no xerophthalmia meaning

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Xerophthalmia

What is xerophthalmia?

Xerophthalmia is pronounced "zeer-of- thal -mee-uh” or “zeer-op- thal -mee-uh.” The Greek root words literally mean “dry eye.”

While the group of conditions that is xerophthalmia includes dry eyes , it covers other signs and symptoms that affect your eyes. Xerophthalmia is caused by a lack of vitamin A and can cause blindness.

The vitamin A deficiency can happen in two ways:

How common is xerophthalmia?

According to the World Health Organization, there are some 254 million children worldwide with vitamin A deficiency. There are about 2.8 million children with xerophthalmia. In addition, it causes about 350,000 cases per year of childhood blindness, making it the leading cause of blindness in children.

Symptoms and Causes

What are the signs and symptoms of xerophthalmia.

The signs and symptoms of xerophthalmia include the following items presented in the order, or stage, in which they generally happen:

What causes xerophthalmia?

Vitamin A deficiency causes xerophthalmia. Vitamin A is important to your vision in two major ways: for moisture and for pigments.

Your eyes need vitamin A to produce moisture to keep your corneas properly lubricated. If your corneas get too dry, they can become damaged, which can lead to blindness.

Also, your eyes need vitamin A to make specific pigments for your retinas to work correctly. A lack of vitamin A hinders your eyes’ ability to make these pigments, which can lead to night blindness. Rods are the parts of your eye that allow you to see in darkness or dim light.

You may lack vitamin A because you don’t get enough vitamin A in your diet or because you can’t use vitamin A effectively.

Dietary causes of vitamin A deficiency and xerophthalmia

Vitamin A deficiency doesn’t happen often in the U.S. and other developed countries. Many of the people who are affected are children in developing nations who aren’t able to get the nutrients they need.

Diagnosis and Tests

How is xerophthalmia diagnosed.

Your provider may use these methods to diagnose xerophthalmia:

Management and Treatment

How is xerophthalmia treated.

Your healthcare provider will recommend vitamin A supplements. Your provider may also suggest using artificial tears and topical antibiotics if you have an infection.

When your skin and eyes improve, you’ll be better.

How can I reduce my risk of developing xerophthalmia?

The best way to avoid xerophthalmia is to include adequate amounts of vitamin A in your diet. These foods provide vitamin A:

Treatment for people with vitamin A deficiency includes supplements. Providers need to monitor these people because too much vitamin A can be fatal.

Outlook / Prognosis

What can i expect if i have xerophthalmia.

If xerophthalmia is treated, you can expect to recover. Without treatment, there’s a possibility of blindness.

Living With

When should i see my healthcare provider about xerophthalmia.

If you’re having any vision issues, see your healthcare provider as soon as possible, even if you just feel like your eyes are dry.

Your provider, or your child’s provider, will check the eyes and skin during a health examination and will notice dryness of the skin and eyes. Providers will be able to see some of the changes to the eyes, which can happen because of vitamin A deficiency.

Your provider may also ask about your food intake or your child’s dietary habits and make suggestions.

Frequently Asked Questions

What is the difference between xerophthalmia and keratomalacia.

Xerophthalmia is a term for a group of eye problems that happen as a result of not getting enough vitamin A. Keratomalacia, or a softening of your cornea, is one of the conditions that are grouped under xerophthalmia. Keratomalacia is like a subset of xerophthalmia.

What is the difference between xerophthalmia and xerostomia?

The difference is that they refer to dryness of different parts of your body. Xerophthalmia refers to having dry eyes. Xerostomia refers to having a dry mouth.

A note from Cleveland Clinic

Experiencing symptoms of eye disease can be scary. If you do have symptoms, see your provider as soon as you can. In the case of xerophthalmia, vitamin A tablets are a simple fix. It’s important to get a diagnosis early because early treatment leads to the best outcome. Global health organizations are working to eliminate vitamin A deficiency in developing countries to reduce cases of preventable blindness and illness among children.

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What Is Xerophthalmia?

‌Xerophthalmia is a disease that causes dry eyes due to vitamin A deficiency . If it goes untreated, it can progress into night blindness or spots on your eyes. It can even damage the cornea of your eye and cause blindness.

This disease is rare in the U.S. It’s more commonly seen in developing countries, where people are more likely to have nutrient deficiencies. It can be treated with vitamin A supplements.

Causes of Xerophthalmia

Vitamin A , or retinol, is an essential nutrient. Its main function is to help maintain your eye health and vision. It also protects your vital organs, including your lungs and heart, and supports your immune system. ‌

Your body can’t make its own vitamin A. You need to eat foods — like carrots and meat — or take supplements that are rich in vitamin A. Getting enough vitamin A is important for your health. ‌

A lack of vitamin A in your diet may cause dry eyes, which is called xerophthalmia.

Risk Factors of Xerophthalmia

‌Xerophthalmia can happen because of underlying conditions that cause vitamin A deficiency. It has the following risk factors: ‌

Young age. Vitamin A deficiency is more common in infants and children. It can hinder a child’s growth, have negative effects on vital organs, and complicate other diseases or infections. If a child doesn’t get enough vitamin A as they are growing, it may cause xerophthalmia or childhood blindness.

Vitamin A deficiency can also occur in children due to diseases like measles and respiratory infections . Such infections increase the chances of xerophthalmia in children. ‌

Severe xerophthalmia affects infants far more than adults. Children 3 to 6 years of age are at a higher risk of developing night blindness due to xerophthalmia.

Other factors. These are some other risk factors of xerophthalmia in children and adults, including: ‌

Symptoms of Xerophthalmia

‌Xerophthalmia is a progressive disease that begins with dry eyes and may keep getting worse. These are the typical symptoms of xerophthalmia:‌

‌ ‌Xerophthalmia is a preventable disease that can be easily treated. But in extreme cases, it can cause permanent blindness.

Diagnosis of Xerophthalmia

‌If you have obvious symptoms like dry eyes, talk to your doctor. They may physically examine you and check your symptoms and history. They may ask you questions about your diet. ‌

Your doctor may also order a blood test to check the vitamin A levels in your body. If you have severe xerophthalmia or night blindness, your doctor may start your treatment right away.

Treatment of Xerophthalmia

‌The main treatment for xerophthalmia is vitamin A therapy or supplementation. It can be given orally or by injection. Your doctor may also give you other medications like antibiotics to prevent eye infections.

Vitamin A therapy is used to treat xerophthalmia in adults and children. The dose depends on your age and the severity of your xerophthalmia.

