corneal fistula

Introduction

Introduction Sometimes the cornea is not completely healed after perforation of the cornea. In the center of the white spot on the ruin, a small, dark black bulge appears, while the anterior chamber disappears and the eyeball becomes soft. At this time, the eyeball immediately compensates, increasing the water production to maintain the normal hardness of the eye. If this bulge is blocked by a new film, the increased aqueous humor production will inevitably lead to a gradual increase in intraocular pressure causing secondary glaucoma. If the intraocular pressure continues to increase, it can cause symptoms of acute glaucoma, and this layer of film breaks through, the symptoms disappear, and the eyeballs become soft again. However, soon after the pupil was closed by the new film, the eye pressure increased again. Repeatedly repeated, the end of the eye due to violent bacterial infection, endophthalmitis, full eye pus or intraocular hemorrhage, and finally the eyeball atrophy. It is also due to the long-term softening of the eyeball, flattening of the cornea, opacity of the lens, and even the retinal detachment. The corneal fistula is not a fistula, but a loose tissue is embedded in the corneal pores, and the aqueous humor seeps out from the crack. The corneal ridge is most likely to occur in patients with a pupillary edge that is incarcerated in the perforated area of the cornea. The aqueous humor often exudes along the edge of the pupil, and the epithelial cells are not easily repaired. It can be seen that the main symptoms of corneal spasm are the deep black bulge on the surface of the cornea, the disappearance of the anterior chamber and the softening of the eyeball. In addition, it can also be proved by fluorescent staining.

Cause

Cause

1. External causes: Most of the corneal infections caused by external causes have two conditions:

a. Damage and shedding of corneal epithelial cells.

b. Simultaneous infection. Infectious corneal ulcers are more likely to occur only if both conditions are available.

2. Internal cause: refers to an intrinsic disease from the whole body.

There is no blood vessel in the cornea, so acute infectious diseases are not easy to invade the cornea. However, the corneal tissue participates in the systemic immune response, although the degree of immune response is lower than that of other tissues, but because it has no blood vessels and the metabolism is slow, the change of this immune response lasts for a long time, and the cornea is in a long time. It is in a sensitive state, so that allergic diseases such as vesicular keratitis are prone to occur.

3. Due to the spread of adjacent tissues, due to embryonic homology and anatomical continuity, the disease that spreads to the corneal epithelium mostly comes from the conjunctiva, such as severe conjunctivitis and superficial keratitis.

Examine

an examination

Related inspection

Corneal examination of the eye and eyelid ultrasound

1. History: The cornea is often accompanied by a history of traumatic diseases such as plant and soil, and long-term application of glucocorticoids and broad-spectrum antibiotics to the eyes and the whole body.

2. Typical clinical manifestations: mainly typical signs of the eye.

3. According to the laboratory examination and histopathological examination results can help the diagnosis.

Diagnosis

Differential diagnosis

Severe FK, especially Fusarium keratitis, due to rapid onset, often combined with anterior chamber empyema and corneal perforation, often misdiagnosed as Pseudomonas aeruginosa corneal ulcer, the main identification is the former with typical mycelium By the lesion, the latter ulcer is pale green, the surface is moist and shiny (consisting of viscous necrotic tissue and secretions), the edge is smooth, and there is an infiltration edema between the normal cornea. In addition, the disease is very similar to the clinical manifestations of the herpes simplex keratitis (necrotic keratitis) and the late discoid ovarian abscess of the Acanthamoeba keratitis, which can be identified by medical history and laboratory diagnosis.

It is also often necessary to identify with bacterial keratitis and viral keratitis.

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