Pathology of corneal ulcers

2021-02-02 12:00 AM

Superficial keratitis can also be found in acute or chronic diseases of the eyelids and conjunctiva such as tear secretion disorder (dry eye), cleft palate, poisoning.


In terms of pathological anatomy, inflammatory lesions in the cornea are divided into two types of keratitis and corneal ulcer.

Keratitis: the phenomenon of inflammatory cells penetrating the layers of the cornea, there is no phenomenon of necrosis. Inflammation can be in the superficial layer (corneal epithelium) or the corneal parenchyma layer (deep keratitis).

Ulcerative corneal is the loss of substance of the corneal organs, forming a real ulcer.

Causes and risk factors

The cause of the illness

Causes of keratitis

Superficial keratitis: pathogens often caused by viruses such as Herpes, Zona, Adenovirus.

Superficial keratitis can also be found in acute or chronic diseases of the eyelids and conjunctiva such as tear secretion disorder (dry eye), cleft palate, poisoning.

Deep keratitis: the causative agent is usually in the bloodstream, possibly due to tuberculosis, syphilis, leprosy, virus, toxin.

Corneal ulcers

Bacteria: staphylococci, streptococci, pneumococcus, green pus bacillus.

Viruses: Herpes, zone.

Fungi: Aspergillus, Fusarium, Cephalosporin, mycelium, ...


Risk factors for corneal ulcers

Complications of trachoma: conjunctivitis, eyelash, eyelash, dry eyes.

Dry eyes due to lack vitamin A.

Nerve damage: nerve VII (open eyelid), menstrual V

Eye injury: causes corneal damage.

The anti-scientific eye treatment methods such as hitting buttocks with bamboo buds, and applying cigarettes to the eyes.

Due to wearing contact glasses.


According to Mac Donnell, there are 30,000 people with corneal ulcers every year in the US.

Keratitis and corneal ulcers cause vision loss and are a cause of blindness. The disease is common in the working age so it affects production (blue pus corneal ulcers are common in agricultural trauma).

In 1999, corneal ulcers accounted for 2.51% of the total number of patients treated at the Central Eye Hospital and 18.69% of the patients treated at the Corneal Department. The main pathogens are bacteria and fungi.




Subjective symptoms

The patient feels discomfort, eye strain, and foreign body sensation. Some patients experience dull aches and pains in the eyes, glare, photophobia, watery eyes, and blurred vision.

Physical symptoms

Superficial keratitis: visual examination often shows mild marginal erection. The cornea may be slightly blurred or have no damage. Examination of the cornea by microscopy (fluorescein staining), can show the corneal lesions:

Dot keratitis (shallow dot keratitis): epithelial clusters that are swollen and slightly raised on the normal corneal surface, clusters of epithelial cells can be seen as opaque white spots. Gray.

In the inflammation of the epithelium, the drug fluorescein stains very little, but pink Bengal can highlight cells damaged by the loss of mucus of the normal surface. The individual lesions can be concentrated or scattered. Fusing inflamed spots can form lines, stars, or branches.

Dot-like exfoliation: manifested as small, slightly concave spots due to loss of epithelial cells. These dots clearly capture the color of the fluorescein dye.

Deep keratitis:

Tuberculous keratitis: the tuberculosis bacteria that directly causes disease in the primitive cornea are very rare. Often secondary tuberculosis lesions: TB bacteria from primary tuberculosis in the body to cause disease in the cornea by two mechanisms:

Mechanism of metastasis: TB bacteria damage the cornea.

Allergic mechanism: allergic to toxins of tuberculosis bacteria.

Tuberculosis keratitis usually has the following forms:

Cystitis puffiness:

The disease usually appears in teenagers after getting the flu, measles, or whooping cough. Lesions on the cornea may be one or more yellow-white, tall blisters about 2 mm in diameter. There is an epithelial infiltration, neovascularization goes from the edge to surround the blister.

Systemic: the patient has tuberculosis lesions in the body (tuberculosis, intestinal tuberculosis).

Progression: The injury can penetrate deep into the cornea causing parenchymal keratitis. Sometimes blistering causes corneal thinning and corneal ulcers.

Parenchymal keratitis:

The disease appears silently, chronic.

Injury to the cornea: the layers of infected corneal parenchyma cells are gray-white. Infiltration is irregular, thick spots are scattered in clumps. The blood vessels are deep in the parenchyma, branching into small branches.

Progression: The disease usually lasts without a pronounced stage, and can cause inflammation of the blood vessels (veins).

Inflammation of the cornea of ​​the bud wall:

Lesions often appear on the infiltrative background of the parenchyma. Presents a denser infiltration area, gray-white, less neovascularized.

Progressive development lasts many episodes or relapses.


Injury to the cornea: the peripheral cornea has infiltration, presenting a gray-white area. Sclerosis is adjacent to the inflamed cornea, red erection.

Diseases often recur, easily causing complications of iritis.

TB membrane:

Blood membrane appears close to the edge, possibly mistaken for trachoma. Infiltration penetrates deep parenchymal layers. New vessels diffuse, dividing many branches deep into the parenchyma.

Lesions are usually localized in one eye, with no trachoma. There is tuberculosis in the sclera.

Keratitis caused by syphilis:

Usually, due to congenital syphilis, many people are from 7 to 20 years old.

Congenital syphilis usually manifests itself in both eyes. It is possible that both eyes appear to be sick (80%) or one eye is affected first and then the second eye.

Congenital syphilis keratitis progresses through three phases: infiltrative, neovascular, and regressive.

Infiltration stage:

Inflammation of the parenchyma above and precipitate behind the cornea. Infiltrates are widespread in the deep layers of the parenchyma. Infiltrates can be thin or dense, covering the pupil, causing rapid, severe vision loss. The epithelium has no lesions at first.

