Entropion is an anomaly of the location of the eyelid, in which the conjunctiva and cornea are injured by its ciliated edge. Clinically, the disease is manifested by the sensation of a foreign body, lacrimation, photophobia and painful sensations that increase when blinking or closing the eyes. The diagnosis is established on the basis of anamnesis, objective examination, visometry and biomicroscopy. Specific treatment is reduced to blepharoplasty. Conservative therapy is effective only in the early stages and includes the use of artificial tear preparations, gels and ointments to moisturize the conjunctiva and cornea.
Entropion is a disease characterized by an incorrect position of the eyelid, in which the eyelashes are turned to the eyeball. In ophthalmology, the inversion of the lower eyelid is much more common than the inversion of the upper eyelid. The disease is common among the elderly. There is no racial or sexual predisposition. The congenital form occurs only in combination with other genetic abnormalities in Larsen syndrome or against the background of congenital microphthalmia. Pathology rarely leads to a total decrease in visual acuity and disability of patients, but causes daily discomfort and causes a pronounced cosmetic defect. Simultaneously with the increase in the number of patients with drug hypersensitivity, entropion in Lyell’s syndrome and Stevens-Johnson syndrome is becoming increasingly widespread.
The most common cause of entropion in old age is involutional degeneration of muscle and connective tissue. After 60 years, orbital fat accumulates intensively, and the skin loses its elastic properties, so even the usual closing of the eyes can provoke an abnormal location of the eyelid. Congenital inversion is a consequence of spastic contraction of the circular muscle of the eye or cartilage deformation. With a spasm of the circular muscle, the ciliated edge shifts towards the eyeball. Horizontal deformation occurs when the Riolan beam spasms. Normally, this anatomical structure, due to its high tone, ensures a tight fit of the eyelid, spastic contraction further enhances the effect and provokes a twist. Abnormal hypertonus of the ciliary muscle is more common in early childhood. Congenital entropion is detected in combination with other manifestations (hypertelorism, multiple dislocations, skeletal disorders) of Larsen syndrome, more than 5 stigmas of dysembriogenesis indicate the genetic nature of the disease. Also, the eyelid can be wrapped inside with microphthalmos.
Acquired inversion develops against the background of toxic epidermal necrolysis or malignant exudative erythema, which in most cases become a manifestation of drug hypersensitivity. Chronic conjunctivitis is one of the causes of periodic irritation of the Riolan muscle bundle, provoking its spastic contractions. Pronounced spasm leads to the eversion of cartilage towards the eyeball. In addition, the role of etiological entropion factors may be eyelid scars, conjunctival damage as a result of mechanical eye injury, chemical or thermal burn.
There are cicatricial, involutional (spastic, atonic) and congenital entropion. The clinical picture of entropion in all forms has similar manifestations, the features of the course are determined by the type of pathology. Constant rubbing of eyelashes becomes a trigger factor for the development of all symptoms of the disease. When the ciliated edge of the eyelid comes into contact with the conjunctiva, its irritation increases, followed by edema, pronounced hyperemia and microscopic damage. Most patients have a feeling of a foreign body in the eye. Another early symptom is lacrimation, which develops as a result of mechanical friction of the eyelashes, and due to a violation of the normal path of tear fluid outflow. Corneal damage is indicated by the appearance of photophobia. Symptoms of the disease increase when blinking and closing your eyes.
Patients with scarring of the eyelid indicate traumatic injuries or burns, less often – a history of conjunctivitis. These factors cause scarring between the conjunctiva and the eyelid. The disease develops gradually. Usually the eyelid takes the form of a convex arch in front, and the ciliated edge is wrapped inside and constantly injures the eye. The severity of clinical manifestations depends on the location and size of the scar, even small defects lead to severe discomfort.
The main difference between the involution entropion and other forms is the absence of scarring. With spastic inversion at the onset of the disease, patients can independently return the ciliated edge to its normal position. Symptoms worsen with intense closing of the eyes. The long course of pathology leads to the formation of a roller-like seal of the circular eye muscle in the tarsal plate area. A feature of the atonic inversion is that the lower edge of the eyelid prolapses forward, while the upper one faces the eyeball. Clinically, the disease resembles trichiasis.
