Index
They are the accumulation of keratin located superficially in the conjunctiva of human eyes.
They can be oval, triangular or irregular in shape. The spots are a sign of vitamin A deficiency and are associated with drying out of the cornea .
It is a clearly defined gray or white lesion that affects the exposed portion of the bulbar conjunctiva. Often bilateral, it is based on the temporal limbus and its apex extends towards the lateral canthus.
The raised, dry, and dull surface of the Bitot stain is distinctively foamy in appearance.
The white deposit consists of keratin, which the conjunctiva begins to produce because the deficiency has led to “squamous metaplasia,” and the cells of the conjunctiva look more like skin than mucous membrane.
To some extent, the white foamy material can be cleaned from the surface of the conjunctiva, but it does not go away completely, even after vitamin A deficiency has been treated.
As such, Bitot’s spot may be accompanied by night blindness or be followed by extensive xerosis of the conjunctiva, xerosis of the cornea, and keratomalacia.
However, there is a great deal of evidence showing that a vitamin A deficiency is not the only cause of a Bitot’s spot.
Indian physician Dr. Caccamise had a patient in Rochester, New York, with a subtle Bitot spot due to a patch of conjunctival xerosis and no vitamin A deficiency.
For example, Bitot’s spots have been seen in patients with pellagra, a state of vitamin B deficiency.
Bitot’s stain consistency
The classic Bitot spot consists of whipped meibomia secretions and conjunctival debris with bacteria that adhere to a xerotic patch of the conjunctiva. Usually, but not always found temporarily.
It can be removed with a swab to reveal the underlying xerosis. It reforms quickly.
Why is Bitot’s point black?
In India, kohl, a powder of antimony or other black pigment in the form of a mask, is a preparation that is used as a cosmetic around the eyes, even in babies.
“My rural patients often said it was used to ward off the evil eye.” This is a blackened type of Bitot’s stain that has rarely been mentioned in an atlas.
History of Bitot’s spots
In 1863, the French physician Pierre Bitot (1822-1888) first described these points in 1863 in debilitated children, they are an important sign to diagnose vitamin A deficiency.
Bitot’s spots are dry-looking triangular patches of xerosified conjunctiva with a layer of foam on the surface, usually located temporarily on the cornea.
These lesions are not wet from the tear film. Bitot’s spots are more extensive than lesions caused by focal ocular surface conditions such as trachoma, burns, and pemphigoid.
The spots can diminish with replacement therapy. In ancient Egypt, this was treated with animal liver, which is where vitamin A is stored.
Vitamin A is a fat soluble vitamin that is made from a family of compounds called retinoids. Vitamin A deficiency can manifest with difficulty in night vision, dry skin, and hair.
While the most common cause of vitamin A deficiency (VAD) is malnutrition, any gastrointestinal disorder that causes lipid malabsorption can also lead to vitamin A deficiency.
Vitamin A deficiency can cause a variety of ocular manifestations, including night blindness, conjunctiva, and corneal xerosis and keratomalacia.
It is a major cause of preventable blindness. Although it is generally a result of malnutrition, vitamin A deficiency can accompany malabsorption syndrome.
Symptoms of bitot spots
Night blindness
This can affect children as well as pregnant and lactating women, and is one of the most common manifestations of deficiency. If vitamin A deficiency is prevalent in the community, there are often local names for it.
It is helpful to find out what these terms are so that they can be used when asking about night blindness. It is more difficult to find out if a child has night blindness, since children do not complain.
Mothers should be asked if they have noticed that their child behaves differently after the sun goes down or when they are in a dark room.
The child will become less active and fear moving. Night blindness tends to affect women who are pregnant or breastfeeding, and children ages 2 to 6.
Xerosis conjuntival
This presents as dryness of the conjunctiva and is another long-standing sign of deficiency. It can be quite difficult to detect and is therefore not a very reliable sign.
Sudden onset acute vitamin A deficiency leads to potentially blinding ocular signs and is associated with a very high mortality rate in children.
Xerosis corneal
This is drying of the cornea and is a sign of sudden and acute deficiency. The cornea becomes dry because the glands in the conjunctiva no longer function normally.
This leads to loss of tears and also loss of mucus, which acts as a ‘wetting agent’.
The lack of mucus along with the lack of tears not only leads to the dry appearance, but also increases the risk of infection.
corneal ulcer
If the acute deficiency is not reversed as a matter of urgency, the cornea may ulcerate and disappear. The ulcer may have the appearance of a small perforated area on the cornea, or the ulcer may have a spongier appearance.
In the absence of secondary infection, the eye may appear strikingly white; however, secondary infection of the ulcer is common, leading to an acutely inflamed eye.
keratomalacia
The most serious form of xerophthalmia is keratomalacia, in which more than a third of the cornea is affected. The cornea may become edematous and thickened, then melt away.
This occurs because the structure of collagen in the cornea is affected by a process known as necrosis. The cornea can be destroyed in just a few days.
Children with keratomalacia are often malnourished, but children who previously seemed relatively healthy can also develop keratomalacia after measles infection or bouts of diarrhea.
This is usually because they were vitamin A deficient and the measles infection caused their vitamin A stores to be depleted.
If you are not sure whether the child you are seeing has keratomalacia, ask about a recent illness, particularly measles.
Therefore, these signs do not necessarily mean that the child is currently deficient in vitamin A. Bitot’s spots usually appear in children aged 3 to 6 years.