Your doctor may ask you to eat more yellow-colored fruits and vegetables rich in beta-carotene . They may also suggest that you add green leafy vegetables, meat, and dairy to your diet. If your xerophthalmia is due to other factors, your doctor can work with you to treat the underlying cause.

Prevention of Xerophthalmia

‌Xerophthalmia can be prevented with vitamin A supplements . Increasing the levels of vitamin A in your diet can also help prevent this disease. Some foods that are rich in vitamin A that you can easily add to your meals include:‌

‌Adding these vitamin A-rich foods to your diet will not only help to prevent xerophthalmia but may also help you to maintain your overall health.

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no xerophthalmia meaning

Everything You Should Know About Xerophthalmia

no xerophthalmia meaning

What is xerophthalmia?

Xerophthalmia is a progressive eye disease caused by vitamin A deficiency. Lack of vitamin A can dry out your tear ducts and eyes. Xerophthalmia can develop into night blindness or more serious damage to your cornea, the outer layer of your eye. This damage may take the form of white spots on your eyes and ulcers on your corneas. Xerophthalmia usually can be reversed with vitamin A therapy.

Read on to learn the symptoms of and risks for this condition, and what treatment options are available.

What are the symptoms?

The symptoms of xerophthalmia start out mild, and then get progressively worse if a vitamin A deficiency isn’t treated. If you have this condition, the thin lining of your eyelid and eyeball, called the conjunctiva, dries out, thickens, and begins to wrinkle. That drying out and wrinkling causes various symptoms.

Night blindness is an early symptom. This is an inability to see in dim light. The World Health Organization and public health workers have used number of cases of night blindness as a gauge of vitamin A deficiency in a population.

As xerophthalmia progresses, lesions form on your cornea. These deposits of tissue are called Bitot’s spots. You can also get corneal ulcers . In the latest stages of the condition, part or all of your cornea liquefies. This eventually leads to blindness.

What causes xerophthalmia?

Xerophthalmia is caused by a lack of vitamin A. Your body doesn’t produce vitamin A on its own. Instead, you have to get vitamin A from the foods you eat. Vitamin A is essential for vision because it’s an element of the protein that absorbs light in the receptors in your retina.

Vitamin A is also important for the function and maintenance of your heart, lungs, kidneys, and other organs.

Xerophthalmia is rare in the United States, United Kingdom, and other developed countries. It’s still seen in developing countries where people may have limited access to animal products, however.

Where is vitamin A found?

Vitamin A is also known as retinol. It’s a fat-soluble substance found in animal products like:

dairy products

It’s also possible to get vitamin A from vegetable sources in the form of beta carotenes. Beta carotenes are converted into retinol in your gut. But this process is inefficient as a vitamin A source compared with eating animal products. Sources of beta carotenes include:

How common is this condition?

Xerophthalmia is rare in the United States: There are only isolated clinical reports of the disease, according to Dr. Alfred Sommer, a professor at the Johns Hopkins Bloomberg School of Public Health and an international expert on vitamin A deficiency.

Vitamin A deficiency and xerophthalmia are a major public health problem in the developing world, affecting millions of women and children. It’s a leading cause of blindness in children. A 2002 study found that worldwide:

Who’s at risk for xerophthalmia?

The major risk for xerophthalmia is poverty and lack of adequate diet, especially a lack of animal products. Infants and children are at greater risk. The younger the child, the more severe the effects of vitamin A deficiency.

Children require a lot of vitamin A in order to grow. Vitamin A deficiency also affects the ability to survive common childhood infections and diseases, such as diarrhea, measles , and respiratory infections.

Other risk factors affect a much smaller number of people in the United States and other countries. The following are risk factors because they affect a person’s ability to absorb vitamin A:

How much vitamin A do you need?

According to the National Institutes of Health (NIH) , recommended daily allowances for vitamin A differ depending on your age and, in some cases, gender.

The NIH gives separate recommendations for pregnant or breast-feeding women.

These recommendations are for people who are healthy and well-nourished. Your doctor may make different recommendations if you have a medical condition or a vitamin deficiency.

What should you expect when you see your doctor?

Your doctor will do a physical examination and ask you questions about your symptoms and diet.

If you have night blindness, your doctor may start you on vitamin A therapy, even before doing blood tests.

Sometimes corneal ulcers of xerophthalmia are mistaken for bacterial infections. As a result, your doctor may prescribe an antibiotic. Further testing for vitamin A deficiency may be needed.

How is xerophthalmia treated?

Vitamin A supplementation is the immediate treatment for xerophthalmia. Vitamin A can be taken by mouth or injected. The dose varies according to your age and general health condition.

In more advanced cases where the cornea is damaged, you may receive antibiotics to prevent secondary infections. You may need to keep your eye covered to protect it until the lesion heals.

Vitamin A supplements can quickly reverse symptoms of xerophthalmia and help protect children from dying of other childhood diseases.

Vitamin A supplements are given preventively in areas where xerophthalmia is a known problem. This is a low-cost way to prevent human suffering and deaths. A 2007 study estimated that 500 million vitamin A capsules are distributed annually, at a relatively low cost of 10 cents per capsule.

Nutrition education can be important in helping people make the best use of their food resources. Fortifying commercial foods with vitamin A also helps reduce vitamin A deficiency. Some foods that may be fortified include:

oils and fats

Another possible source of vitamin A is golden rice, which is genetically engineered to contain beta carotene. It has been opposed by groups that are against any genetic modification of food.

What can you expect?

Xerophthalmia improves quickly with vitamin A supplements. In very advanced cases, scarring may remain and impair vision. In the worst cases, permanent blindness may occur.

Vitamin A deficiency and xerophthalmia remain a significant public health problem in the developing world and in areas of war or natural disasters. The availability and affordability of an adequate diet, including animal products and green leafy vegetables, is key.

If you or your child are at risk for vitamin A deficiency, talk to your doctor about taking vitamin A supplements. Also, vary your diet as much as possible to include animal products, and vegetables and fruits with beta carotene.

Read next: Preventing eye problems »

Last medically reviewed on January 24, 2017

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no xerophthalmia meaning

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Xerophthalmia

Disease Entity

Xerophthalmia refers to the spectrum of ocular disease caused by severe Vitamin A deficiency (VAD). Vitamin A serves several essential functions in the eye, and deficiency can lead to a constellation of ocular signs and symptoms that affect the conjunctiva, cornea, and retina. Xerophthalmia continues to be a leading cause of preventable blindness in developing countries [1] . Unfortunately, xerophthalmia signifies a severity of VAD that causes significant morbidity and mortality from malnutrition and increased susceptibility to mucosal infections.