Entropion in Stevens-Johnson and Lyell syndromes is accompanied by pronounced blepharospasm and photophobia. The symptoms are caused by dysplasia of the epidermis of the eyelids with its subsequent increase on the posterior rib and the surface of the eyelids. Severe forms of the disease lead to scarring of the bulbar and palpebral conjunctiva, complete overgrowth of tear points is possible. The progression of entropion causes the development of secondary chronic conjunctivitis. Subsequently, when the cornea is damaged, keratopathy develops, point erosive defects appear. In the absence of timely treatment, minimal dystrophic manifestations are replaced by ulcerative keratitis and the formation of a cataract. The ingrowth of newly formed vessels into the cornea leads to a decrease in visual acuity.
The diagnosis of entropion is based on information about the anamnesis of life and disease, data from objective examination, visometry and biomicroscopy. Anamnestic data may indicate injuries, burns of the eyelids or drug hypersensitivity. In some cases, burdened heredity is revealed by the abnormal location of the eyelids. An external examination determines entropion towards the eyeball, hyperemia and swelling of the conjunctiva, pronounced lacrimation. The skin around the eyes is irritated, hyperemic.
During biomicroscopy of the eye, erosive defects of the cornea, damage to the bulbar conjunctiva, and fusion between the bulbar and palpebral sections are visualized. Biomicroscopy with fluorescein is recommended for clearer visualization of defects. The tear film is usually unstable, which is confirmed by an additional Norn test. Visual acuity is determined by the method of visiometry. A decrease in this indicator occurs only with intensive ingrowth of newly formed vessels and with entropion, complicated by clouding of the cornea in the form of an eyesore.
Specific treatment of eyelid inversion is reduced to blepharoplasty. In the preoperative period, the use of special adhesive bandages for the prevention of intraoperative complications is shown. In the early stages of the disease, it is recommended to apply U-shaped sutures from the area of the skin under the ciliated edge to the lower parts of the tarsal plate. These measures ensure the correct anatomical position of the eyelid, the effect persists for 3-4 months. The technique of surgical intervention in spastic entropion involves a small incision of the circular muscle of the eye in the pre-parsal region or complete excision of the muscle bundle of Riolan. With the atonic form, it is necessary to remove the triangular section of the tarsal plate together with the adjacent layers of muscles and skin. This technique ensures that the eyelid is fixed in a horizontal position.
With scar entropion, a small part of the mucous membrane should be transplanted into the area of the posterior rib of the eyelid or intercostal zone (Sapezhko method). The technique of surgical intervention according to the Uis is ineffective, since in most cases it leads to the re-formation of a keloid scar. To eliminate entropion after injury or burn, it is necessary to reconstruct the posterior plate of the eyelid with subsequent transplantation of its own mucous membrane from the lips to the damaged areas. This technique is also recommended for Lyell and Stevens-Johnson syndromes.
Conservative treatment is based on the daily use of artificial tear preparations, gels containing dexpanthenol, and eye ointments at night (alternating thiamine ointment with antibacterial agents). In case of spastic entropion, instillation of topical anesthetics is recommended in the early stages. Drug therapy is unable to eliminate the organic pathology of the eyelids and is used only in the early stages to reduce the clinical manifestations of pathology.
Prognosis and prevention
The prognosis for entropion in the case of timely treatment is favorable for life and work capacity. Only irreversible damage to the cornea (formation of a cataract, ingrowth of newly formed vessels) leads to a decrease in visual acuity. With entropion formed as a result of toxic epidermal necrolysis or malignant exudative erythema, the prognosis is doubtful.
No specific measures have been developed to prevent entropion. To prevent further progression of pathology, it is necessary to observe hygiene of the eyelids, to carry out their timely moistening together with moistening of the conjunctiva and cornea. In the early stages of the disease, an ophthalmologist’s examination is indicated with a frequency of 2 times a year. An obligatory stage of the examination is the biomicroscopy of the eyes.