Bitot’s spots that do not respond to vitamin A treatment are more common in school-age children.
Bitot’s spots pathophysiology
The lesion is due to keratinization of the conjunctival epithelium and is considered one of the classic characteristics of vitamin A deficiency.
Vitamin A is necessary for the development of normal epithelium, vitamin A deficiency causes Bitot’s spots through metaplasia of the conjunctival epithelium and keratin tangles mixed with Corynebacterium xerosis, which live in the stratum corneum of the conjunctiva.
The typical foamy appearance is due to the gas produced by these bacteria. Histologically, Bitot’s spots show keratinization, irregular maturation, inflammatory infiltration, and accumulation of gram-positive bacilli.
In developing countries, primary vitamin A deficiency is mainly caused by malnutrition, particularly by decreased consumption of provitamin carotenoids.
Pregnant and lactating women and young children are at the greatest risk, due to the higher nutritional demands. Also, in children with measles, vitamin A deficiency increases morbidity and mortality.
In developed countries, vitamin A deficiency is generally secondary to gastrointestinal disorders that cause malabsorption or impaired storage or transport of vitamin A, such as liver, intestine, or pancreatic disease.
The deficiency can also occur in people who follow strict vegetarian or vegan diets.
Causes of Bitot’s spots
The main underlying causes of vitamin A deficiency can be summarized as follows.
Reduced consumption
- Inadequate supply of food.
- Alcoholism.
- Mental illness.
- Dysphagia .
Impaired absorption
- Crohn’s disease.
- Celiac disease.
- Pancreatic insufficiency.
- Short bowel syndrome
- Chronic diarrhea.
Messy transportation
- Abetalipoproteinemia.
Reduced storage
- Liver disease
- Cystic fibrosis.
Role of zinc : Zinc deficiency may also be related to the pathogenesis of secondary vitamin A deficiency.
Inadequate zinc can depress hepatic synthesis of retinol-binding protein (RBP), which is necessary for the mobilization of retinol from the liver.
Additionally, zinc may play a role in the conversion of beta-carotene to retinol through the enzyme 15-15 dioxygenase.
Observe the intestines
Eponymous after Charles Bitot who first described them, Bitot’s spots represent an ocular manifestation of vitamin A deficiency.
Vitamin A deficiency is a major cause of preventable blindness in the developing world.
The clinical detection of Bitot’s spots offers an opportunity for the early diagnosis of vitamin A deficiency.
Although vitamin A deficiency may have disappeared in the developed world, the condition is still common in the developing world.
Since determination of serum retinol levels is not routinely available in ocular features ranging from night blindness, conjunctival xerosis, and corneal xerosis, Bitot’s spots and corneal ulceration and scarring can provide a clinical clue. for the diagnostic.
Lack of vitamin A affects the development of goblet cells in the conjunctiva resulting in the accumulation of keratin debris.
Bitot’s spots also demonstrate keratinization, irregular maturation, inflammatory infiltration, and accumulation of Gram-positive bacilli.
Generally seen as triangular spots, Bitot’s spots are usually tipped laterally and can have a variable surface area.
These can be cheesy, foamy whitish lesions and are the most common indicator used to estimate vitamin A deficiency in the community.
Bitot’s spots are generally due to nutritional deficiency, which is a common public health problem among preschool-age children in the developing world. Other conditions associated with systemic vitamin A deficiency may include:
A reduced intake (alcoholism, mental illness and dysphagia), disordered absorption (Crohn’s disease, celiac disease, pancreatic insufficiency and short bowel syndrome), disorderly transport (Abetalipoprotenemia) and reduced storage (liver disease).
Clinical detection of Bitot’s spots confirms vitamin deficiency. Confirmation can be made by estimating serum levels of retinol or retinol-binding protein.
Efforts should be directed at evaluating the cause of vitamin A deficiency, including reduced intake or any malabsorption state.
Evaluation
In addition to an eye exam, evaluation of a patient with Bitot’s spots involves a careful history, a general health exam, and laboratory investigations to determine the underlying cause.
In patients with Bitot’s spots, first assess malnutrition in the youngest age group and malabsorption in the elderly.
History
The physician should consult with the patient or guardian regarding aspects of medical or social history potentially associated with reduced intake or impaired absorption of vitamin A.
Relevant factors include age, diet, weight loss, alcohol intake, gastrointestinal disorders or surgery, and night blindness or other eye conditions.
General examination
This should include an evaluation of the patient’s constitution and weight, signs of jaundice, and abdominal palpation to rule out hepatomegaly.
Eye exam
The physician should look for possible subconjunctival fibrosis and simblepharon. The condition of the ocular surface can be evaluated by means of the Schirmer test, rose bengal or lysamine green staining and conjunctival impression cytology.
Blood test
Measurement of serum retinol-binding protein is relatively simple, inexpensive, has high specificity and sensitivity, and can be performed in less advanced laboratories. The reference range is 30 to 75 mg / L.
Serum vitamin A / retinol : the reference range is 30 to 80 μg / dL.
Serum zinc : the reference range is 75 to 120 μg / dL.
Bitot’s stain treatment
High-dose vitamin A is the treatment for all people with dry eye and for infants or children with severe malnutrition or measles.
The improvement of Bitot’s spots is observed within 2 weeks after the administration of a high dose of vitamin A.
However, the retinal manifestations of vitamin A deficiency are slower to respond to treatment, with night blindness and dark adaptation problems often persisting for 4 weeks.