Epidemiology

VAD is among the leading causes of blindness worldwide, estimated to blind half a million children each year [2] . Although VAD is rarely seen in developed countries, it remains a public health concern in more than half of all countries, mostly affecting young children in impoverished regions. The World Health Organization (WHO) estimates that 228 million children have VAD, causing 1-3 million childhood deaths and 5-10 million cases of eye disease. VAD is especially prevalent in Africa and South-East Asia, where young children and pregnant women in low-income countries are disproportionally affected [3] [4] .

In the United States, VAD is rare. In 2013, it was estimated at 0.3% [5] [6] . VAD usually involves a malabsorptive process, such as inflammatory bowel disease or post-gastric bypass surgery, or a severely restrictive diet.

In resource-poor regions, the most common cause of VAD is insufficient nutrition complicated by chronic inflammation from regular gastrointestinal infections. In the developed world, the leading causes of VAD are pancreatic, liver, and intestinal pathology. Some of the more common causes of VAD are listed below:

Risk Factors

Pathophysiology

Vitamin A is a fat-soluble vitamin that humans derive primarily from diet. It has several essential functions in the body, including cell development, metabolism, immune function, vision, and reproductive function.

Dietary sources of preformed vitamin A include dark leafy greens, orange-colored vegetables, fish liver oils, liver, egg yolks, butter, and vitamin A-fortified dairy products. A variety of other foods contain beta-carotene and other provitamin carotenoids, which get converted into vitamin A. These include green leafy and yellow vegetables, carrots, and deep- or bright-colored fruits. Once consumed, Vitamin A is hydrolyzed by pancreatic and intestinal enzymes, emulsified with dietary fats and bile acids, and absorbed in the duodenum. The liver stores 80-90% of the body’s vitamin A in hepatic stellate cells, and the remainder is stored in adipose tissue and the pancreas. Stored vitamin A is released into the circulation bound to prealbumin (transthyretin) and retinol-binding protein. Disruption in any of these processes can lead to VAD [5] .

The recommended dietary allowance of vitamin A is 700ug/day in females and 900ug/day in the males. For children and pregnant or lactating women, the recommended amount is 300-900, 770, and 1300ug/day, respectively. Children aged 1-5 years old require a minimum of 200ug/day to prevent symptomatic VAD [5] .

In the eye, Vitamin A is essential for maintenance of conjunctival and corneal epithelia as well as night vision. VAD causes metaplasia and keratinization of mucus-secreting epithelium, which can cause conjunctival and corneal xerosis, corneal ulcers, keratomalacia, and corneal scarring. Rods are the retinal photoreceptor that is responsible for night vision. Rods have a singular photopigment, rhodopsin. Retinol is a vitamin A-derived cofactor that is required for the formation of rhodopsin; thus, VAD leads to impairment of rod function and causes nyctalopia, or night blindness due to the eye’s inability to adapt from light to dark [7] .

Clinical Signs [8]

Night blindness (Grade XN): Defective vision in dim light or night blindness is one of the most common manifestations of VAD, especially in children age 2-6 or pregnant or lactating women. Although it is considered one of the earliest manifestations, children with VAD may develop one of the more severe signs, such as corneal ulcers, after infection or diarrhea without any of the classically early signs. Children may not be able to verbalize their symptoms, and parents need to be asked if they have noticed their children behaving differently in the dark, e.g. becoming less active or fearful. Night blindness is considered to be both a sensitive and specific indicator for serum retinol levels.

no xerophthalmia meaning

Conjunctival xerosis (Grade X1A): Conjunctival xerosis is characterized by a dull and dry appearance of the conjunctiva with slight wrinkling. It is caused by the loss of goblet cells and insufficient mucin secretion, and it can be subtle and difficult to detect clinically.

no xerophthalmia meaning

Bitot spots (Grade X1B): Bitot spots are collections of desquamated, keratinized epithelial cells mixed with the gas-forming bacteria Corynebacterium xerosis. They appear as triangular patches of foamy, whitish, opaque deposits, typically located on the bulbar conjunctiva near the limbus at the 3 and 9 o’clock positions. They are more common temporally.

no xerophthalmia meaning

Corneal xerosis (Grade X2): Conjunctival xerosis is characterized by a dull and hazy appearance of the cornea that is caused by drying of the cornea secondary to conjunctival gland dysfunction. It may initially present with bilateral punctate corneal epithelial erosions, and it can quickly progress to the stage of corneal ulceration. Up to this stage, high-dose Vitamin A supplementation can result in the full preservation of vision.

Corneal ulceration (Grade X3A and B): Corneal xerosis can lead corneal ulceration and melting if not treated urgently. Keratomalacia, the melting away of the cornea by liquefactive necrosis, is the most severe form of xerophthalmia. It can perforate and destroy the cornea in just a matter of days. A child who appears relatively healthy but develops keratomalacia should be questioned about a recent history of measles or diarrhea, which could rapidly deplete already deficient vitamin A stores.

Corneal scar (Grade XS): Corneal scarring due to VAD is often symmetric and bilateral. Other causes of corneal scarring must be ruled out.

Xerophthalmic fundus (Grade XF): prolonged VAD can lead to structural changes in the retina. Fundus changes appear as small, white, deep retinal lesions scattered throughout the posterior pole.

Grading System

The World Health Organization (WHO) has a grading system for xerophthalmia as seen in the following table [9] . More detailed descriptions of the clinical signs of Xerophthalmia are below.

Patients presenting with clinical signs of xerophthalmia (or, in the case of a pediatric patient, their parents) must be questioned on dietary, medical, and social history, including alcohol intake. Be sure to ask about any malabsorptive process, as described above, or risk factors such as living in a resource-poor country or current pregnancy or lactation. Because xerophthalmia is a manifestation of moderate-to-severe VAD, it is important to ask about the systemic signs of milder VAD, including frequent GI and respiratory tract infections, anemia, iron deficiency, and development of xeroderma and phrynoderma (follicular hyperkeratosis often found on extensor surfaces, shoulders, and buttocks) [10] [7] .

Physical exam

Aside from the ocular exam, the physical exam should include assessments for weight/body habitus, jaundice, and abdominal exam for hepatomegaly.

Blood tests [11]

Other testing [5] [12]

Differential Diagnosis

Keratomalacia should be treated as a medical emergency, as it is an indicator of very severe VAD. High-dose vitamin A is the treatment for all patients, and treatment can either be oral or intramuscular. Recommended Vitamin A deficiency treatment regimens are described in the following table [13] . Treatment can be adjusted as needed based on regular serum retinol level monitoring

Patients with concomitant zinc deficiency should also undergo zinc supplementation. VAD associated with malabsorptive or other processes is treated based on the severity of deficiency and provider discretion, usually involving daily treatment.

