rare cases, surgery is the treatment of last resort.

Xeropthalmia is a medical condition that describes an excessive dryness of the eyes. It is caused by a multitude of factors, although the most important of them is vitamin A deficiency. Patients tend to be older than 65 and women are more commonly affected than men. Systematic diseases such as diabetes, dysfunctions of the thyroid gland or autoimmune disease can also result in the development of eye dryness. If the condition is not properly treated, it can lead to blindness or ulcerations of the cornea.

Patients with xerophthalmia usually present with a sensation of a foreign body within their eyes, irritation and mild pain. Some may also complain of eye redness. Their symptoms are usually exacerbated by the end of the day, by smoking, sitting for a long time in front of a television or a computer screen, central heating or air conditioning. Diagnosis is established with history, although it can only be conclusively confirmed by an opthalmologist after the performance of special tests.

Treatment depends on the severity of the disease. Mild disease is treated with artificial tears and avoidance of exacerbating factors. Moderate or severe disease can be treated with anti-inflammatory agents and drugs that increase the secretion of tears. Surgery is performed very rarely as last resort. 

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