In the later stage, the entire cornea is opaque as a translucent glass due to infiltration, the cornea thickens due to edema.

The infiltration phase lasts from 4 to 8 weeks.

Phase with the new circuit:

New vessels appear from the edge into the parenchyma layer. The blood vessels spread throughout the cornea, making the cornea pink. If a few blood vessels can be localized in each area. The neovascular phase lasts from 6 to 8 weeks.

Degradation stage:

Infiltration gradually shrinks thin places; the infiltration center lasts longer. Small blood vessels, thinning, deep parenchyma may exist hollow vessels. Blood circulation decreased or stopped. The cornea gradually clears. Eyesight increased very little.

Systemic: the patient has congenital syphilis.

Oral signs: incisors are crossed with a V-shape (Hutchinson), incisors are strawberry-shaped, with an open palate.

Signs of ear, nose, and throat: stuffy nose, saddle shape, deafness, drowsiness.

Osteoarthritis signs: No sternum, tibial plateau, joint effusion.

Leprosy keratitis:

Usually appears late at the end of the leprosy stage. Injury to the cornea has three forms.

Corneal ulcers

Swollen lashes. The patient has difficulty opening eyes (signs of eyelid curl).

Marginal convergence: deep conjunctival blood vessels red accumulation around the cornea, fading towards the same map. Possible erection and edema of the entire conjunctiva.

The cornea is cloudy due to the inflammatory cell infiltration, the surface is shiny and rough. If there is an injury to the epithelium or ulcer: fluorescein (+) staining. There may be anterior purulent, iris-lashes.

Injury to the cornea may have one or more ulcers, the ulcer may be round or oval in shape; can be in the center or at the edge, can be small or wide almost all of the cornea.

Caused by bacteria: The damaged parenchyma, dense purulent inflammation, and surrounding edema. Necrotic parenchyma exfoliates creating a deep concave ulcer, the edge of the ulcer is jagged, the base of the ulcer often has dirty necrosis with mucus secretions attached.

Green pus-associated ulcers usually progress very quickly. After only 1-2 days, the ulcer has spread, the infiltrates diffusely in the parenchyma and rapidly develops into a yellow abscess that occupies most or even the entire cornea.

Causes of fungi: the ulcer is usually thick, the surface is dry and around the ulcer often has satellite infiltration foci, possibly with an immune ring image that surrounds the inflammation. The ulcer margin is usually neat and clearly defined. The ulcer is covered with a thick layer of dry, dirty grey necrosis that is high on the surface of the cornea. Pus appeared, then disappeared, then reappeared

Figure: Bacterial corneal ulcers - Fungal corneal ulcers

Viral causes: ulcers are often twigging or maps, reduced or lost corneal sensation. The disease or recurrence is often caused by the Herpes virus or shingles.

Corneal ulcers caused by the herpes virus

Testing: Taking the ulcer secretion or slightly curling the edge of the ulcer for microbiological testing: fresh, direct microscopy. Then cultured bacteria and made an antibiotic. In the case of ulcerative keratitis due to viruses, cytological tests are required.

Progression and complications:

If the ulcer is superficial and the ulcer is small, the prognosis is generally good.

If the ulcer is extensive, strong necrosis, especially fungal ulcers, the prognosis is bad.

Possible complications are loss of corneal substance that causes Cartesian swelling, corneal perforation, iritis of the eyelids, endocarditis.


In the community

Detecting corneal ulcer patients: Reduced vision in one eye or both, red eyes, cornea cloudy, concave.

In a specialist hospital

Based on clinical and subclinical symptoms (fresh microscopy test, direct microscopy, the culture of bacteria as an antibiotic).

The principles of treatment

In the community

Vision measurement.

Antiseptic or antibiotic look up: Acgyrol 3- 10%, Thimerosal 0.03%, Betadine 5% or Chloramphenicol 0.4%, Oflovid ...

Transfer the patient to the hospital.

Do not use corticosteroids (Polydexa, Dexaclo).

In a specialist hospital

Internally medical treatment

Treatment of corneal ulcers, whatever the cause, follows the general principle:

Specific anti-inflammatory (antibiotic) and nonspecific (non-steroidal anti-inflammatory).

Bacterial corneal ulcers: antibiotics are required depending on the cause or broad-spectrum (Oflovid, okacin, gentamycin, ...)

Viral corneal ulcers: need to use specific antiviral drugs (Triherpin, Zovirax ...).

Fungal corneal ulcers: need to use specific antifungal drugs (Natacin, Ketoconazole, Sporal, ...). Dot Lugol 5% ulcers.

Prevention of pupil adhesion to the front of the vitreous: apply Atropin 1-4%, if the pupil is not dilated, the combination of Atropine 1% and Adrenalin 0.1% is injected under the conjunctiva 4 points close to the edge of the cornea with the dose 0.1ml.

Corneal nutrition: Apply oil A and take vitamins A, CB2.

If the cornea threatens perforation or perforation, it is necessary to give antihypertensive drugs (oral acetazolamide).

Pain relief, sedation.

Contraindicated to use corticosteroids.

Surgical treatment

Corneal transplant.

Washroom latex.

Removing the eyeball, taking internal eye: when the disease progresses, medical treatment does not result.


It is necessary to educate patients about awareness of the use of labor protection equipment.

Need to treat eye diseases that can cause corneal ulcers:


Treatment of dry eyes caused by lack of vitamin A.

Eyecare in cases of nerve paralysis VII, III, V.

It is necessary to treat systemic diseases that are at risk of causing corneal ulcers.