Localized ocular treatment includes intense lubrication, topical retinoid acid, and management of perforation.

Patient education is a large component of management, and patients and their families should be educated on dietary sources of vitamin A and well-balanced, nutrient-rich diets. Alcohol abuse should be addressed if applicable. In resource-poor countries, large-scale vitamin A supplementation programs are in place.

Xerophthalmia signifies a severity of VAD that can cause mortality from malnutrition and increased susceptibility to mucosal infections. Nearly 2/3 of children with keratomalacia die within months. Mortality in children with night blindness is triple the mortality found in children with subclinical VAD, and mortality in children with both Bitot spots and night blindness is reported to be nine times that of children with subclinical VAD [9] .

With prompt treatment of high-dose vitamin A, the early ophthalmologic signs, such as a rod function, conjunctival xerosis, and night blindness, can resolve completely within about 2 months of supplementation, without long-term sequelae [14] [15] . Corneal xerosis and ulceration may also improve; however, they can lead to scarring and permanent vision loss [5] .

no xerophthalmia meaning

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Xerophthalmia: Findings from the Eye Lead to Diagnosis of a Fatal Intestinal Disease

Beril tulu aygun.

1 Department of Ophthalmology, University of Health Sciences Beyoglu Eye Training and Research Hospital, Istanbul, Turkey

Burcin Kepez Yildiz

Deniz ogutmen koc.

2 Department of Gastroenterology, University of Health Sciences Gaziosmanpasa Taksim Training and Research Hospital, Istanbul, Turkey

Yusuf Yildirim

Vitamin A has an essential role in the maintenance of corneal and conjunctival epithelization, as well as photoreceptor transduction in the retina. A deficiency of vitamin A causes keratinization of the surface epithelium, and night blindness is often the first symptom. This report describes a case of chronic intestinal pseudo-obstruction (CIPO), a rare and potentially fatal disease, diagnosed following detection of a vitamin A deficiency in an ophthalmological examination. A 25-year-old female patient presented with a 3-month history of dryness, a burning sensation, and decreased vision, especially at night, in both eyes. She appeared cachectic and ill, and reported having lost 10 kg in the previous year. An ophthalmological examination revealed conjunctival and corneal keratinization in addition to punctate keratopathy with xerosis in both eyes, which raised the suspicion of a vitamin A deficiency. Her serum vitamin A level confirmed the diagnosis, and she was referred to the gastroenterology clinic, where she was diagnosed with CIPO and treated with parenteral multivitamin supplementation. A vitamin A deficiency should be suspected in patients with malnourishment and xerosis. Rapid diagnosis and treatment can be life-saving in cases with a severe underlying pathology.

Introduction

Vitamin A is a lipid-soluble vitamin absorbed from the intestinal lumen and stored in the liver, and it is crucial for a healthy immune system, skin, ocular surface, and retina. It has an essential role in maintenance of corneal and conjunctival epithelization, as well as photoreceptor transduction in the retina ( 1 ). A deficiency of vitamin A causes keratinization of the surface epithelium, and night blindness in particular, which is a first symptom ( 2 ).

Detection of even mild ocular signs indicating xerophthalmia (Bitot’s spots, xerosis) should alert ophthalmologists to consider a vitamin A deficiency and to seek a gastroenterology consultation in order to reveal the underlying cause, which could be a life-threatening disorder.

This is a report of a case diagnosed with a rare and potentially fatal disease, chronic intestinal pseudo-obstruction (CIPO), following detection of a vitamin A deficiency in an ophthalmological examination and referral to a gastroenterology clinic.

Case Report

A 25-year-old female patient presented at our outpatient clinic with a 3-month history of dryness, a burning sensation, and decreased vision, especially at night, in both eyes. The patient had been referred to us after visiting 2 other university clinics. Topical artificial tear drops and topical cyclosporin treatments had not been beneficial. Her medical history included episodes of vomiting, diarrhea, and considerable weight loss in the previous 3 months. She appeared cachectic and malnourished, and reported feeling exhausted.

The ophthalmological examination revealed a best corrected visual acuity of 20/320, conjunctival and corneal keratinization, and punctate keratopathy with xerosis in both eyes, which raised the suspicion of a vitamin A deficiency ( Fig. 1 ). An analysis of the patient’s serum vitamin A level was ordered, and the result was 0.04 µg/dL (normal range: 30-80 µg/dL). In order to verify the ocular diagnosis, a conjunctival biopsy was performed the next day, and the pathology report revealed diffuse keratinization of the conjunctival epithelium, which is consistent with the clinical diagnosis of xerophthalmia.

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Biomicroscopic view at presentation. (a) Paralimbal corneal and conjunctival keratinization; (b) Bitot’s spot at the temporal conjunctiva.

Following the initial examination, without waiting for the biopsy results, topical retinol palmitate ointment to be applied 3 times a day was added to the existing treatment of topical, preservative-free, artificial tear drops and topical cyclosporine. An urgent referral to the gastroenterology clinic was also arranged for a systemic evaluation and parenteral vitamin A administration.

Upon further investigation at the gastroenterology clinic, the patient disclosed a history of 10 years of intermittent stomachache and constipation relieved after attacks of vomiting and diarrhea for 2 days. She had lost 10 kg in the prior year, and had experienced amenorrhea for the previous 5 months. Her workup revealed a dilated duodenum, air-fluid levels at the intestines, no peristalsis in the esophagus or stomach, and no intestinal obstruction. A rheumatological evaluation yielded no results related to connective tissue diseases. An explorative laparotomy was performed after the patient had an attack of vomiting, hypotension, fever, and distention in the abdomen on the third day of admittance to the gastroenterology service. No mechanical obstruction was found, which concluded in a diagnosis of CIPO. The patient’s ocular pathology of xerophthalmia was attributed to the intestinal malabsorption of vitamin A due to CIPO.

The patient was admitted to the gastroenterology clinic on the day of presentation, and an intravascular multivitamin complex treatment, which includes 3500 IU vitamin A along with vitamins B through E was initiated, since a systemic (oral or parenteral) form of vitamin A alone is not commercially available in Turkey. Additionally, parenteral nutrition and prokinetic drugs were administered. The patient received an intravascular multivitamin treatment daily for 12 days, and was discharged with recommendations for an oral liquid diet and oral multivitamin complex supplementation.

At the 1-month follow-up examination, the patient had no symptoms of dryness or stinging. Additionally, she reported feeling stronger and looked in better general health. Although still not within the normal limits, the serum vitamin A level of the patient had increased significantly to 11.8 µg/dL. An ophthalmological examination indicated improved visual acuity to 20/32, and the corneal and conjunctival keratinization had substantially decreased in both eyes ( Fig. 2 ). A fundus examination, which was suboptimal in the initial presentation due to corneal distortion, did not show any pathologies. An electroretinogram (ERG) was ordered in order to evaluate photoreceptor function at the 1-month visit and revealed normal results. At her 3-month visit, the patient continued to report no ocular symptoms, and a biomicroscopic examination showed no signs of Bitot’s spot or corneal keratinization ( Fig. 3 ).

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The 1-month follow-up examination results. Note the decrease in the size of the Bitot’s spot findings. (a) Right eye; (b) Left eye.

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The 3-month follow-up examination results. There were no signs of corneal or conjunctival keratinization. (a) Right eye; (b) Left eye.

Vitamin A deficiency is uncommon in developed countries; however, there are reports in the literature describing cases that occurred related to eating disorders ( 3 ), bariatric surgery ( 4 ), and intestinal or liver disorders ( 4 , 5 ) where either severe malnourishment or malabsorption is evident. CIPO is a rare and severe pathological condition, frequently misdiagnosed due to its rarity and limited awareness, and is often associated with a poor outcome ( 6 ). Often, there is a long history of severe, non-specific digestive symptoms followed by an acute, exacerbating sub-occlusive attack ( 7 ). In this case, the diagnosis of a rare ocular disease led to the diagnosis of a rare and potentially fatal chronic intestinal disease, which had been symptomatic for almost half of the lifetime of the patient. This case is an example of how it is crucial to consider patient’s full medical history and systemic complaints, and to investigate any underlying pathology.

In addition to topical treatment of xeropthalmia, systemic supplementation is also necessary in cases of a vitamin A deficiency. The World Health Organization recommends 100.000 IU vitamin A intramuscularly for severe corneal disease or malabsorption ( 8 ). In our country, no isolated systemic vitamin A supplementation is commercially available; only multivitamin complexes including vitamins A through E are offered, which was therefore the choice of treatment for our patient. Since our patient required substantial supplementation other than vitamin A, the gastroenterology physicians made the choice to administer the multivitamin complex intravenously, rather than intramuscularly. Since parenteral nutrition had been initiated during the admittance for CIPO treatment, the multivitamin complex was continued intravenously, and then replaced with oral supplementation at discharge, together with an oral feeding recommendation limited to liquid or homogenized food.

Following the initiation of vitamin A therapy, both night blindness and ocular surface symptoms are expected to resolve in days to weeks ( 1 ), as occurred in our patient’s case. At the end of the first month, she reported no ocular symptoms, and felt much more energetic, even though she needed further treatment and nutritional support for CIPO. An ophthalmological examination supported this improvement of ocular surface symptoms. In order to evaluate photoreceptor function, an ERG was ordered at this visit, which resulted in normal findings, as could be anticipated, given reports in the literature that after 10 days of vitamin supplementation, all ERG parameters are expected to return to normal ( 9 ). The improvement of her symptoms with multivitamin supplementation might suggest that it is an alternative option in places where an isolated form of vitamin A is not available, such as Turkey.

Without sufficient awareness, CIPO or vitamin A deficiency leading to xerophthalmia may not be easily recognizable in a metropolitan area. The purpose of this report is to remind physicians in different specialties that rare diseases do exist, and it is essential to meticulously and comprehensively evaluate patients in order to make the right diagnosis and eventually to suggest the correct treatment, which could affect the prognosis of the patient. The rapid diagnosis of vitamin A deficiency and proper referral of patients to determine and treat the underlying pathology can prevent morbidity and mortality, though this might be an additional challenge in cases with a rarely encountered intestinal disease such as CIPO.

Informed consent: Written informed consent was obtained from the patient for the publication of the case report and the accompanying images.

Peer-review: Externally peer-reviewed.

Conflict of Interest: None declared.

Authorship Contributions: Involved in design and conduct of the study (BTA, BKY, YY, DOK); preparation and review of the study (BTA, BKY, YY, DOK); data collection (BTA, YY).

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Xerophthalmia

The term ‘xerophthalmia’ means ‘dryness of the eye,’ i.e., of the cornea and conjunctiva.

From: Encyclopedia of Food Sciences and Nutrition (Second Edition) , 2003

Related terms:

John F. Salmon MD, FRCS, FRCOphth , in Kanski's Clinical Ophthalmology , 2020

Introduction

Vitamin A is essential for the maintenance of the body's epithelial surfaces, for immune function and for the synthesis of retinal photoreceptor proteins. Xerophthalmia refers to the spectrum of ocular disease caused by inadequate vitamin A intake and is a late manifestation of severe deficiency. Lack of vitamin A in the diet may be caused by malnutrition, malabsorption, chronic alcoholism or by highly selective dieting. The risk in infants is increased if their mothers are malnourished and by coexisting diarrhoea or measles.

A World Health Organization (WHO) grading system is set out in Table 7.7 .

Symptoms are night blindness (nyctalopia), discomfort and loss of vision.

Xerosis is characterized by dryness of the conjunctiva in the interpalpebral zone with loss of goblet cells, squamous metaplasia and keratinization.

Bitot spots are triangular patches of foamy keratinized epithelium ( Fig. 7.41A ) in the interpalpebral zone thought to be caused by Corynebacterium xerosis.

Lustreless appearance due to secondary xerosis.

Bilateral punctate corneal epithelial erosions in the interpalpebral zone can progress to epithelial defects but are reversible with treatment.

Keratinization.

Sterile corneal melting by liquefactive necrosis (keratomalacia), which may lead to perforation ( Fig. 7.41B ).

Retinopathy , characterized by yellowish peripheral dots, may occur in advanced cases and is associated with decreased electroretinogram amplitude.

Keratomalacia is an indicator of very severe vitamin A deficiency and should be treated as a medical emergency due to the risk of death, particularly in infants.

Systemic treatment involves oral (oil-based 200 000 IU) or intramuscular (aqueous-based 100 000 IU) vitamin A for keratomalacia. Multivitamin supplements and dietary sources of vitamin A are also administered.

Local treatment consists of intense lubrication, topical retinoic acid and management of perforation.

Autoimmune and Inflammatory Disorders

Russell E. Bartt , Jordan L. Topel , in Textbook of Clinical Neurology (Third Edition) , 2007

Xerophthalmia can be demonstrated by Schirmer's test, staining of the corneal and conjunctival epithelium by rose bengal dye, or demonstration of epithelial strands by slit‐lamp examination. Xerostomia can be assessed by nuclear scanning of the salivary glands, radiological sialography, or calculation of salivary flow rate. Biopsy of minor salivary glands, found on the inner aspect of the lower lip, is well tolerated and diagnostic when lymphocytic aggregation is demonstrated. Anemia, leukopenia, and elevated ESR are common. Hypergammaglobulinemia and positive RF are common but not specific for the diagnosis. SS‐B antibodies are relatively specific for primary SS. SS‐A antibodies are seen in primary SS and SS associated with SLE. Half of SS patients have antibodies against salivary duct antigens.

The EEG is abnormal in nearly 50% of patients with CNS dysfunction, but the findings are nonspecific. CT and MRI scans usually show focal regions of abnormality in patients with clinical evidence of focal disease. Electrophysiological studies are consistent with demyelination, denervation, or both. CSF may be normal or may show pleocytosis and elevated protein. CSF is characterized by protein elevation and evidence of intrathecal immunoglobulin synthesis, with increased IgG and oligoclonal bands. 122 Pathological studies are limited, but perivascular inflammation and diffuse vasculitis involving the cerebral blood vessels, as well as acute necrotizing arteritis of the spinal cord, have been described. 126 Peripheral nerve tissue shows demyelination and acute or chronic vasculitis or perivasculitis. 127 Dorsal root ganglionitis, with lymphocytic infiltration and degeneration of ganglion cells, has also been reported to accompany subacute sensory neuronopathy, which is a rare complication of SS. 128

X – Differential Diagnosis

Fred F. Ferri MD, FACP , in Ferri's Clinical Advisor 2022 , 2022

Xerophthalmia 71

Tricyclic antidepressants: amitriptyline, doxepin.

Antihistamines: diphenhydramine, chlorpheniramine, promethazine, and many cold and decongestant preparations.

Anticholinergic agents: antiemetics such as scopolamine, antispasmodic agents such as oxybutynin chloride.

Abnormalities of Eyelid Function

Neuromuscular disorders.

Thyrotoxicosis.

Abnormalities of Tear Production

Hypovitaminosis A.

Stevens-Johnson syndrome.

Familial diseases affecting sebaceous secretions.

Abnormalities of Corneal Surfaces

Scarring from past injuries and herpes simplex infection.

Vitamin A: Deficiency and Interventions

K.P. West Jr , in Encyclopedia of Human Nutrition (Third Edition) , 2013

Corneal Xerophthalmia

Corneal xerophthalmia is manifested in severe VA deficiency. The earliest corneal lesions appear as superficial punctate defects, evident with a slit lamp, that with advanced deficiency become more numerous and concentrated. The cornea is considered xerotic (X2) when the keratopathy covers large areas of its surface rendering a hazy, nonwetable, lusterless, and irregular appearance on handlight examination. Stromal edema may be present. In more severe cases, thick, elevated X2 plaques may form. Usually both eyes are affected. X3A can be sharply demarcated, round, or oval defects that are usually shallow but may also perforate the cornea. Healed ulcers form a leukoma (scar) or adherent leukoma if the iris has plugged the perforated ulcer. Most ulcers occur peripheral to the visual axis and, thus, may not threaten central vision if treated in time. X3B refers to a full-thickness softening and necrosis of the corneal stroma that can cause protruding, opaque, yellow-to-gray lesions to form ( Figure 2 ) . These may reduce or slough off leaving a descemetocele following VA treatment. X3B usually impairs vision in the involved eye although the degree of visual loss depends on the location, thickness, and extent of corneal necrosis and the resultant scar. Owing to the generally malnourished and ill state of children with corneal xerophthalmia, fatality of hospitalized cases ranges from 4% to 25%.

no xerophthalmia meaning

Figure 2 . Keratomalacia.

Vitamin A Deficiencies and Excess

Robert M. Kliegman MD , in Nelson Textbook of Pediatrics , 2020

Clinical Manifestations of Vitamin A Deficiency

The most obvious symptoms of vitamin A deficiency are associated with changes in epithelial cell morphology and functions. In the intestines, mucus-secreting goblet cells are affected, and loss of an effective barrier against pathogens can cause diarrhea or impairment of epithelial barrier function. Similarly, mucus secretion by the epithelium is essential in the respiratory tract for the disposal of inhaled pathogens and toxicants. Characteristic epithelial changes result from vitamin A deficiency, including proliferation of basal cells, hyperkeratosis, and formation of stratified cornified squamous epithelium. Squamous metaplasia of the renal pelves, ureters, vaginal epithelium, and the pancreatic and salivary ducts can lead to increased infections in these areas. In the urinary bladder, loss of epithelial integrity can result in pyuria and hematuria. In the skin, vitamin A deficiency manifests as dry, scaly, hyperkeratotic patches, typically on the arms, legs, shoulders, and buttocks. The combination of defective epithelial barriers to infection, low immune response, and lowered response to inflammatory stress, all from insufficient vitamin A, can cause poor growth and serious health problems in children.

The most characteristic and specific signs of vitamin A deficiency are eye lesions, but these may manifest rather late in the progression of vitamin A deficiency, develop insidiously, and rarely occur before age 2 yr. An earlier symptom of vitamin A deficiency is delayed dark adaptation, as a result of reduced resynthesis of rhodopsin; this may progress to night blindness . Photophobia is a common symptom. The retinal pigment epithelium (RPE), the structural element of the retina, undergoes keratinization. When the RPE degenerates, the rods and cones have no support and eventually break down, resulting in blindness.

As vitamin A deficiency progresses, the corneal and conjunctival epithelial tissues of the eye become severely altered because of a lack of sufficient RA for normal epithelial cell differentiation. The cornea protects the eye from the environment and is also important in light refraction. Stages in vitamin A deficiency include corneal keratinization and opacity, susceptibility to infection, and formation of dry, scaly layers of cells ( xerophthalmia ) ( Figs. 61.3 and 61.4 ) . The conjunctival membrane undergoes keratinization and may develop foamy-appearing plaques ( Bitôt spots ; Fig. 61.5 ). When lymphocytes infiltrate the cornea in later stages of infection, it degenerates irreversibly ( keratomalacia and corneal ulceration ), resulting in irreversible blindness. These eye lesions are primarily diseases of the young and are a major cause of blindness in developing countries. Although rates of xerophthalmia have fallen, the number of affected children is still too high. Treatment with vitamin A, up to the stage of keratomalacia, is effective in rapidly repleting the individual and saving vision.

Vitamin A Deficiency and Its Prevention

Susanne H. Wedner , David A. Ross , in International Encyclopedia of Public Health (Second Edition) , 2017

Treatment of VAD

Children with xerophthalmia , measles or severe protein-energy malnutrition should be treated with high dose vitamin A ( WHO/UNICEF/IVACG, 1997 ). Children should receive 50 000 IU if they are below 6 months, 100 000 IU if they are between 6 and 12 months, and 200 000 IU if they are older than 12 months. For xerophthalmia, this dosage is recommended three times (on days 1, 2, and 14–30), for measles twice (on successive days), and for severe protein-energy malnutrition once. Although extremely uncommon except in famine situations, adolescents or adults with severe xerophthalmia (i.e., corneal xerosis or ulcer) should receive three doses of vitamin A (as above) as a medical emergency. This even applies to women, in whom the increased risk of teratogenesis in the fetus if the woman is in the early stages of pregnancy is far outweighed by the substantial risk of blindness in the mother.

HYPOVITAMINOSIS A

V. Reddy , in Encyclopedia of Food Sciences and Nutrition (Second Edition) , 2003

Treatment of Xerophthalmia

All individuals with xerophthalmia (except pregnant women) should be treated with large oral doses of 200 000 IU vitamin A according to the WHO guidelines ( Table 4 ). The age-specific dose should be given on the first and second days and again 2 weeks later. This applies to all stages of active xerophthalmia, including night blindness, Bitot's spots, and corneal lesions. Corneal xerophthalmia is a medical emergency and should be treated immediately on diagnosis and then patients should be referred to a hospital for further treatment as they often present complex problems. Topical application of antibiotic ointment (tetracycline or chloramphenicol) is recommended for corneal lesions to prevent secondary infection. In addition, patients should be provided nutritional support and medical therapy.

Table 4 . Treatment of xerophthalmia

Three doses: on diagnosis + next day + 2 weeks later.

Corneal xerosis shows improvement within a week but in more advanced cases (corneal ulcer/keratomalacia), healed scars remain as white opacities, resulting in partial or total blindness. Night blindness responds in a couple of days while Bitot's spots take 3–10 days and some may persist, particularly in older age groups.

Pregnant women should be treated with small doses of vitamin A, not exceeding 10 000 IU daily or 25 000 IU weekly, for about a month. Large doses of vitamin A should be avoided during pregnancy to avoid the risk of teratogenicity.

Why Test BCG in Sjögren’s Syndrome?

Tor Paaske Utheim MD, PhD , in The Value of BCG and TNF in Autoimmunity , 2014

7.3 Symptoms and Signs

Dry eyes ( xerophthalmia ) and dry mouth (xerostomia) are especially frequent symptoms in SS patients. 6 The causes of xerophthalmia can be subdivided into aqueous-deficient and evaporative, with SS belonging to the first group ( Figure 7.2 ). Xerophthalmia can lead to eye infections and corneal ulcerations, whereas hyposalivation can result in dental caries and oral infections. Parotid swelling is a typical, but rare, trait. Dryness of other structures such as the skin, nose, throat, and vagina are also common. 7

no xerophthalmia meaning

Figure 7.2 . The causes of dry eye disease can broadly be divided into aqueous-deficient and evaporative. SS belongs to the first category.

About half of SS patients develop systemic involvement, either before or after pSS is diagnosed. 8 As many as 70% of patients experience fatigue, which, for some, can be crippling. The quality of life is found to be reduced in patients with SS. 9,10 Almost half of pSS patients have various cutaneous presentations (e.g., angular cheilitis, dry skin, Reynaud’s phenomena, purpura, maculopapular lesions, or urticarial manifestations). 11 Several neurological manifestations can occur, the most common being sensory polyneuropathies. 2,12 Effects on the peripheral nervous system are more frequent than involvement of the central nervous system (CNS). However, CNS involvement can lead to seizures, optic neuritis, encephalopathy, and dementia. 13

A number of organs can be affected in SS. Patients often present with lung abnormalities, 14 including irritating dry cough due to dryness of the tracheobronchial mucosa, 15 dyspnea secondary to small airway obstruction 16 , and increased bronchial responsiveness. 17 Autoimmune thyroiditis affects up to one-third of patients 6 and often manifests as hypothyroidism. Effects on the liver can include hepatomegaly and autoimmune hepatitis (rare). Autoimmune cholangitis develops in less than 10% of patients. Kidney involvement is usual, especially interstitial nephritis. 18 Gastrointestinal features include dysphagia, nausea, and/or epigastric pains, often due to dryness and/or dysmotility. Many patients with SS experience arthralgia and myalgia. Arthritis occasionally occurs, although it is typically mild and without erosion of the joints. 19 In one study, SS was found to increase the likelihood for non-Hodgkin B-cell lymphoma development by as much as 44 times 20 , and up to 5% of patients with SS will eventually develop non-Hodgkin B-cell lymphomas. 21 A chronic antigenic drive is thought to select B cells for neoplastic transformation. 22 Most patients with SS who develop lymphoma have a good prognosis, but some progress to disseminated disease. 23 The parotid gland is the most common site of lymphoma in SS.

Neuroparasitology and Tropical Neurology

Gustavo C. Román , in Handbook of Clinical Neurology , 2013

Vitamin A deficiency

Vitamin A deficiency causes xerophthalmia (Greek, xeros dry + ophthalmos eye); this vitamin is critical for synthesis of corneal and conjunctival epithelial cell RNA, glycoproteins, and retinal; the latter combines with both rod and cone opsins to form rhodopsin. The earliest clinical manifestation of vitamin A deficiency is night blindness due to lack of rhodopsin in retinal rods; children get lost at night or stumble into objects in the dark. Progressive conjunctival xerosis is manifested by dry and thickened conjunctiva resulting in Bitot spots, i.e., the accumulation of keratin and debris with a cheesy or foamy appearance on the temporal side of the conjunctiva ( Fig. 30.6 ). Xerophthalmia progresses to corneal xerosis that may lead to corneal ulceration, keratomalacia, and permanent blindness ( Smith and Steinemann, 2000 ).

no xerophthalmia meaning

Fig. 30.6 . Vitamin A deficiency causes xerophthalmia and night blindness. The typical lesion is called Bitot spot and is characterized by accumulation of keratin and debris with a cheesy or foamy appearance on the temporal side of the conjunctiva.

Vitamin A deficiency also has a negative effect on metabolic and immune functions, worsening morbidity and mortality in children. Supplementation of vitamin A in endemic areas results in 23–30% reduction in mortality rates for children aged 6 months to 5 years ( Gogia and Sachdev, 2011 ); in particular, vitamin A contributes to attenuate the severity of diarrhea. Vitamin A is recommended also for the treatment of measles in children admitted to the hospital in areas with high case fatality ( D'Souza and D'Souza, 2002 ).

The recommended dose of vitamin A for lactating mothers should be 10 000 IU/day. A dietary intake of 1500 IU/day is recommended in the first year of life. Because of the common deficiency of multiple vitamins and minerals in children from endemic areas, a microcapsule technique has been used to create triple-fortified salt containing iodine, iron, and vitamin A.

The deficit of vitamin A has teratogenic effects and increases the susceptibility of laboratory animals to cancer. Likewise, an excess of vitamin A ( > 10 000 IU/day) during early pregnancy is teratogenic due to increased placental transfer and exposure to all-trans-retinoic acid affecting organogenesis and embryonic development ( Collins and Mao, 1999 ). Abnormalities include cleft palate, harelip, macroglossia, hydrocephalus, and malformations of the eyes.

Ophthalmology in the Tropics and Sub-tropics

Nicholas A.V. Beare , Andrew Bastawrous , in Manson's Tropical Infectious Diseases (Twenty-third Edition) , 2014

Eye Changes in Vitamin A Deficiency (Xerophthalmia)

The symptoms and signs of xerophthalmia are listed in Table 67.8 . Blindness results from bilateral severe corneal disease. In corneal xerosis (X2) the cornea appears dry and dull and may ulcerate due to epithelium break down (X3A). The cornea may melt dramatically (keratomalacia, X3B), with an acute onset, sometimes over a few hours. Children aged 1–3 years are particularly at risk. Keratomalacia usually leads to irreversible blindness from corneal scarring (XS) ( Figure 67.39 ).

Apart from vision loss, many children with severe VADD will die because they are susceptible to infections, such as respiratory infections and diarrhoea. If a child has vitamin A deficiency, others in the same family and community are also at risk.

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Everything You Need to Know About Xerophthalmia

Complications

Dr Katherine Duncan

Xerophthalmia is an eye condition that results from vitamin A deficiency. Symptoms include dry eyes, night vision difficulty, and lesions on the eyeball’s mucous membrane. Treatment for xerophthalmia can involve increasing your vitamin A intake or using artificial tears. Some people may require surgery.

According to the National Institutes of Health, vitamin A deficiency is one of the most common causes of preventable blindness in children. Promptly addressing a vitamin A deficiency is critical to preventing complications.

This article will explain xerophthalmia, including its symptoms and causes. It will also discuss the diagnostic and treatment methods for the condition.

What are the causes of xerophthalmia?

A person covering their eyes

Xerophthalmia results when you eat too little vitamin A. It can also happen if your body is unable to absorb the nutrient.

Vitamin A is essential for vision. It is a component of rhodopsin, an eye protein that enables you to see in dim light. It also helps keep the outside covering of your eyes clear.

Common sources of vitamin A include green leafy vegetables, meats, and fish.

Many factors can cause vitamin A deficiency, including:

What are the symptoms of xerophthalmia?

Xerophthalmia is a progressive condition . This means that without treatment, symptoms will typically get worse with time.

The progression usually happens as follows:

Contact your doctor if you have symptoms of xerophthalmia.

How do doctors diagnose xerophthalmia?

To diagnose xerophthalmia, your doctor will ask you questions related to your symptoms, medical history, and eating habits. They may also conduct a lab test to check the levels of vitamin A in your body.

Other possible tests include:

What are the treatments for xerophthalmia?

Xerophthalmia treatment typically focuses on increasing the levels of vitamin A in your body. Your doctor may give you vitamin A supplements by mouth or injection.

Your doctor may also recommend:

These treatments can typically relieve symptoms in the early stages. However, surgery may be necessary if you have developed corneal ulcers.

You may also require additional treatment for any underlying health conditions contributing to vitamin A deficiency.

What is the outlook for people with xerophthalmia?

Without treatment, xerophthalmia can have serious implications. Researchers estimate that only 4 in 10 people with corneal xerophthalmia survive, and many survivors become partially blind.

If you have symptoms consistent with xerophthalmia, it is essential to contact your doctor right away. Prompt treatment can help prevent complications.

What are some potential complications of xerophthalmia?

Besides maintaining eye health and vision, vitamin A also supports your immune system and protects your vital organs. Vitamin A deficiency can lead to various complications, including:

Can you prevent xerophthalmia?

You can help prevent xerophthalmia by preventing vitamin A deficiency. Start by eating foods rich in vitamin A , such as:

You may also wish to take vitamin A supplements. Be sure to consult your doctor before making these dietary changes.

Managing health conditions that contribute to nutritional deficiencies, such as celiac disease or chronic diarrhea, can help in preventing xerophthalmia.

Other frequently asked questions

Here are a few other commonly asked questions about xerophthalmia. Dr. Katherine Duncan has reviewed the answers.

Is xerophthalmia the same as night blindness?

Night blindness is a common symptom of xerophthalmia. Xerophthalmia results from a vitamin A deficiency, which can affect your ability to see in dim light.

Who is at risk for vitamin A deficiency?

According to experts , certain people may not be able to consume adequate amounts of vitamin A. In addition, some people cannot absorb the nutrient as needed. This can include people in developing countries, premature infants, or people with underlying conditions such as cystic fibrosis .

Xerophthalmia is an eye condition that results from vitamin A deficiency. Initial symptoms can include dry eyes , wrinkled eyeballs and eyelids, and night blindness.

To diagnose the condition, your clinician will ask questions related to your symptoms, medical history, and eating habits. They may also run tests to assess your eye health and check the levels of vitamin A in your body.

Treatments focus on increasing the levels of vitamin A in your body and managing your symptoms. This may involve vitamin A supplementation, preservative-free artificial tears, and antibiotics . You can reduce your risk of xerophthalmia by consuming more vitamin A-rich foods. You can also reduce your risk by managing underlying conditions that affect your body’s ability to absorb nutrients.

Schedule an appointment with your doctor if you have symptoms of xerophthalmia.

About the Author

Top Definitions

xerophthalmia

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The development of deficiency diseases (scurvy, rickets, xerophthalmia , rickets and malnutrition).

He'd have blubbered like any old ZeuglodonHad Xerophthalmia not come on.

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